Search results for "Protection"

showing 10 items of 1623 documents

Aspirin protects striatal dopaminergic neurons from neurotoxin-induced degeneration: an in vivo microdialysis study.

2006

The effect of aspirin on dopaminergic neuronal damage induced by in vivo infusion of 1-methyl-4-phenylpiridinium iodide (MPP(+)) and 6-hydroxydopamine (6-OHDA) was studied in rats, using microdialysis. Rat striata were perfused with 1 mM MPP(+) or 6-OHDA for 10 min, causing peak levels of dopamine (DA) in the dialytic fluid, after 40 min. After 24 h, 1 mM MPP(+) was perfused again for 10 min and DA levels measured in the dialytic fluid, as an index of neuronal cell integrity. Pretreatment with Aspidol (lysine acetylsalicylate), 180 mg/kg i.p., 1 h before MPP(+) or 6-OHDA perfusion, did not modify DA extracellular output, on day 1, but restored MPP(+)-induced DA release on day 2, indicating …

MaleMicrodialysisTyrosine 3-MonooxygenaseDopamineMicrodialysisNeurotoxinsPharmacologyNeuroprotectionSettore BIO/09 - FisiologiaRats Sprague-Dawleychemistry.chemical_compoundIn vivoHydroxybenzoatesNeurotoxinAnimalsDrug InteractionsMolecular BiologyChromatography High Pressure LiquidNeuronsAnalysis of VarianceAspirinGeneral NeuroscienceMPTPDopaminergicImmunohistochemistryCorpus StriatumRatsNeuroprotective Agentsnervous systemchemistryAnesthesiaNerve DegenerationNeurology (clinical)Aspirin in vivo microdialysisPerfusionOxidopamineDevelopmental Biology
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Inhibition of myosin light chain kinase reduces brain edema formation after traumatic brain injury.

2010

The role of the endothelial contractile apparatus in the process of brain edema formation after brain trauma is not characterized. Phosphorylation of myosin light chains by myosin light chain kinases (MLCK) activates endothelial contractile elements and results in a rearrangement of the cytoskeleton. This may enhance post-traumatic blood-brain barrier dysfunction. In order to investigate the role of the MLCK on brain edema formation and blood-brain barrier permeability after brain injury, mice were anesthetized and subjected to a controlled cortical impact (CCI). MLCK expression is significantly up-regulated after CCI with a maximum 12 h post-injury. Specific inhibition of MLCK by ML-7 resu…

MaleMyosin light-chain kinaseMyosin Light ChainsTime FactorsEndotheliumIntracranial PressureTraumatic brain injuryCentral nervous systemBrain Edemamacromolecular substancesBrain damageNaphthalenesBlood–brain barrierBiochemistryNeuroprotectionDrug Administration ScheduleFunctional LateralityStatistics NonparametricCerebral edemaCellular and Molecular NeuroscienceMicemedicineAnimalsEnzyme InhibitorsMyosin-Light-Chain KinaseNeurologic Examinationbusiness.industryAzepinesmedicine.diseaseConstrictionCell biologyMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureGene Expression RegulationBlood-Brain BarrierBrain Injuriesmedicine.symptombusinessNeuroscienceEvans BlueJournal of neurochemistry
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Erythropoietin and erythropoietin receptor expression after experimental spinal cord injury encourages therapy by exogenous erythropoietin

2005

OBJECTIVE: Erythropoietin (EPO) is a pleiotropic cytokine originally identified for its role in erythropoiesis. Recent studies have demonstrated that EPO and its receptor (EPO-R) are expressed in the central nervous system, where EPO exerts neuroprotective functions. Because the expression of the EPO and EPO-R network is poorly investigated in the central nervous system, the aim of the present study was to investigate whether the resident EPO and EPO-R network is activated in the injured nervous system. METHODS: A well-standardized model of compressive spinal cord injury in rats was used. EPO and EPO-R expression was determined by immunohistochemical analysis at 8 hours and at 2, 8, and 14 …

MaleNervous systemmedicine.medical_specialtyCentral nervous systemSpinal cord injuryNeuroprotectionErythropoietin receptorRats Sprague-Dawleyhemic and lymphatic diseasesInternal medicineReceptors ErythropoietinmedicineAnimalsSpinal cord injuryErythropoietinSpinal Cord InjuriesNeuronsbusiness.industryNervous tissuemedicine.diseaseAneurysmRecombinant ProteinsNeuroprotectionRatsErythropoietin receptorDisease Models Animalmedicine.anatomical_structureEndocrinologyGene Expression Regulationerythropoietin; erythropoietin receptor; neuroprotection; spinal cord injuryErythropoietinImmunologyNeurogliaSurgeryNeurology (clinical)businessSpinal Cord Compressionmedicine.drug
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Transcription factor gene expression profiling after acute intermittent nicotine treatment in the rat cerebral cortex

2004

Several studies in different in vitro and in vivo models have demonstrated neuroprotective effects of nicotinic receptor agonists and indirect trophic actions of nicotine on brain are suggested from observations describing nicotine as a cognitive enhancer by increasing vigilance and improving learning and memory. While an increasing number of studies have given evidence of neuroprotective and neurotrophic effects of nicotine treatment, the molecular mechanism mediating the neurotrophic effects of nicotine are not fully understood. Previously in an analysis of several neurotrophic factors as possible mediators of nicotine-induced neuroprotection and/or neurotrophic effects we could reveal th…

MaleNicotineGene ExpressionBiologyNeuroprotectionNicotineCerebral Cortex/drug effectNeurotrophic factorsmedicineAnimalsNicotinic AgonistsRats WistarIn Situ HybridizationOligonucleotide Array Sequence AnalysisCerebral CortexMicroarray analysis techniquesGene Expression ProfilingGeneral NeuroscienceRatsGene expression profilingNicotinic agonistNicotine/pharmacology Nicotinic Agonistsbiology.proteinGene Expression/drug effectImmediate early geneNeuroscienceTranscription Factorsmedicine.drugNeurotrophinNeuroscience
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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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Cohort Profile: the EPI-CT study: a European pooled epidemiological study to quantify the risk of radiation-induced cancer from paediatric CT

2018

International audience; •The multinational EPI-CT study was set-up in 2011 to provide direct estimates of risk of solid tumours and leukaemia among children and young adults who underwent computed tomography (CT) scanning and to consolidate the scientific basis for optimization of paediatric CT protocols and patient protection.•Under a common protocol, cohort studies were conducted in Belgium, Denmark, France, Germany, the Netherlands, Norway, Spain, Sweden and the United Kingdom, coordinated by the International Agency for Research on Cancer (IARC). •The study recruited a total of about 950,000 patients having undergone at least one CT-scan before the age of 22 years. A total of 8.7 millio…

MaleOncologymedicine.medical_specialtyNeoplasms Radiation-InducedAdolescentEpidemiology[SDV]Life Sciences [q-bio]PediatricsRisk Assessment030218 nuclear medicine & medical imagingYoung Adult03 medical and health sciencesRadiation Protection0302 clinical medicineRisk FactorsRadiation IonizingInternal medicineEpidemiologymedicineHumansYoung adultChildCohort ProfilesRetrospective Studiesbusiness.industryInfant NewbornInfantCancerRetrospective cohort studyGeneral Medicinemedicine.disease3. Good healthEuropeEpidemiologic StudiesMulticenter studyChild Preschool030220 oncology & carcinogenesisCohortFemaleRadiation-induced cancerTomography X-Ray ComputedRisk assessmentbusinessInternational Journal of Epidemiology
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Increased Hypoxic Tolerance by Chemical Inhibition of Oxidative Phosphorylation: “Chemical Preconditioning”

1997

A short ischemic episode preceding sustained ischemia is known to increase tolerance against ischemic cell death. We report early-onset long-lasting neuroprotection against in vitro hypoxia by preceding selective chemical inhibition of oxidative phosphorylation: “chemical preconditioning.” The amplitude of CA1population spikes (psap) in hippocampal slices prepared from control animals (control slices) was 31 ± 27% (mean ± SD) upon 45-min recovery from 15-min in vitro hypoxia. In slices prepared from animals treated in vivo with 20 mg/kg 3-nitropropionate (3-np) 1–24 h prior to slice preparation (preconditioned slices), psap improved to 90 ± 15% (p < 0.01). Posthypoxic oxygen free radical…

MalePotassium ChannelsFree RadicalsPopulationIschemiaNerve Tissue ProteinsBiologyPharmacologyHippocampusNeuroprotectionOxidative PhosphorylationBrain Ischemia030218 nuclear medicine & medical imagingGlibenclamide03 medical and health sciencesAdenosine Triphosphate0302 clinical medicineSlice preparationIn vivoGlyburidemedicineAnimalsEnzyme InhibitorsRats WistarHypoxia BraineducationNeuronseducation.field_of_studyAntagonistHypoxia (medical)NADNitro Compoundsmedicine.diseaseCell HypoxiaRatsSuccinate DehydrogenaseNeuroprotective AgentsNeurologyAnesthesiaNeurology (clinical)Propionatesmedicine.symptomReactive Oxygen SpeciesCardiology and Cardiovascular Medicine030217 neurology & neurosurgerymedicine.drugJournal of Cerebral Blood Flow & Metabolism
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External photon radiation treatment for prostate cancer: Uncomplicated and cancer-free control probability assessment of 36 plans

2019

[Purpose] To perform a systematic and thorough assessment, using the Uncomplicated and Cancer-Free Control Probability (UCFCP) function, of a broad range of photon prostate cancer RT treatments, on the same scenario (a unique pelvic CT set). UCFCP considers, together with the probabilities of local tumour control (TCP) and deterministic (late) sequelae (NTCP), the second primary cancer risk (SPCR) due to photon and neutron peripheral doses.

MaleProbability assessmentmedicine.medical_treatmentRadiobiological modellingBiophysicsGeneral Physics and AstronomyProstate radiotherapy treatmentNormal tissue complication probabilityTumour control probabilityRadiation protection of the patient030218 nuclear medicine & medical imaging03 medical and health sciencesProstate cancer0302 clinical medicinemedicineHumansDosimetryRadiology Nuclear Medicine and imagingConformal radiationProbabilityPhotonsbusiness.industryRadiotherapy Planning Computer-AssistedCancer-FreePhoton radiationProstatic NeoplasmsRadiotherapy DosageGeneral MedicineSecond primary cancermedicine.diseaseRadiation therapySecond primary cancer risk030220 oncology & carcinogenesisRadiotherapy plan optimisationRadiotherapy Intensity-ModulatedRadiotherapy ConformalTomography X-Ray ComputedNuclear medicinebusinessPhysica Medica 66: 88-96 (2019)
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Neuroprotection of lipoic acid treatment promotes angiogenesis and reduces the glial scar formation after brain injury

2012

After trauma brain injury, a large number of cells die, releasing neurotoxic chemicals into the extracellular medium, decreasing cellular glutathione levels and increasing reactive oxygen species that affect cell survival and provoke an enlargement of the initial lesion. Alpha-lipoic acid is a potent antioxidant commonly used as a treatment of many degenerative diseases such as multiple sclerosis or diabetic neuropathy. Herein, the antioxidant effects of lipoic acid treatment after brain cryo-injury in rat have been studied, as well as cell survival, proliferation in the injured area, gliogenesis and angiogenesis. Thus, it is shown that newborn cells, mostly corresponded with blood vessels …

MaleProgrammed cell deathAngiogenesisBlotting WesternNeovascularization PhysiologicPharmacologyBiologyNeuroprotectionAntioxidantsGlial scarNeovascularizationLesionCicatrixchemistry.chemical_compoundMicroscopy Electron TransmissionIn Situ Nick-End LabelingmedicineAnimalsRats WistarChromatography High Pressure LiquidGliogenesisThioctic AcidGeneral NeuroscienceImmunohistochemistryRatsLipoic acidNeuroprotective AgentschemistryBrain Injuriesmedicine.symptomNeurogliaNeuroscienceNeuroscience
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Molecular mechanisms of Id2 down-regulation in rat liver after acetaminophen overdose. Protection by N-acetyl-L-cysteine.

2010

Id2 is a pleiotropic protein whose function depends on its expression levels. Id2-deficient cells show increased cell death. This study explored the molecular mechanisms for the modulation of Id2 expression elicited by GSH and oxidative stress in the liver of acetaminophen (APAP)-intoxicated rats. APAP-overdose induced GSH depletion, Id2 promoter hypoacetylation, RNApol-II released and, therefore, Id2 down-regulation. Id2 expression depends on c-Myc binding to its promoter. APAP-overdose decreased c-Myc content and binding to Id2 promoter. Reduction of c-Myc was not accompanied by decreased c-myc mRNA, suggesting a mechanism dependent on protein stability. Administration of N-acetyl-cystein…

MaleProgrammed cell deathProteasome Endopeptidase ComplexGenes mycDown-RegulationBiologymedicine.disease_causeBiochemistrychemistry.chemical_compoundDownregulation and upregulationmedicineCoding regionAnimalsRats WistarPsychological repressionAcetaminophenInhibitor of Differentiation Protein 2Messenger RNAdigestive oral and skin physiologyGeneral MedicineGlutathioneAnalgesics Non-NarcoticMolecular biologyGlutathioneAcetaminophenAcetylcysteineRatsOxidative StresschemistryGene Expression RegulationLiverCytoprotectionDrug OverdoseOxidative stressmedicine.drugSignal TransductionFree radical research
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