Search results for " pigment"

showing 10 items of 309 documents

ApoB100,LDLR-/- mice exhibit reduced electroretinographic response and cholesteryl esters deposits in the retina

2008

International audience; PURPOSE. To evaluate the retinal phenotype of 7- and 14-month-old apoB100,LDLR–/– mice, a relevant animal model of lipid metabolism dysfunction. METHODS. Single-flash electroretinograms were obtained from 7- and 14-month-old apoB100,LDLR–/– and control mice fed a standard diet under both scotopic and photopic conditions. Visual cycle retinoids were analyzed in eyes from dark-adapted mice. Retinal and choroidal vascularization was evaluated with scanning laser ophthalmoscopy. Fatty acids were analyzed in the retina. Esterified and free cholesterol was detected in eye cryosections. RESULTS. Scotopic and photopic b-wave amplitudes were significantly reduced in apoB100,L…

MaleHUMAN BRUCHS MEMBRANEgenetic structuresHIGH-FAT DIETLipid Metabolism DisordersBasement MembraneAGE-RELATED MACULOPATHYchemistry.chemical_compoundMice0302 clinical medicine[SDV.IDA]Life Sciences [q-bio]/Food engineeringFluorescein AngiographyPigment Epithelium of EyeTRANSGENIC MICE0303 health sciencesmedicine.diagnostic_testROD OUTER SEGMENTSmedicine.anatomical_structureBiochemistryHUMAN APOLIPOPROTEIN-BApolipoprotein B-100Femalelipids (amino acids peptides and proteins)Cholesterol EstersPhotopic visionVisual phototransductionmedicine.medical_specialtyDark AdaptationMice TransgenicBiologyRetinaRECEPTOR-NEGATIVE MICE03 medical and health sciencesRetinoidsRetinal DiseasesBASAL DEPOSITSInternal medicinemedicineElectroretinographyAnimals[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process EngineeringFilipinHUMAN ATHEROSCLEROTIC LESIONS030304 developmental biologyRetinaRetinal pigment epitheliumRetinalMacular degenerationmedicine.diseaseMACULAR DEGENERATIONeye diseasesMice Inbred C57BLOphthalmoscopyEndocrinologychemistryReceptors LDLLDL receptor030221 ophthalmology & optometrysense organsPhotic StimulationElectroretinography
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Carotenoid trade-off between parasitic resistance and sexual display: an experimental study in the blackbird (Turdus merula).

2008

Many parasites depress the expression of the carotenoid-based colour displays of their hosts, and it has been hypothesized that animals face a trade-off in carotenoid allocation between immune functions and ‘degree of ornamentation’. While numerous correlative studies suggest that parasite infection decreases the intensity of carotenoid-based colour displays, the existence of this trade-off has never been demonstrated experimentally in a host–parasite model. In this study, we used the blackbird ( Turdus merula ) and Isospora (an intestinal parasite) to assess whether this trade-off does indeed exist. Blackbirds were supplemented with carotenoids while simultaneously being exposed to parasi…

MaleMESH : Host-Parasite InteractionsMESH : Analysis of VarianceTrade-offmedicine.disease_causeSongbirds[ SDV.BBM.BC ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM][ SDV.EE.IEO ] Life Sciences [q-bio]/Ecology environment/SymbiosisParasite hostingbill colourCarotenoidGeneral Environmental Sciencetrade-offchemistry.chemical_classificationPigmentationMESH : PigmentationBeakcarotenoidsfood and beveragesMESH : IsosporaGeneral MedicineIsosporaBeakGeneral Agricultural and Biological SciencesResearch Article[ SDV.MP.PAR ] Life Sciences [q-bio]/Microbiology and Parasitology/ParasitologyMESH : MaleZoologyIntestinal parasiteBiologyParasitic infectionGeneral Biochemistry Genetics and Molecular BiologyHost-Parasite InteractionsCoccidiaBotanymedicineAnimalsBody Weights and MeasuresMESH : Dietary SupplementsMESH : SongbirdsMESH : CarotenoidsAnalysis of VarianceIsosporaGeneral Immunology and Microbiologyorganic chemicalscoccidiaMESH : Body Weights and Measuresbiology.organism_classificationMESH : Beakchemistryexperimental infectionDietary SupplementsMESH : Animals
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Occupational sun exposure and mycosis fungoides: a European multicenter case-control study.

2006

International audience; OBJECTIVE: We sought to study the association between occupational sun exposure and mycosis fungoides (MF), a peripheral T-cell lymphoma. SUBJECTS AND METHODS: A European multicenter case-control study including seven rare cases (one being MF) was conducted between 1995 and 1997. From the 118 accepted cases, 104 were interviewed, of which 76 were definite cases. Population controls were selected randomly from the regions of case ascertainment. Information based on occupational experiences was coded according to industry types. A job exposure matrix was created according to the expected exposure to sunlight. RESULTS: Once exposures to aromatic halogenated hydrocarbons…

MaleMESH: Occupational Exposure030207 dermatology & venereal diseases0302 clinical medicineRisk FactorsMESH: Risk FactorsEpidemiologyOdds RatioMESH: Agededucation.field_of_studyMESH: Middle AgedPigmentationMiddle AgedMESH: Case-Control StudiesCausalityEuropeOccupational Diseases030220 oncology & carcinogenesisSunlightFemaleMESH: Occupational Diseasesmedicine.medical_specialtyMESH: SunlightPopulationJob-exposure matrixMESH: CausalityMESH: PigmentationOccupational medicine03 medical and health sciencesMycosis FungoidesOccupational ExposuremedicineHumanseducationAgedMycosis fungoidesMESH: Humansbusiness.industryMESH: Mycosis FungoidesPublic Health Environmental and Occupational HealthCase-control studyOdds ratiomedicine.diseaseDermatologyConfidence intervalMESH: Odds RatioMESH: MaleSurgery[SDV.SPEE] Life Sciences [q-bio]/Santé publique et épidémiologieCase-Control Studies[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologieMESH: EuropebusinessMESH: Female
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Identification of three novel mutations in the MYO7A gene

1999

Three new mutations in the myosin VIIA gene involved in the pathogenesis of Usher syndrome type Ib are reported. These mutations are K1080X in exon 25, E1170K in exon 28, and Y1719C in exon 37. It is presumed that these mutations are involved in the Usher syndrome Ib phenotype. Hum Mutat 14:181, 1999. Copyright 1999 Wiley-Liss, Inc.

MaleMYO7AHearing Loss SensorineuralUsher syndromeMyosinsBiologymedicine.disease_causeExonRetinitis pigmentosaMyosinotorhinolaryngologic diseasesGeneticsmedicineHumansGenePolymorphism Single-Stranded ConformationalGenetics (clinical)GeneticsMutationBase SequenceChromosomes Human Pair 11fungiDyneinsSyndromemedicine.diseasePhenotypeeye diseasesPedigreePhenotypeMyosin VIIaMutationFemaleRetinitis PigmentosaHuman Mutation
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Translational read-through of the RP2 Arg120stop mutation in patient iPSC-derived retinal pigment epithelium cells.

2014

Mutations in the RP2 gene lead to a severe form of X-linked retinitis pigmentosa. RP2 patients frequently present with nonsense mutations and no treatments are currently available to restore RP2 function. In this study, we reprogrammed fibroblasts from an RP2 patient carrying the nonsense mutation c.519C>T (p.R120X) into induced pluripotent stem cells (iPSC), and differentiated these cells into retinal pigment epithelial cells (RPE) to study the mechanisms of disease and test potential therapies. RP2 protein was undetectable in the RP2 R120X patient cells, suggesting a disease mechanism caused by complete lack of RP2 protein. The RP2 patient fibroblasts and iPSC-derived RPE cells showed phe…

MaleNonsense mutationInduced Pluripotent Stem CellsGene ExpressionRetinal Pigment EpitheliumBiologymedicine.disease_causeBioinformaticschemistry.chemical_compoundYoung AdultGTP-Binding ProteinsRetinitis pigmentosaGeneticsmedicineHumansCiliaFibroblastInduced pluripotent stem cellEye ProteinsMolecular BiologyGenetics (clinical)MutationOxadiazolesRetinal pigment epitheliumIntracellular Signaling Peptides and ProteinsMembrane ProteinsRetinalCell DifferentiationEpithelial CellsGeneral MedicineArticlesFibroblastsmedicine.diseaseCellular Reprogramming3. Good healthAtalurenCell biologyProtein Transportmedicine.anatomical_structurePhenotypechemistryProtein BiosynthesisMutationHuman molecular genetics
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Ultraviolet vision in lacertid lizards: evidence from retinal structure, eye transmittance, SWS1 visual pigment genes, and behaviour

2014

Abstract Ultraviolet (UV) vision and UV colour patches have been reported in a wide range of taxa and are increasingly appreciated as an integral part of vertebrate visual perception and communication systems. Previous studies with Lacertidae, a lizard family with diverse and complex coloration, have revealed the existence of UV-reflecting patches that may function as social signals. However, confirmation of the signalling role of UV coloration requires demonstrating that the lizards are capable of vision in the UV waveband. Here we use a multidisciplinary approach to characterize the visual sensitivity of a diverse sample of lacertid species. Spectral transmission measurements of the ocula…

MaleOpsinVisual perceptiongenetic structuresUltraviolet RaysPhysiologyAquatic ScienceRetinaOpticsbiology.animalmedicineAnimalsLacertidaePhotopigmentMolecular BiologyPhylogenyVision OcularEcology Evolution Behavior and SystematicsRetinabiologyLizardbusiness.industryLizardsbiology.organism_classificationeye diseasesPodarcis muralismedicine.anatomical_structureMicroscopy FluorescenceEvolutionary biologyInsect ScienceOil dropletRetinal Cone Photoreceptor CellsVisual PerceptionAnimal Science and Zoologysense organsbusinessRetinal PigmentsJournal of Experimental Biology
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A comparative evaluation of NB30, NB54 and PTC124 in translational read-through efficacy for treatment of an USH1C nonsense mutation

2012

Translational read-through-inducing drugs (TRIDs) promote read-through of nonsense mutations, placing them in the spotlight of current gene-based therapeutic research. Here, we compare for the first time the relative efficacies of new-generation aminoglycosides NB30, NB54 and the chemical compound PTC124 on retinal toxicity and read-through efficacy of a nonsense mutation in the USH1C gene, which encodes the scaffold protein harmonin. This mutation causes the human Usher syndrome, the most common form of inherited deaf-blindness. We quantify read-through efficacy of the TRIDs in cell culture and show the restoration of harmonin function. We do not observe significant differences in the read…

MaleRetinal DisorderUsher syndromemedia_common.quotation_subjectNonsenseNonsense mutationPeptide Chain Elongation TranslationalCell Cycle ProteinsIn Vitro TechniquesBiologyPharmacologymedicine.disease_causeRetinaCell LineMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRetinal DiseasesIn vivoretinitis pigmentosaRetinitis pigmentosaotorhinolaryngologic diseasesmedicineAnimalsHumansResearch ArticlesAdaptor Proteins Signal Transducingpharmacogenetics030304 developmental biologymedia_commonOxadiazoles0303 health sciencesMutationsensoneuronal degenerationRetinalmedicine.diseasedrug therapy3. Good healthMice Inbred C57BLCytoskeletal ProteinsAminoglycosideschemistryCodon NonsenseMolecular MedicineFemaleUsher syndrome030217 neurology & neurosurgeryEMBO Molecular Medicine
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Mutation ofPOC1Bin a Severe Syndromic Retinal Ciliopathy

2014

We describe a consanguineous Iraqi family with Leber congenital amaurosis (LCA), Joubert syndrome (JBTS), and polycystic kidney disease (PKD). Targeted next-generation sequencing for excluding mutations in known LCA and JBTS genes, homozygosity mapping, and whole-exome sequencing identified a homozygous missense variant, c.317G>C (p.Arg106Pro), in POC1B, a gene essential for ciliogenesis, basal body, and centrosome integrity. In silico modeling suggested a requirement of p.Arg106 for the formation of the third WD40 repeat and a protein interaction interface. In human and mouse retina, POC1B localized to the basal body and centriole adjacent to the connecting cilium of photoreceptors and in …

MaleRetinal degenerationgenetic structuresAmino Acid MotifsLeber Congenital AmaurosisMolecular Sequence DataCell Cycle ProteinsBiologyKidneyArticleRetinaJoubert syndromeMiceCerebellar DiseasesCerebellumCiliogenesisRetinitis pigmentosaGeneticsmedicineAnimalsHumansAbnormalities MultipleAmino Acid SequenceCiliaEye AbnormalitiesChildZebrafishGenetics (clinical)Cystic kidneyGeneticsCiliumKidney Diseases Cysticmedicine.diseaseDisease gene identificationeye diseasesPedigreeCiliopathyGene Knockdown TechniquesIraqMutationsense organsHuman Mutation
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USH3A transcripts encode clarin-1, a four-transmembrane-domain protein with a possible role in sensory synapses.

2002

Usher syndrome type 3 (USH3) is an autosomal recessive disorder characterised by the association of post-lingual progressive hearing loss, progressive visual loss due to retinitis pigmentosa and variable presence of vestibular dysfunction. Because the previously defined transcripts do not account for all USH3 cases, we performed further analysis and revealed the presence of additional exons embedded in longer human and mouse USH3A transcripts and three novel USH3A mutations. Expression of Ush3a transcripts was localised by whole mount in situ hybridisation to cochlear hair cells and spiral ganglion cells. The full length USH3A transcript encodes clarin-1, a four-transmembrane-domain protein…

MaleUsher syndromeMolecular Sequence DataBiologyPhotoreceptor cellSynapse03 medical and health sciencesExonMice0302 clinical medicineSequence Analysis ProteinRetinitis pigmentosaHair Cells Auditoryotorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansAmino Acid SequenceGenetics (clinical)Spiral ganglionIn Situ HybridizationPhylogeny030304 developmental biology0303 health sciencesGene Expression ProfilingChromosome MappingMembrane ProteinsSequence Analysis DNAmedicine.diseaseCell biologyPedigreeTransmembrane domainmedicine.anatomical_structureMutationSynapsesFemalesense organsHair cellCalcium ChannelsSequence Alignment030217 neurology & neurosurgeryEuropean journal of human genetics : EJHG
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Detection of a novel Cys628STOP mutation of the myosin VIIA gene in Usher syndrome type Ib.

1998

A Spanish family with three Usher I syndrome-affected members was linked to markers located on chromosome 11q. A search for mutations on the myosin VIIA gene revealed a novel mutation (Cys628STOP) on exon 16 segregating with the disorder in a homozygous state. This nonsense mutation could be responsible for the disease since it leads to a truncated protein that presumably has no function.

MaleUsher syndromeNonsense mutationDNA Mutational AnalysisGenes RecessiveBiologyDeafnessMyosinsPolymerase Chain ReactionExonotorhinolaryngologic diseasesmedicineHumansCysteineMolecular BiologyGenePolymorphism Single-Stranded ConformationalGeneticsMyosin VIIaChromosomeDyneinsCell BiologyDNAExonsSyndromeMiddle Agedmedicine.diseasePedigreeMyosin VIIaMutation (genetic algorithm)MutationCodon TerminatorFemaleNovel mutationRetinitis PigmentosaMolecular and cellular probes
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