Search results for " Type II"

showing 10 items of 542 documents

Inflammation-Induced Alteration of Astrocyte Mitochondrial Dynamics Requires Autophagy for Mitochondrial Network Maintenance

2013

Accumulating evidence suggests that changes in the metabolic signature of astrocytes underlie their response to neuroinflammation, but how proinflammatory stimuli induce these changes is poorly understood. By monitoring astrocytes following acute cortical injury, we identified a differential and region-specific remodeling of their mitochondrial network: while astrocytes within the penumbra of the lesion undergo mitochondrial elongation, those located in the core-the area invaded by proinflammatory cells-experience transient mitochondrial fragmentation. In brain slices, proinflammatory stimuli reproduced localized changes in mitochondrial dynamics, favoring fission over fusion. This effect w…

MaleLipopolysaccharidesPhysiologyDnm1l protein mouseInterleukin-1betaNitric Oxide Synthase Type IIMitochondrionAstrocytes/metabolismMitochondrial DynamicsAutophagy-Related Protein 7Mice0302 clinical medicinemetabolism [Reactive Oxygen Species]PhosphorylationCells Culturedcytology [Astrocytes]0303 health sciencesmetabolism [Inflammation]metabolism [Astrocytes]Inflammation/metabolismCytokines/metabolismdrug effects [Mitochondria]Mitochondria/drug effectsMitochondriaCell biologyAstrocytes/drug effectsmedicine.anatomical_structureMicrotubule-Associated Proteins/metabolismPhosphorylationCytokinesmetabolism [Dynamins]Nitric Oxide Synthase Type II/metabolismMicrotubule-Associated ProteinsAstrocytegenetics [Microtubule-Associated Proteins]DynaminsProgrammed cell deathAstrocytes/cytologydrug effects [Astrocytes]Mice TransgenicBiologypharmacology [Interferon-gamma]Proinflammatory cytokine03 medical and health sciencesInterferon-gammametabolism [Interleukin-1beta]reactive astrocytesReactive Oxygen Species/metabolismddc:570Mitochondria/metabolismtoxicity [Lipopolysaccharides]medicineAutophagyAnimalsAutophagy-Related Protein 7Molecular BiologyNeuroinflammation030304 developmental biologypathology [Inflammation]Dynamins/metabolismInflammationdrug effects [Mitochondrial Dynamics]Autophagymetabolism [Cytokines]Interferon-gamma/pharmacologyCell Biologymetabolism [Microtubule-Associated Proteins]Microtubule-Associated Proteins/geneticsMitochondrial Dynamics/drug effectsmetabolism [Mitochondria]metabolism [Nitric Oxide Synthase Type II]Mice Inbred C57BLLipopolysaccharides/toxicityAtg7 protein mouseAstrocytesInterleukin-1beta/metabolismReactive Oxygen Species030217 neurology & neurosurgeryInflammation/pathologyCell Metabolism
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Immunohistochemical characteristics of the Implant-Hosted Bon : preliminary findings of 9 mandibular cores

2010

Objectives: The aims of this study were to investigate the biochemical topography of collagen types I and III and to describe the histological structure at the implant placement site to determine the clinical significance of the findings and their possible interaction with bone healing around dental implants. Material and Methods: Bone cores from 9 mandibles were taken from the site of placement of dental implants. The reliable technique for rapid preparation of fresh-frozen undecalcified bone sections and the indirect immunofluorescent technique as an immunohistochemical procedure were applied. All sections were viewed under U.V light. For comparative purposes the tissue blocks remaining w…

MaleMature BoneDentistryBone healingMandibleBiologyCollagen Type ICollagen Type IIIYoung AdultOsseointegrationHumansGeneral DentistryAgedDental Implantsbusiness.industryHistologyMiddle Aged:CIENCIAS MÉDICAS [UNESCO]ImmunohistochemistryStainingImplant placementCollagen Type IIIOtorhinolaryngologyUNESCO::CIENCIAS MÉDICASImmunohistochemistrySurgeryFemaleImplantbusiness
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Putative role of nitric oxide synthase isoforms in the changes of nitric oxide concentration in rat brain cortex and cerebellum following sevoflurane…

2005

We have previously observed an increase in nitric oxide (NO) content in rat brain cortex following halothane, sevoflurane or isoflurane anaesthesia. This study was undertaken in order to determine whether isoform-specific nitric oxide synthase (NOS) inhibitors and inducers could modify these increases in NO contents. Rats were subjected to isoflurane and sevoflurane anaesthesia with concomitant administration of neuronal nitric oxide synthase (nNOS) inhibitor 7-Nitro-indazole (7-NI), inducible nitric oxide synthase (iNOS) inhibitor 2-amino-5,6-dihydro-6-methyl-4H-1,3-thiazine (AMT) or lipopolysaccharide. NO concentration in different organs was measured by electron paramagnetic resonance (E…

MaleMethyl Ethersmedicine.medical_specialtyCentral nervous systemNitric Oxide Synthase Type IINerve Tissue ProteinsNitric Oxide Synthase Type INitric OxideSevofluraneNitric oxidechemistry.chemical_compoundSevofluraneInternal medicineCortex (anatomy)CerebellummedicineAnimalsRats WistarPharmacologyCerebral CortexbiologyIsofluraneRecombinant ProteinsRatsNitric oxide synthaseIsoenzymesmedicine.anatomical_structureEndocrinologyIsofluranechemistryBiochemistryCerebral cortexAnesthetics Inhalationbiology.proteinHalothaneNitric Oxide Synthasemedicine.drugEuropean journal of pharmacology
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Influence of a Brief Episode of Anesthesia during the Induction of Experimental Brain Trauma on Secondary Brain Damage and Inflammation

2011

It is unclear whether a single, brief, 15-minute episode of background anesthesia already modulates delayed secondary processes after experimental brain injury. Therefore, this study was designed to characterize three anesthesia protocols for their effect on molecular and histological study endpoints. Mice were randomly separated into groups that received sevoflurane (sevo), isoflurane (iso) or an intraperitoneal anesthetic combination (midazolam, fentanyl and medetomidine; comb) prior to traumatic brain injury (controlled cortical impact, CCI; 8 m/s, 1 mm impact depth, 3 mm diameter). Twenty-four hours after insult, histological brain damage, neurological function (via neurological severit…

MaleMouseGeneral AnesthesiaNitric Oxide Synthase Type IIFentanylMiceAnesthesiologyAnesthesiaNeurosurgical CareMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionMicrofilament ProteinsQRAnimal ModelsSurvival RateHead InjuryNeurologyNeurointensive CareAnesthesiaMedicineRegional Anesthesiamedicine.symptomResearch Articlemedicine.drugTraumatic brain injuryScienceBlotting WesternImmunologyBrain damageAnesthetic MechanismsMicrobiologySevofluraneModel OrganismsNeuropharmacologymedicineAnimalsRNA MessengerBiologyInflammationInterleukin-6business.industryCalcium-Binding ProteinsImmunityBrain Contusionmedicine.diseaseMice Inbred C57BLIsofluraneCyclooxygenase 2Brain InjuriesAnestheticMidazolamClinical ImmunologybusinessPLoS ONE
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Intramural delivery of Sirolimus prevents vascular remodeling following balloon injury

2005

Abstract Objective. Several studies have demonstrated that Sirolimus-eluting stents reduce restenosis in patients with coronary artery disease. Here, we tested whether direct delivery of Sirolimus into the vessel wall during balloon angioplasty can modify vascular remodeling over several weeks. Methods and Results. During angioplasty of the rabbit iliac artery we administered an intramural infusion of Sirolimus or its vehicle directly through a balloon catheter into the vessel wall. After 3 weeks neointimal formation was decreased (0.71 ± 0.1 vs. 1.4 ± 0.12 intima/media ratio), and this process was attributed to the inhibitory properties of Sirolimus on ECM deposition and smooth muscle cell…

MaleNeointimaPathologymedicine.medical_specialtymedicine.medical_treatmentBiophysicsBalloonIliac ArteryBiochemistryMuscle Smooth VascularArticleAnalytical ChemistryRestenosisAngioplastymedicineAnimalsVimentincardiovascular diseasesMolecular BiologyCell ProliferationSirolimusbiologybusiness.industryGraft Occlusion VascularBalloon catheterequipment and suppliesmedicine.diseaseTunica intimaActinsExtracellular MatrixFibronectinsCollagen Type IIImedicine.anatomical_structurealpha 1-AntitrypsinSirolimuscardiovascular systembiology.proteinLamininRabbitsTunica IntimabusinessElastinAngioplasty Balloonmedicine.drugBiochimica et Biophysica Acta (BBA) - Proteins and Proteomics
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Antiatherosclerotic Effects of Small-Molecular-Weight Compounds Enhancing Endothelial Nitric-Oxide Synthase (eNOS) Expression and Preventing eNOS Unc…

2008

Many cardiovascular diseases are associated with reduced levels of bioactive nitric oxide (NO) and an uncoupling of oxygen reduction from NO synthesis in endothelial NO synthase (eNOS uncoupling). In human endothelial EA.hy 926 cells, two small-molecular-weight compounds with related structures, 4-fluoro-N-indan-2-yl-benzamide (CAS no. 291756-32-6; empirical formula C16H14FNO; AVE9488) and 2,2-difluoro-benzo[1,3]dioxole-5-carboxylic acid indan-2-ylamide (CAS no. 450348-85-3; empirical formula C17H13F2NO3; AVE3085), enhanced eNOS promoter activity in a concentration-dependent manner; with the responsible cis-element localized within the proximal 263 base pairs of the promoter region. RNA int…

MaleNeointimamedicine.medical_specialtyNitric Oxide Synthase Type IIINitric Oxide Synthase Type IINitric OxideProtective AgentsUmbilical veinCell LineNitric oxideMicechemistry.chemical_compoundApolipoproteins EEnosInternal medicinemedicineAnimalsHumansBenzodioxolesRNA MessengerAortaMice KnockoutPharmacologychemistry.chemical_classificationSp1 transcription factorReactive oxygen speciesGene knockdownbiologyEndothelial CellsAtherosclerosisbiology.organism_classificationVasoprotectiveMice Inbred C57BLMolecular WeightEndocrinologychemistryBenzamidesIndansMolecular MedicineJournal of Pharmacology and Experimental Therapeutics
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Modulatory effect of bolinaquinone, a marine sesquiterpenoid, on acute and chronic inflammatory processes

2002

The marine metabolite bolinaquinone is a novel inhibitor of secretory phospholipase A(2) (sPLA(2)), with a potency on the human synovial enzyme (group II) higher than that of manoalide. This activity on the sPLA(2) was confirmed in vivo in the 8-h zymosan rat air pouch on the secretory enzyme accumulation in the pouch exudate. Additionally, bolinaquinone decreased potently the synthesis and release of leukotriene B(4) (LTB(4)) in calcimycin (A23187)-stimulated human neutrophils as a consequence of the inhibition of 5-lipoxygenase activity, as well as PGE(2) and NO production on zymosan-stimulated mouse peritoneal macrophages. This compound exerted anti-inflammatory effects by topical and or…

MaleNeutrophilsGene ExpressionNitric Oxide Synthase Type IIMarine BiologyPharmacologyBone resorptionMicechemistry.chemical_compoundManoalideIn vivoEdemamedicineAnimalsEdemaHumansRats WistarPharmacologybiologyZymosanMembrane ProteinsArthritis ExperimentalPoriferaRatsCarrageenanIsoenzymesRadiographyNitric oxide synthaseDisease Models AnimalchemistryCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesImmunologyMacrophages Peritonealbiology.proteinMolecular MedicineTumor necrosis factor alphaNitric Oxide Synthasemedicine.symptomSesquiterpenes
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Neuroprotective Properties of Mildronate, a Small Molecule, in a Rat Model of Parkinson’s Disease

2010

Previously, we have found that mildronate [3-(2,2,2-trimethylhydrazinium) propionate dihydrate], a small molecule with charged nitrogen and oxygen atoms, protects mitochondrial metabolism that is altered by inhibitors of complex I and has neuroprotective effects in an azidothymidine-neurotoxicity mouse model. In the present study, we investigated the effects of mildronate in a rat model of Parkinson’s disease (PD) that was generated via a unilateral intrastriatal injection of the neurotoxin 6-hydroxydopamine (6‑OHDA). We assessed the expression of cell biomarkers that are involved in signaling cascades and provide neural and glial integration: the neuronal marker TH (tyrosine hydroxylase); …

MaleNitric Oxide Synthase Type IIlcsh:ChemistryUbiquitinNeurotoxinlcsh:QH301-705.5Receptor Notch3SpectroscopyNeuronsReceptors NotchbiologyGlial fibrillary acidic proteinMicrofilament ProteinsGeneral MedicineComputer Science ApplicationsCell biologySubstantia NigraNitric oxide synthaseNeuroprotective Agentsmedicine.anatomical_structureBiochemistryNeurogliaNeurogliaMethylhydrazinesneuroimmunological biomarkersTyrosine 3-Monooxygenasesmall moleculeSubstantia nigraParkinson’s disease; 6-OHDA model; neuroimmunological biomarkers; mildronate; small moleculeNeuroprotectionArticleCatalysisInorganic ChemistryGlial Fibrillary Acidic ProteinmedicineAnimalsParkinson Disease SecondaryRats WistarPhysical and Theoretical ChemistryOxidopamineMolecular BiologyTyrosine hydroxylase6-OHDA modelCalcium-Binding ProteinsmildronateOrganic ChemistryCorpus StriatumRatslcsh:Biology (General)lcsh:QD1-999nervous systemParkinson’s diseasebiology.proteinBiomarkersInternational Journal of Molecular Sciences
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Redox Regulation of Dihydrofolate Reductase: Friend or Troublemaker?

2015

Oxidative stress is a hallmark of cardiovascular diseases1 and a major contributor to vascular dysfunction.2 On the basis on recent concepts, vascular oxidative stress is caused mainly by infiltrating inflammatory cells such as monocytes/macrophages or leucocytes,3,4 producing so-called kindling radicals that lead to the activation of secondary, vascular enzymatic sources of reactive oxygen species (mainly superoxide).2,5 A prominent example is the uncoupled nitric oxide (NO) synthase, which means that an NO-producing antiatherosclerotic enzyme is getting switched to a superoxide-producing proatherosclerotic enzyme.2 Molecular mechanisms causing endothelial NO synthase (eNOS) uncoupling or …

MaleNitric Oxide Synthase Type IIIAorta ThoracicOxidative phosphorylationBiologymedicine.disease_causeNitric OxideArticleNitric oxidechemistry.chemical_compoundEnosmedicineAnimalschemistry.chemical_classificationReactive oxygen speciesSuperoxideNitric Oxide Synthase Type IIIEndothelial CellsTetrahydrobiopterinbiology.organism_classificationTetrahydrofolate DehydrogenasechemistryBiochemistryCardiology and Cardiovascular MedicineOxidative stressmedicine.drugArteriosclerosis, thrombosis, and vascular biology
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Nitroglycerin-induced endothelial dysfunction and tolerance involve adverse phosphorylation and S-glutathionylation of endothelial nitric oxide synth…

2011

Continuous administration of nitroglycerin (GTN) causes tolerance and endothelial dysfunction by inducing reactive oxygen species (ROS) production from various enzymatic sources, such as mitochondria, NADPH oxidase, and an uncoupled endothelial nitric oxide synthase (eNOS). In the present study, we tested the effects of type 1 angiotensin (AT(1))-receptor blockade with telmisartan on GTN-induced endothelial dysfunction in particular on eNOS phosphorylation and S-glutathionylation sites and the eNOS cofactor synthesizing enzyme GTP-cyclohydrolase I.Wistar rats were treated with telmisartan (2.7 or 8 mg/kg per day PO for 10 days) and with GTN (50 mg/kg per day SC for 3 days). Aortic eNOS phos…

MaleNitric Oxide Synthase Type IIIPhysiologyVasodilator AgentsPharmacologyBenzoatesCell LineNitroglycerinmedicineAnimalsHumansTelmisartanEnzyme InhibitorsPhosphorylationRats WistarS-GlutathionylationEndothelial dysfunctionGTP CyclohydrolaseBeneficial effectsNitroglycerinPharmacologyAngiotensin II receptor type 1Dose-Response Relationship DrugEndothelial nitric oxide synthaseChemistryEndothelial CellsDrug ToleranceAldehyde Dehydrogenasemedicine.diseaseGlutathioneMitochondriaRatsVasodilationOxidative StressTetrahydrofolate DehydrogenaseMolecular MedicinePhosphorylationBenzimidazolesEndothelium VascularTelmisartanReactive Oxygen SpeciesAngiotensin II Type 1 Receptor BlockersProtein Processing Post-Translationalmedicine.drugVascular Pharmacology
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