Search results for "type"

showing 10 items of 10618 documents

Therapeutic considerations in cerebellopontine angle lipomas inducing hemifacial spasm.

2000

Lipoma is a very rare tumour at the cerebellopontine angle. We report a case of incomplete hemifacial spasm, associated with a lipoma involving and compressing both facial and acoustic nerves at their origin in the brainstem. The patient was treated with medical therapy (botulinum toxin A) and surgery. We present a review of the last ten years of the literature, with particular regard to management.

medicine.medical_specialtyNeurologyDermatologyCerebellopontine Angleotorhinolaryngologic diseasesMedicineHumansHemifacial SpasmBotulinum Toxins Type ACerebellar NeoplasmsNeuroradiologymedicine.diagnostic_testbusiness.industryMagnetic resonance imagingGeneral MedicineLipomaMiddle Agedmedicine.diseaseCerebellopontine angleBotulinum toxinMagnetic Resonance ImagingSurgerybody regionsstomatognathic diseasesPsychiatry and Mental healthTreatment OutcomeNeuromuscular AgentsFemaleNeurology (clinical)NeurosurgeryLipomabusinessmedicine.drugHemifacial spasmNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
researchProduct

Baseline data from a prospective international disease registry for Niemann-Pick disease type C

2011

medicine.medical_specialtyNiemann–Pick disease type Cbusiness.industryEndocrinology Diabetes and MetabolismBaseline datamedicine.diseaseBiochemistryEndocrinologyDisease registryInternal medicineGeneticsmedicinebusinessMolecular BiologyMolecular Genetics and Metabolism
researchProduct

Differential blockade by nifedipine and ω-conotoxin GVIA of α1- and β1-adrenoceptor-controlled calcium channels on motor nerve terminals of the rat

1990

Electrically evoked release of [3H]acetylcholine ([3H]ACh) from the rat phrenic nerve and its facilitation by stimulation of presynaptic alpha 1- and beta 1-adrenoceptors were investigated in the absence and presence of nifedipine and omega-conotoxin GVIA. Both calcium channel antagonists did not modify electrically evoked [3H]ACh release, but selectively blocked the effect triggered by both facilitatory adrenergic receptors. The increase in [3H]ACh release mediated via beta 1-adrenoceptor activation was abolished by low concentrations (1 nM) of omega-conotoxin GVIA, whereas nifedipine (100 nM) abolished the facilitatory effect mediated via alpha 1-adrenoceptor stimulation. Therefore, the b…

medicine.medical_specialtyNifedipineNeuromuscular JunctionMollusk Venomschemistry.chemical_elementIn Vitro TechniquesCalciumN-type calcium channelMotor Endplatecomplex mixturesNeuromuscular junctionNifedipineomega-Conotoxin GVIAInternal medicinemedicineAnimalsL-type calcium channelVoltage-dependent calcium channelChemistryGeneral NeuroscienceCalcium channelRats Inbred StrainsCalcium Channel BlockersAcetylcholineElectric StimulationRatsReceptors AdrenergicPhrenic Nervemedicine.anatomical_structureEndocrinologyCalcium ChannelsAcetylcholinemedicine.drugNeuroscience Letters
researchProduct

NADPH Oxidase Accounts for Enhanced Superoxide Production and Impaired Endothelium-Dependent Smooth Muscle Relaxation in BKβ1 −/− Mice

2006

Objective— Nitric oxide (NO)-induced vasorelaxation involves activation of large conductance Ca 2+ -activated K + channels (BK). A regulatory BKβ1 subunit confers Ca 2+ , voltage, and NO/cGMP sensitivity to the BK channel. We investigated whether endothelial function and NO/cGMP signaling is affected by a deletion of the β1-subunit. Methods and Results— Vascular superoxide in BKβ1 −/− was measured using the fluorescent dye hydroethidine and lucigenin-enhanced chemiluminescence. Vascular NO formation was analyzed using electron paramagnetic resonance (EPR), expression of NADPH oxidase subunits, the endothelial NO synthase (eNOS), the soluble guanylyl cyclase (sGC), as well as the activity a…

medicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumAorta ThoracicNitric OxideMuscle Smooth VascularNitric oxideMicechemistry.chemical_compoundSuperoxidesInternal medicineCyclic GMP-Dependent Protein KinasesmedicineAnimalsHumansProtein IsoformsNADH NADPH OxidoreductasesLarge-Conductance Calcium-Activated Potassium ChannelsMice KnockoutNADPH oxidasebiologySuperoxideMicrofilament ProteinsNADPH OxidasesPhosphoproteinsMolecular biologyVasodilationEndocrinologymedicine.anatomical_structurechemistryGuanylate CyclaseNAD(P)H oxidaseNOX1ApocyninNADPH Oxidase 1biology.proteinEndothelium VascularCardiology and Cardiovascular MedicineSoluble guanylyl cyclaseCell Adhesion MoleculesSignal TransductionArteriosclerosis, Thrombosis, and Vascular Biology
researchProduct

Nitric oxide synthases: regulation and function

2011

Nitric oxide (NO), the smallest signalling molecule known, is produced by three isoforms of NO synthase (NOS; EC 1.14.13.39). They all utilize l-arginine and molecular oxygen as substrates and require the cofactors reduced nicotinamide-adenine-dinucleotide phosphate (NADPH), flavin adenine dinucleotide (FAD), flavin mononucleotide (FMN), and (6R-)5,6,7,8-tetrahydrobiopterin (BH(4)). All NOS bind calmodulin and contain haem. Neuronal NOS (nNOS, NOS I) is constitutively expressed in central and peripheral neurons and some other cell types. Its functions include synaptic plasticity in the central nervous system (CNS), central regulation of blood pressure, smooth muscle relaxation, and vasodila…

medicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumNeovascularization PhysiologicNitric Oxide Synthase Type IIVasodilationNitric Oxide Synthase Type IReviewArginineNitric OxideEndothelial NOSNitric oxideMicechemistry.chemical_compoundEnosInternal medicineRenin–angiotensin systemmedicineAnimalsHumansbiologybusiness.industryCardiovascular AgentsGenetic Therapybiology.organism_classificationBiopterinIsoenzymesNitric oxide synthaseEndocrinologymedicine.anatomical_structurechemistryCardiovascular DiseasescGMP-specific phosphodiesterase type 5biology.proteinEndothelium VascularHydroxymethylglutaryl-CoA Reductase InhibitorsNitric Oxide SynthaseCardiology and Cardiovascular MedicinebusinessEuropean Heart Journal
researchProduct

Nitric oxide in the pathogenesis of vascular disease

2000

Nitric oxide (NO) is synthesized by at least three distinct isoforms of NO synthase (NOS). Their substrate and cofactor requirements are very similar. All three isoforms have some implications, physiological or pathophysiological, in the cardiovascular system. The endothelial NOS III is physiologically important for vascular homeostasis, keeping the vasculature dilated, protecting the intima from platelet aggregates and leukocyte adhesion, and preventing smooth muscle proliferation. Central and peripheral neuronal NOS I may also contribute to blood pressure regulation. Vascular disease associated with hypercholesterolaemia, diabetes, and hypertension is characterized by endothelial dysfunct…

medicine.medical_specialtyNitric Oxide Synthase Type IIIHypercholesterolemiaNitric Oxide Synthase Type IIVasodilationNitric OxideEndothelial NOSPathology and Forensic MedicineNitric oxidePathogenesischemistry.chemical_compoundInternal medicineHumansMedicineEndothelial dysfunctionbiologybusiness.industryVascular diseasemedicine.diseaseNitric oxide synthaseEndothelial stem cellOxidative StressEndocrinologychemistryCardiovascular DiseasesHypertensionbiology.proteinEndothelium VascularNitric Oxide SynthasebusinessDiabetic AngiopathiesThe Journal of Pathology
researchProduct

eNOS Uncoupling in Cardiovascular Diseases - the Role of Oxidative Stress and Inflammation

2013

Many cardiovascular diseases and drug-induced complications are associated with - or even based on - an imbalance between the formation of reactive oxygen and nitrogen species (RONS) and antioxidant enzymes catalyzing the break-down of these harmful oxidants. According to the “kindling radical” hypothesis, the formation of RONS may trigger in certain conditions the activation of additional sources of RONS. According to recent reports, vascular dysfunction in general and cardiovascular complications such as hypertension, atherosclerosis and coronary artery diseases may be connected to inflammatory processes. The present review is focusing on the uncoupling of endothelial nitric oxide synthas…

medicine.medical_specialtyNitric Oxide Synthase Type IIIInflammationOxidative phosphorylationmedicine.disease_causechemistry.chemical_compoundEnosInternal medicineDrug DiscoverymedicineHumansEndothelial dysfunctionInflammationPharmacologybiologyTetrahydrobiopterinbiology.organism_classificationmedicine.diseaseReview articleOxidative StressEndocrinologychemistryCardiovascular Diseasesmedicine.symptomAsymmetric dimethylarginineOxidative stressmedicine.drugCurrent Pharmaceutical Design
researchProduct

Dexamethasone suppresses eNOS and CAT-1 and induces oxidative stress in mouse resistance arterioles

2004

Long-term treatment with glucocorticoids is associated with mild to moderate hypertension. We reported previously that downregulation of endothelial NO synthase (eNOS) expression and activity is likely to contribute to this increase in blood pressure. In the present study, we tested the effects of dexamethasone on the vasodilation of microvascular arterioles using implanted dorsal skin-fold chambers in anesthetized C57BL/6J mice. Experiments were performed on control mice or on mice treated with dexamethasone (0.1–3 mg/kg of body wt). Endothelium-dependent vasodilation in response to ACh (0.1–10 μM) was reduced by dexamethasone in a dose-dependent fashion. Comparable inhibition was seen in …

medicine.medical_specialtyNitric Oxide Synthase Type IIIPhysiologyNitric Oxide Synthase Type IIAscorbic AcidBiologyArgininemedicine.disease_causeAntioxidantsDexamethasoneMicrocirculationMiceDownregulation and upregulationEnosArteriolePhysiology (medical)medicine.arteryInternal medicinemedicineAnimalsHumansGlucocorticoidsCells CulturedNitritesDexamethasoneCationic Amino Acid Transporter 1NitratesMyocardiumEndothelial Cellsbiology.organism_classificationAcetylcholineMice Inbred C57BLVasodilationNitric oxide synthaseArteriolesOxidative StressEndocrinologybiology.proteinVascular ResistanceNitric Oxide SynthaseCardiology and Cardiovascular MedicineOxidative stressGlucocorticoidmedicine.drugAmerican Journal of Physiology-Heart and Circulatory Physiology
researchProduct

PPARγ as an indicator of vascular function in an experimental model of metabolic syndrome in rabbits

2021

Abstract Background and aims Underlying mechanisms associated with vascular dysfunction in metabolic syndrome (MetS) remain unclear and can even vary from one vascular bed to another. Methods In this study, MetS was induced by a high-fat, high-sucrose diet, and after 28 weeks, aorta and renal arteries were removed and used for isometric recording of tension in organ baths, protein expression by Western blot, and histological analysis to assess the presence of atherosclerosis. Results MetS induced a mild hypertension, pre-diabetes, central obesity and dyslipidaemia. Our results indicated that MetS did not change the contractile response in either the aorta or renal artery. Conversely, vasodi…

medicine.medical_specialtyNitric Oxide Synthase Type IIIVasodilationmedicine.disease_causeEnosmedicine.arteryInternal medicineAnimalsMedicineRenal arteryProtein kinase BSistema cardiovascularMetabolic SyndromeAortaDiabetisbiologybusiness.industryModels Theoreticalmedicine.diseasebiology.organism_classificationPPAR gammaVasodilationEndocrinologyEndothelium VascularRabbitsSodium nitroprussideMetabolic syndromeCardiology and Cardiovascular MedicinebusinessProto-Oncogene Proteins c-aktOxidative stressmedicine.drugAtherosclerosis
researchProduct

Genotype 1 Relapsers and Non‐Responders

2011

medicine.medical_specialtyNon respondersbusiness.industryInternal medicineGenotypeMedicinebusinessGastroenterologyAdvanced Therapy for Hepatitis C
researchProduct