Search results for "Retinal"

showing 10 items of 631 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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Altered antioxidant-oxidant status in the aqueous humor and peripheral blood of patients with retinitis pigmentosa.

2013

Retinitis Pigmentosa is a common form of hereditary retinal degeneration constituting the largest Mendelian genetic cause of blindness in the developed world. It has been widely suggested that oxidative stress possibly contributes to its pathogenesis. We measured the levels of total antioxidant capacity, free nitrotyrosine, thiobarbituric acid reactive substances (TBARS) formation, extracellular superoxide dismutase (SOD3) activity, protein, metabolites of the nitric oxide/cyclic GMP pathway, heme oxygenase-I and inducible nitric oxide synthase expression in aqueous humor or/and peripheral blood from fifty-six patients with retinitis pigmentosa and sixty subjects without systemic or ocular …

Retinal degenerationAdultMalePathologymedicine.medical_specialtygenetic structuresSOD3lcsh:MedicineGene ExpressionPharmacologymedicine.disease_causeNitric OxideAntioxidantsNitric oxideAqueous Humorchemistry.chemical_compoundRetinitis pigmentosaTBARSmedicineCluster AnalysisHumanslcsh:ScienceCyclic GMPMultidisciplinarybiologySuperoxide DismutaseNitrotyrosinelcsh:RMiddle Agedmedicine.diseaseOxidantseye diseasesNitric oxide synthasechemistryCase-Control Studiesbiology.proteinLeukocytes MononuclearMetabolomelcsh:QFemalesense organsOxidative stressBiomarkersHeme Oxygenase-1Retinitis PigmentosaResearch ArticlePloS one
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Molecular genetics of autosomal dominant retinitis pigmentosa (ADRP): a comprehensive study of 43 Italian families

2005

Retinitis pigmentosa is the most common form of retinal degeneration and is heterogeneous both clinically and genetically. The autosomal dominant forms ( ADRP) can be caused by mutations in 12 different genes. This report describes the first simultaneous mutation analysis of all the known ADRP genes in the same population, represented by 43 Italian families. This analysis allowed the identification of causative mutations in 12 of the families (28% of the total). Seven different mutations were identified, two of which are novel (458delC and 6901C --> T (P2301S), in the CRX and PRPF8 genes, respectively). Several novel polymorphisms leading to amino acid changes in the FSCN2, NRL, IMPDH1, and…

Retinal degenerationDNA Mutational Analysismedicine.disease_causeGene FrequencyPrevalenceAge of OnsetSPLICING-FACTOR GENESChildGenetics (clinical)Genes DominantGeneticsMutationeducation.field_of_studyRNA-Binding ProteinsMiddle AgedDNA-Binding ProteinsBasic-Leucine Zipper Transcription FactorsItalyChild PreschoolMESSENGER-RNAMicrotubule-Associated ProteinsRetinitis PigmentosaFORMAdultRhodopsinmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesAdolescentPopulationRHODOPSIN GENEBiologyMolecular geneticsRetinitis pigmentosaGeneticsmedicineHumansFamilyEye ProteinseducationGeneAllele frequencyHomeodomain ProteinsMUTATIONSmedicine.diseaseeye diseasesMutationTrans-ActivatorsMutation testingOnline Mutation ReportCarrier Proteins
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The mitotic spindle protein SPAG5/Astrin connects to the Usher protein network postmitotically

2011

Abstract Background Mutations in the gene for Usher syndrome 2A (USH2A) are causative for non-syndromic retinitis pigmentosa and Usher syndrome, a condition that is the most common cause of combined deaf-blindness. To gain insight into the molecular pathology underlying USH2A-associated retinal degeneration, we aimed to identify interacting proteins of USH2A isoform B (USH2AisoB) in the retina. Results We identified the centrosomal and microtubule-associated protein sperm-associated antigen (SPAG)5 in the retina. SPAG5 was also found to interact with another previously described USH2AisoB interaction partner: the centrosomal ninein-like protein NINLisoB. Using In situ hybridization, we foun…

Retinal degenerationGenetics and epigenetic pathways of disease [NCMLS 6]Usher syndromeBiologyPhotoreceptor cell03 medical and health sciences0302 clinical medicineMicrotubuleEvaluation of complex medical interventions Genomic disorders and inherited multi-system disorders [NCEBP 2]Retinitis pigmentosamedicineotorhinolaryngologic diseasesBasal bodylcsh:QH573-671Ganglion cell layer030304 developmental biologyGenetics0303 health sciencesRetinalcsh:CytologyResearchPathogenesis and modulation of inflammation Infection and autoimmunity [N4i 1]Cell Biologymedicine.diseaseGenetics and epigenetic pathways of disease Plasticity and memory [NCMLS 6]eye diseasesCell biologyGenetics and epigenetic pathways of disease DCN MP - Plasticity and memory [NCMLS 6]medicine.anatomical_structure030220 oncology & carcinogenesissense organs
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Translational read-through as an alternative approach for ocular gene therapy of retinal dystrophies caused by in-frame nonsense mutations

2014

AbstractThe eye has become an excellent target for gene therapy, and gene augmentation therapy of inherited retinal disorders has made major progress in recent years. Nevertheless, a recent study indicated that gene augmentation intervention might not stop the progression of retinal degeneration in patients. In addition, for many genes, viral-mediated gene augmentation is currently not feasible due to gene size and limited packaging capacity of viral vectors as well as expression of various heterogeneous isoforms of the target gene. Thus, alternative gene-based strategies to stop or delay the retinal degeneration are necessary. This review focuses on an alternative pharmacologic treatment s…

Retinal degenerationGeneticsGene isoformOxadiazolesRetinal DisorderPhysiologyNonsense mutationContext (language use)Genetic TherapyBiologyBioinformaticsmedicine.diseaseSensory SystemsAminoglycosidesCodon NonsenseProtein BiosynthesisRetinal DystrophiesmedicineAnimalsHumansCoding regionGeneRetinal DystrophiesSignal TransductionVisual Neuroscience
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Mutation Analysis Identifies GUCY2D as the Major Gene Responsible for Autosomal Dominant Progressive Cone Degeneration

2008

PURPOSE. Heterozygous mutations in the GUCY2D gene, which encodes the membrane-bound retinal guanylyl cyclase-1 protein (RetGC-1), have been shown to cause autosomal dominant inherited cone degeneration and cone–rod degeneration (adCD, adCRD). The present study was a comprehensive screening of the GUCY2D gene in 27 adCD and adCRD unrelated families of these rare disorders. METHODS. Mutation analysis was performed by direct sequencing as well as PCR and subsequent restriction length polymorphism analysis (PCR/RFLP). Haplotype analysis was performed in selected patients by using microsatellite markers. RESULTS. GUCY2D gene mutations were identified in 11 (40%) of 27 patients, and all mutation…

Retinal degenerationMaleDNA Mutational AnalysisReceptors Cell SurfaceBiologyPolymerase Chain ReactionArticlemedicineElectroretinographyMissense mutationHumansGenetic Predisposition to DiseaseCodonGeneGeneticsHaplotypeRetinal DegenerationDNAmedicine.diseasePrognosisRod Cell Outer SegmentMajor geneMolecular biologyPedigreeHaplotypesGuanylate CyclaseMutationMutation testingDisease ProgressionGUCY2DFemaleRestriction fragment length polymorphism
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Disruption of the retinitis pigmentosa 28 gene Fam161a in mice affects photoreceptor ciliary structure and leads to progressive retinal degeneration.

2014

Mutations in the FAM161A gene were previously identified as the cause for autosomal-recessive retinitis pigmentosa 28. To study the effects of Fam161a dysfunction in vivo, we generated gene-trapped Fam161a(GT/GT) mice with a disruption of its C-terminal domain essential for protein-protein interactions. We confirmed the absence of the full-length Fam161a protein in the retina of Fam161a(GT/GT) mice using western blots and showed weak expression of a truncated Fam161a protein by immunohistochemistry. Histological analyses demonstrated that photoreceptor segments were disorganized in young Fam161a(GT/GT) mice and that the outer retina was completely lost at 6 months of age. Reactive microglia…

Retinal degenerationMaleOpsinGenotypeVision DisordersAction PotentialsGene ExpressionMice TransgenicRetinal Pigment EpitheliumBiologyRetinaMiceRetinitis pigmentosaGeneticsmedicineAnimalsHumansPhotoreceptor CellsPeripherin 2Eye ProteinsMolecular BiologyGenetics (clinical)Retinal regenerationRetinaGene therapy of the human retinaCiliumRetinal DegenerationGeneral Medicinemedicine.diseaseeye diseasesCell biologyProtein Transportmedicine.anatomical_structureGenetic LociGene TargetingMutationFemalesense organsMicrogliaCarrier ProteinsProtein BindingHuman molecular genetics
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A key role for cyclic nucleotide gated (CNG) channels in cGMP-related retinitis pigmentosa.

2011

The rd1 natural mutant is one of the first and probably the most commonly studied mouse model for retinitis pigmentosa (RP), a severe and frequently blinding human retinal degeneration. In several decades of research, the link between the increase in photoreceptor cGMP levels and the extremely rapid cell death gave rise to a number of hypotheses. Here, we provide clear evidence that the presence of cyclic nucleotide gated (CNG) channels in the outer segment membrane is the key to rod photoreceptor loss. In Cngb1(-/-) x rd1 double mutants devoid of regular CNG channels, cGMP levels are still pathologically high, but rod photoreceptor viability and outer segment morphology are greatly improve…

Retinal degenerationMaleProgrammed cell deathgenetic structuresMutantchemistry.chemical_elementCyclic Nucleotide-Gated Cation ChannelsNerve Tissue ProteinsCalciumBiologyCyclic nucleotidechemistry.chemical_compoundMiceRetinal Rod Photoreceptor CellsRetinitis pigmentosaGeneticsmedicineAnimalsHumansRod cellCyclic nucleotide-gated ion channelMolecular BiologyCyclic GMPGenetics (clinical)Mice KnockoutMice Inbred C3HGeneral MedicineAnatomymedicine.diseaseeye diseasesCell biologyMice Inbred C57BLDisease Models Animalmedicine.anatomical_structurechemistryCalciumFemalesense organsRetinitis PigmentosaHuman molecular genetics
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Dynamics, alterations, and consequences of minimally invasive intraocular pressure elevation in rats.

2014

PURPOSE: An important, yet not exclusive, aspect of primary open angle glaucoma is elevated intraocular pressure (IOP) profiles within fluctuations and pressure peaks. The study aimed at establishing minimally invasive methods for recurrent IOP elevation in rats to investigate the impact of IOP dynamics and pathomorphologic retinal alterations during and after IOP elevation. METHODS: Intraocular pressure was elevated unilaterally in Long Evans rats to a level of ≈35 mm Hg for 1 hour in a total of 30 manipulations within 6 weeks, by using two methods: (1) suction-cup oculopression and (2) loop-adjusted oculopression. Retinal thickness (RT) was measured via optical coherence tomography (OCT),…

Retinal degenerationMaleRetinal Ganglion Cellsmedicine.medical_specialtyIntraocular pressuregenetic structuresOpen angle glaucomachemistry.chemical_compoundTonometry OcularOptical coherence tomographyOphthalmologymedicineAnimalsRats Long-EvansRetinal thinningIntraocular Pressuremedicine.diagnostic_testbusiness.industryRetinal DegenerationRetinalmedicine.diseaseeye diseasesRatsDisease Models Animalmedicine.anatomical_structureRetinal ganglion cellchemistryAnesthesiaOptic nerveDisease Progressionsense organsbusinessGlaucoma Open-AngleTomography Optical CoherenceFollow-Up StudiesInvestigative ophthalmologyvisual science
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PRCD is concentrated at the base of photoreceptor outer segments and is involved in outer segment disc formation.

2019

Abstract Mutations of the PRCD gene are associated with rod-cone degeneration in both dogs and humans. Prcd is expressed in the mouse eye as early as embryonic day 14. In the adult mouse retina PRCD is expressed in the outer segments of both rod and cone photoreceptors. Immunoelectron microscopy revealed that PRCD is located at the outer segment rim, and that it is highly concentrated at the base of the outer segment. Prcd-knockout mice present with progressive retinal degeneration, starting at 20 weeks of age and onwards. This process is reflected by a significant and progressive reduction of both scotopic and photopic electroretinographic responses, and by thinning of the retina, and spec…

Retinal degenerationMalegenetic structuresImmunoelectron microscopyRetinal Pigment EpitheliumBiologyRetinachemistry.chemical_compoundMicePhagocytosisGeneticsmedicineAnimalsScotopic visionOuter nuclear layerEye ProteinsMolecular BiologyGenetics (clinical)Mice KnockoutRetinaRetinal DegenerationMembrane ProteinsRetinalGeneral Medicinemedicine.diseaseRod Cell Outer SegmentPhotoreceptor outer segmenteye diseasesCell biologyMice Inbred C57BLmedicine.anatomical_structurechemistryRetinal Cone Photoreceptor CellsFemalesense organsCone-Rod DystrophiesRetinitis PigmentosaPhotopic visionSignal TransductionHuman molecular genetics
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