Search results for " III"

showing 10 items of 562 documents

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
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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
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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
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Esophageal cancer: Clinical Practice Guidelines for diagnosis, treatment and follow-up

2010

Esophageal cancer: Clinical Practice Guidelines for diagnosis, treatment and follow-up M. Stahl, W. Budach, H.-J. Meyer & A. Cervantes On behalf of the ESMO Guidelines Working Group* Department of Medical Oncology and Centre of Palliative Care, Kliniken Essen-Mitte, Essen; Department of Radiation Oncology, University of Dusseldorf, Dusseldorf; Department of Surgery, Stadt Klinikum Solingen, Germany; Department of Hematology and Medical Oncology, INCLIVA, University of Valencia, Valencia, Spain

medicine.medical_specialtyPalliative careEsophageal NeoplasmsMeta-Analysis as TopicRadiation oncologymedicineHumansNeoplasm MetastasisNeoplasm StagingEsophageal diseasebusiness.industryIncidenceGeneral surgeryFollow up studiesCancerHematologyEsophageal cancermedicine.diseasehumanitiesSurgeryEsophagectomyEuropeClinical PracticeTreatment OutcomeClinical Trials Phase III as TopicOncologyDiagnosis treatmentEsophagoscopybusinessFollow-Up StudiesAnnals of Oncology
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Clinical Efficacy of Laquinimod for the Treatment of Multiple Sclerosis; Pooled Analyses from the ALLEGRO and BRAVO Phase III Trials (S01.007)

2012

Objective: The current report provides detail on pooled analyses assessing the effect of laquinimod on relapse, disability, and brain atrophy measures from the recently completed phase III trials ALLEGRO and BRAVO. Background Laquinimod is an oral, CNS acting immunomodulator in development for the treatment of multiple sclerosis. Its impact on disability progression and brain atrophy, two indices of longterm outcome for patients with multiple sclerosis (MS) are being studied in its phase III trials. Design/Methods: MS patients (N=2437) were randomized to laquinimod (n=984) or placebo (n = 1006). In both trials, patients underwent neurological examinations including the Expanded Disability S…

medicine.medical_specialtyPhase iii trialsbusiness.industryRelapse ratePharmacologyClinical trialSafety profilechemistry.chemical_compoundchemistryFamily medicineMedicinemedia_common.cataloged_instanceDisability progressionNeurology (clinical)Clinical efficacyEuropean unionbusinessLaquinimodmedia_commonNeurology
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Estradiol, acting through estrogen receptor alpha, restores dimethylarginine dimethylaminohydrolase activity and nitric oxide production in oxLDL-tre…

2011

Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO) synthase. ADMA accumulation, mainly due to a decreased dimethylarginine dimethylaminohydrolase (DDAH) activity, has been related to the development of cardiovascular diseases. We investigate whether estradiol prevents the changes induced by oxidized low density lipoprotein (oxLDL) on the DDAH/ADMA/NO pathway in human umbilical artery endothelial cells (HUAEC). HUAEC were exposed to estradiol, native LDL (nLDL), oxLDL and their combinations for 24 h. In some experiments, cells were also exposed to the unspecific estrogen receptor (ER) antagonist ICI 182780, the specific ERα antagonist MPP or specific agonists …

medicine.medical_specialtyProtein-Arginine N-MethyltransferasesEndotheliumNitric Oxide Synthase Type IIImedicine.drug_classBlotting WesternArginineNitric OxideBiochemistryUmbilical ArteriesNitric oxideAmidohydrolasesReceptors G-Protein-Coupledchemistry.chemical_compoundEndocrinologyEnosInternal medicinemedicineEstrogen Receptor betaHumansEstrogens Non-SteroidalMolecular BiologyCells CulturedbiologyEstradiolArtèriesProtein StabilityEstrogen AntagonistsEstrogen Receptor alphaEndoteli vascularbiology.organism_classificationNitric oxide synthaseIsoenzymesLipoproteins LDLRepressor Proteinsmedicine.anatomical_structureEndocrinologychemistryReceptors EstrogenEstrogenbiology.proteinlipids (amino acids peptides and proteins)Endothelium VascularAsymmetric dimethylarginineEstrogen receptor alphaGPER
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Biopterin metabolism and eNOS expression during hypoxic pulmonary hypertension in mice.

2013

International audience; Tetrahydrobiopterin (BH$_4$), which fosters the formation of and stabilizes endothelial NO synthase (eNOS) as an active dimer, tightly regulates eNOS coupling / uncoupling. Moreover, studies conducted in genetically-modified models demonstrate that BH$_4$ pulmonary deficiency is a key determinant in the pathogenesis of pulmonary hypertension. The present study thus investigates biopterin metabolism and eNOS expression, as well as the effect of sepiapterin (a precursor of BH$_4$) and eNOS gene deletion, in a mice model of hypoxic pulmonary hypertension. In lungs, chronic hypoxia increased BH$_4$ levels and eNOS expression, without modifying dihydrobiopterin (BH$_2$, t…

medicine.medical_specialtySepiapterinNitric Oxide Synthase Type III[SDV]Life Sciences [q-bio]Hypertension PulmonaryBiopterinlcsh:Medicine[SDV.BC]Life Sciences [q-bio]/Cellular Biology[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]030204 cardiovascular system & hematology03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineEnosRight ventricular hypertrophyDihydrobiopterinInternal medicinemedicine[SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]AnimalsHypoxialcsh:Science[SDV.BC] Life Sciences [q-bio]/Cellular Biology030304 developmental biology0303 health sciencesMultidisciplinarybiologylcsh:RHypoxia (medical)biology.organism_classificationmedicine.diseasePulmonary hypertensionBiopterin[SDV] Life Sciences [q-bio]Disease Models AnimalTetrahydrofolate DehydrogenaseEndocrinologychemistryVentricular pressurelcsh:Qmedicine.symptomResearch ArticlePLoS ONE
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Prevention of Atherosclerosis by Interference with the Vascular Nitric Oxide System

2009

Nitric oxide (NO) produced by endothelial NO synthase (eNOS) represents an anti-atherosclerotic principle. NO bioavailability is decreased in atherosclerosis due to increased NO inactivation by reactive oxygen species and reduced NO synthesis. Various types of vascular pathophysiology are associated with oxidative stress, with NADPH oxidases as the major source of reactive oxygen species. These inactivate NO. Also, oxidative stress is likely to be the main cause for oxidation of the essential NOS cofactor, tetrahydrobiopterin (BH(4)). A lack of BH(4) leads to eNOS uncoupling (i.e., uncoupling of oxygen reduction from NO synthesis in eNOS). Based on these pathomechanisms, the therapeutic pot…

medicine.medical_specialtySepiapterinNitric Oxide Synthase Type IIImedicine.drug_classGTP cyclohydrolase INitric Oxidemedicine.disease_causeRenin inhibitorNitric oxidechemistry.chemical_compoundEnosInternal medicineDrug DiscoverymedicineAnimalsHumansHypolipidemic AgentsPharmacologybiologyArteriesTetrahydrobiopterinAtherosclerosisbiology.organism_classificationNitric oxide synthaseOxidative StressTreatment OutcomeEndocrinologychemistrybiology.proteinOxidative stressSignal Transductionmedicine.drugCurrent Pharmaceutical Design
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Nonreamed flexible locked intramedullary nailing in tibial open fractures

1998

Thirty-nine open unstable tibial shaft fractures were treated with a nonreamed flexible locked intramedullary nail between 1992 and 1995. There were 23 Grade I, 12 Grade II, three Grade IIIA, and one Grade IIIB fractures. The average time of followup assessment was 24 months. The average time to fracture union was 24 weeks. Complications were related in most cases to fractures with highly unstable patterns and extensive soft tissue lesions. There were five (12.5%) delayed unions and one (2.5%) nonunion. Deep infections developed in three (7.7%) patients. One patient required an additional procedure to correct a varus malunion. There were no implant failures. It was concluded that nonreamed …

medicine.medical_specialtybusiness.industryNonunionFracture unionSoft tissueGeneral Medicinemedicine.diseaselaw.inventionSurgeryIntramedullary rodFixation (surgical)lawmedicineOrthopedics and Sports MedicineSurgeryMalunionImplantbusinessGrade IIIa
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Influence of blood sampling from venipunctures and catheter systems on serial determinations of prothrombin activation fragment 1 + 2 and thrombin-an…

1993

To evaluate the influence of different blood sampling techniques on test results of thrombin-antithrombin III complex (TAT) and prothrombin fragment 1 + 2 (F1 + 2) serial determinations were performed. In six groups of nonrandomized patients (ten patients each) the concentrations of the coagulation markers of blood samples from central catheters (internal jugular, caval, Shaldon, pulmonary artery) and peripheral cannulas (17G and 18G) were compared with those of blood samples obtained simultaneously from direct venipunctures of the contralateral arm. Medians and 25th-75th percentiles of TAT and F1 + 2 concentrations of plasmas obtained from central catheters were not different from those ta…

medicine.medical_specialtymedicine.drug_classAntithrombin IIICatheterizationInternal medicinemedicine.arterymedicineHumansProtein PrecursorsVeinBloodlettingHematologyVenipuncturebusiness.industryPROTHROMBIN FRAGMENT 1.2AnticoagulantHematologyGeneral MedicinePeptide FragmentsCatheterBloodmedicine.anatomical_structureAnesthesiaPulmonary arteryProthrombinbusinessPeptide HydrolasesBlood samplingAnnals of Hematology
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