Search results for "Retinal Neurons"

showing 4 items of 4 documents

A novel automated segmentation method for retinal layers in OCT images proves retinal degeneration after optic neuritis.

2015

Aim The evaluation of inner retinal layer thickness can serve as a direct biomarker for monitoring the course of inflammatory diseases of the central nervous system such as multiple sclerosis (MS). Using optical coherence tomography (OCT), thinning of the retinal nerve fibre layer and changes in deeper retinal layers have been observed in patients with MS. Here, we first compare a novel method for automated segmentation of OCT images with manual segmentation using two cohorts of patients with MS. Using this method, we also aimed to reproduce previous findings showing retinal degeneration following optic neuritis (ON) in MS. Methods Based on a 5×5 expansion of the Prewitt operator to efficie…

Retinal degenerationAdultMalePathologymedicine.medical_specialtyMultiple SclerosisOptic Neuritisgenetic structuresDiagnostic Techniques Ophthalmological03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compoundYoung Adult0302 clinical medicineNerve FibersOptical coherence tomographyOphthalmologyMedicineHumansSegmentationOptic neuritisGanglion cell layerRetinamedicine.diagnostic_testbusiness.industryRetinal DegenerationReproducibility of ResultsRetinalMiddle Agedmedicine.diseaseeye diseasesSensory SystemsOphthalmologymedicine.anatomical_structurechemistry030221 ophthalmology & optometryOptic nerveFemalesense organsbusiness030217 neurology & neurosurgeryAlgorithmsBiomarkersTomography Optical CoherenceRetinal NeuronsThe British journal of ophthalmology
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The Small Heat Shock Protein α-Crystallin B Shows Neuroprotective Properties in a Glaucoma Animal Model

2017

Glaucoma is a neurodegenerative disease that leads to irreversible retinal ganglion cell (RGC) loss and is one of the main causes of blindness worldwide. The pathogenesis of glaucoma remains unclear, and novel approaches for neuroprotective treatments are urgently needed. Previous studies have revealed significant down-regulation of α-crystallin B as an initial reaction to elevated intraocular pressure (IOP), followed by a clear but delayed up-regulation, suggesting that this small heat-shock protein plays a pathophysiological role in the disease. This study analyzed the neuroprotective effect of α-crystallin B in an experimental animal model of glaucoma. Significant IOP elevation induced b…

0301 basic medicineProteomicsRetinal Ganglion Cellsgenetic structuresNerve fiber layerGlaucomaCell CountMass Spectrometrylcsh:ChemistryPathogenesischemistry.chemical_compound0302 clinical medicineexperimental glaucoma; α-crystallin B; neuroprotection; proteomicsProtein Interaction Mapslcsh:QH301-705.5Spectroscopyα-crystallin BGeneral MedicineComputer Science ApplicationsUp-Regulationmedicine.anatomical_structureNeuroprotective AgentsRetinal ganglion cellneuroprotectionRetinal Neuronsmedicine.medical_specialtyDown-RegulationBiologyNeuroprotectionCatalysisArticleInorganic Chemistry03 medical and health sciencesCrystallinOphthalmologyHeat shock proteinmedicineElectroretinographyAnimalsPhysical and Theoretical ChemistryMolecular BiologyIntraocular Pressureexperimental glaucomaOrganic Chemistryalpha-Crystallin B ChainRetinalGlaucomamedicine.diseaseeye diseasesDisease Models Animal030104 developmental biologylcsh:Biology (General)lcsh:QD1-999chemistry030221 ophthalmology & optometrysense organsInternational Journal of Molecular Sciences; Volume 18; Issue 11; Pages: 2418
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Serum and antibodies of glaucoma patients lead to changes in the proteome, especially cell regulatory proteins, in retinal cells.

2012

PURPOSE: Previous studies show significantly specifically changed autoantibody reactions against retinal antigens in the serum of glaucoma and ocular hypertension (OHT) patients in comparison to healthy people. As pathogenesis of glaucoma still is unknown the aim of this study was to analyze if the serum and antibodies of glaucoma patients interact with neuroretinal cells. METHODS: R28 cells were incubated with serum of patients suffering from primary open angle glaucoma (POAG), normal tension glaucoma (NTG) or OHT, POAG serum after antibody removal and serum from healthy people for 48 h under a normal or an elevated pressure of 15000 Pa (112 mmHg). RGC5 cells were additionally incubated wi…

ProteomicsRetinal Ganglion CellsSerumProteomegenetic structuresOcular hypertensionGlaucomalcsh:MedicineAutoimmunityPathogenesischemistry.chemical_compoundMolecular Cell Biologylcsh:ScienceCellular Stress ResponsesMultidisciplinarySpectrometric Identification of ProteinsbiologyNeurodegenerative DiseasesBlood proteinsSignaling CascadesNeurologyMedicineRetinal DisordersElectrophoresis Polyacrylamide GelAntibodyGlaucoma Open-AngleRetinal NeuronsSignal TransductionResearch ArticleSpectrometry Mass Electrospray IonizationImmunologyImmunoglobulinsPeptide MappingAntibodiesStress Signaling CascadeCell LineAntigenmedicinePressureAnimalsHumansBiologylcsh:RAutoantibodyRetinalGlaucomamedicine.diseaseeye diseasesRatsOphthalmologychemistrySpectrometry Mass Matrix-Assisted Laser Desorption-IonizationImmunologybiology.proteinOcular HypertensionClinical Immunologylcsh:Qsense organsChromatography LiquidPLoS ONE
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Role of nitric oxide synthase isoforms for ophthalmic artery reactivity in mice.

2014

Abstract Nitric oxide synthases (NOS) are involved in regulation of ocular vascular tone and blood flow. While endothelial NOS (eNOS) has recently been shown to mediate endothelium-dependent vasodilation in mouse retinal arterioles, the contribution of individual NOS isoforms to vascular responses is unknown in the retrobulbar vasculature. Moreover, it is unknown whether the lack of a single NOS isoform affects neuron survival in the retina. Thus, the goal of the present study was to examine the hypothesis that the lack of individual nitric oxide synthase (NOS) isoforms affects the reactivity of mouse ophthalmic arteries and neuron density in the retinal ganglion cell (RGC) layer. Mice defi…

Retinal Ganglion CellsVasodilator AgentsNitric Oxide Synthase Type IIVideo microscopyVasodilationCell CountNitric Oxide Synthase Type IMuscle Smooth Vascularchemistry.chemical_compoundMiceOphthalmic ArteryPhenylephrineEnosEnzyme InhibitorsMice KnockoutbiologyAnatomySensory SystemsNitric oxide synthaseIsoenzymesVasodilationmedicine.anatomical_structureNG-Nitroarginine Methyl EsterRetinal ganglion cellKnockout mouseRetinal NeuronsNitroprussidemedicine.medical_specialtyNitric Oxide Synthase Type IIIEndothelial NOSNitric oxideCellular and Molecular NeuroscienceTonometry OcularInternal medicinemedicineAnimalsNitric Oxide DonorsIntraocular Pressurebusiness.industrybiology.organism_classificationAcetylcholineMice Inbred C57BLOphthalmologyEndocrinologychemistryVasoconstrictionbiology.proteinAdrenergic alpha-1 Receptor AgonistsEndothelium VascularbusinessExperimental eye research
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