Search results for "pigmentos"

showing 10 items of 95 documents

Role of MTHFR (677, 1298) haplotype in the risk of developing secondary leukemia after treatment of breast cancer and hematological malignancies

2007

Therapy-related myelodysplasia and acute myeloid leukemia (t-MDS/AML) is a malignancy occurring after exposure to chemotherapy and/or radiotherapy. Polymorphisms involved in chemotherapy/radiotherapy response genes could be related to an increased risk of developing this neoplasia. We have studied 11 polymorphisms in genes of drug detoxification pathways (NQO1, glutathione S-transferase pi) and DNA repair xeroderma pigmentosum, complementation group (3) (XPC(3), X-ray repair cross complementing protein (1)), Nijmegen breakage syndrome (1), excision repair cross-complementing rodent repair deficiency, complementation group (5) and X-ray repair cross complementing protein (3) and in the methy…

OncologyCancer Researchmedicine.medical_specialtyXeroderma pigmentosumAntineoplastic AgentsBreast NeoplasmsSingle-nucleotide polymorphismPolymorphism Single NucleotideBreast cancerRisk Factorshemic and lymphatic diseasesInternal medicinemedicineHumansMethylenetetrahydrofolate Reductase (NADPH2)Leukemiabiologybusiness.industryHaplotypeMyeloid leukemiaNeoplasms Second PrimaryHematologyMiddle Agedmedicine.diseaseHaplotypesOncologyCase-Control StudiesHematologic NeoplasmsMethylenetetrahydrofolate reductaseImmunologybiology.proteinbusinessNijmegen breakage syndromeNucleotide excision repairLeukemia
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Beneficial Read-Through of aUSH1CNonsense Mutation by Designed Aminoglycoside NB30 in the Retina

2010

PURPOSE. The human Usher syndrome (USH) is the most frequent cause of inherited combined deaf-blindness. USH is clinically and genetically heterogeneous, assigned to three clinical types. The most severe type is USH1, characterized by profound inner ear defects and retinitis pigmentosa. Thus far, no effective treatment for the ophthalmic component of USH exists. The p.R31X nonsense mutation in USH1C leads to a disease causing premature termination of gene translation. Here, we investigated the capability of the novel synthetic aminoglycoside NB30 for the translational read-through of the USH1C-p.R31X nonsense mutation as a retinal therapy option. METHODS. Read-through of p.R31X by three com…

ParomomycinUsher syndromeBlotting WesternNonsense mutationCell Culture TechniquesGene ExpressionCell Cycle ProteinsParomomycinBiologyPharmacologyTransfectionRetinaMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRetinitis pigmentosaIn Situ Nick-End Labelingotorhinolaryngologic diseasesmedicineAnimalsHumansAdaptor Proteins Signal Transducing030304 developmental biologyGenetics0303 health sciencesRetinaDose-Response Relationship DrugAminoglycosideRetinalmedicine.disease3. Good healthMice Inbred C57BLCytoskeletal ProteinsAminoglycosidesElectroporationHEK293 Cellsmedicine.anatomical_structureMicroscopy FluorescencechemistryCodon NonsenseProtein BiosynthesisGentamicinGentamicins030217 neurology & neurosurgerymedicine.drugInvestigative Opthalmology & Visual Science
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Primary ciliary dyskinesia. Ciliopathies

2008

Abstract Primary ciliary dyskinesia is a genetically inherited syndrome characterised by ciliary immotility or dysmotility. Deficiency in mucociliary clearance produces chronic respiratory infections from birth, male sterility by spermatozoid immotility and situs inversus in 40%–50% of patients (Kartagener's syndrome). Diagnosis is made by analysing ciliary motility with high-speed digital video and ciliary ultrastructure. The wide distribution and functions of the cilia in the body mean that this dysfunction can generate other ciliopathies apart from primary ciliary dyskinesia.

Pathologymedicine.medical_specialtyBronchiectasisSterilityMucociliary clearancebusiness.industryCiliumGeneral MedicineAnatomymedicine.diseaseCiliopathiesSitus inversusRetinitis pigmentosaotorhinolaryngologic diseasesmedicineHumansbusinessCiliary Motility DisordersPrimary ciliary dyskinesiaActa Otorrinolaringologica (English Edition)
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Xeroderma Pigmentosum – A case report with oral implications

2012

Xeroderma Pigmentosum is a rare autosomal recessive genetic disorder characterized by defective DNA repair leading to clinical and cellular hypersensitivity to ultraviolet radiation and carcinogenic agents. Important clinical features are: intense cutaneous photosensitivity, xerosis, poikiloderma, actinic keratosis, acute burning under minimal sun exposure, erythemas, hyperpigmented lentiginous macules, and malignant lesions in sun-exposed areas, including basocellular carcinoma, squamous cell carcinoma, and melanoma. There is a great involvement of many parts of the body, especially head and neck. The oral manifestations are mainly related to the occurrence of malignant tumors in the lips,…

Pathologymedicine.medical_specialtyXeroderma pigmentosumScarsPoikilodermaOdontologíaCase ReportTongueCarcinomaMedicineskin and connective tissue diseasesGeneral DentistryOral Medicine and Pathologyintegumentary systembusiness.industryMelanomaActinic keratosisGenetic disordermedicine.disease:CIENCIAS MÉDICAS [UNESCO]Ciencias de la saludstomatognathic diseasesmedicine.anatomical_structureUNESCO::CIENCIAS MÉDICASDERMATOPATIASmedicine.symptombusinessJournal of Clinical and Experimental Dentistry
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Ultrastructural study of primary canine and human pigmentary retinopathy

1985

An electron microscopic study was performed on eyes of Labrador dogs afflicted with progressive retinal atrophy (PRA). There was complete loss of photoreceptors, atrophy of the remaining retina and gliosis in the peripheral part while the central retina showed incomplete loss of photoreceptors and an almost total disappearance of photoreceptor outer segments. Melanin-bearing cells, largely containing melanolysosomes, were found deep inside the retina. This electron microscopic study also incorporated the retina of a middle-aged woman affected by retinopathia pigmentosa (RP). The fine structure of the diseased retina showed a similar pattern of lesions, more pronounced in the periphery of th…

Pathologymedicine.medical_specialtygenetic structuresBiologyRetinalaw.inventionDogsAtrophySpecies SpecificitylawRetinitis pigmentosamedicineAnimalsHumansDog DiseasesGenetics (clinical)Progressive retinal atrophyRetinaPigmentary RetinopathyMiddle Agedmedicine.diseaseeye diseasesOphthalmologymedicine.anatomical_structureGliosisPediatrics Perinatology and Child HealthUltrastructureFemalesense organsAtrophyElectron microscopemedicine.symptomRetinitis PigmentosaOphthalmic Paediatrics and Genetics
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Therapy Strategies for Usher Syndrome Type 1C in the Retina

2014

The Usher syndrome (USH) is the most common form of inherited deaf-blindness with a prevalence of ~ 1/6,000. Three clinical subtypes (USH1–USH3) are defined according to the severity of the hearing impairment, the presence or absence of vestibular dysfunction and the age of onset of retinitis pigmentosa (RP). USH1 is the most severe subtype with congenital severe to profound hearing loss and onset of RP before puberty. Currently only the amelioration of the hearing deficiency is implemented, but no treatment of the senso-neuronal degeneration in the eye exists.

Pediatricsmedicine.medical_specialtyRetinabusiness.industryUsher syndromemacromolecular substancesDegeneration (medical)medicine.diseaseProfound hearing lossmedicine.anatomical_structurenervous systemRetinitis pigmentosaotorhinolaryngologic diseasesmedicineDeaf blindnessVestibular dysfunctionAge of onsetbusiness
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BBS1 Mutations in a Wide Spectrum of Phenotypes Ranging From Nonsyndromic Retinitis Pigmentosa to Bardet-Biedl Syndrome

2012

OBJECTIVE: To investigate the involvement of the Bardet-Biedl syndrome (BBS) gene BBS1 p.M390R variant in nonsyndromic autosomal recessive retinitis pigmentosa (RP). METHODS: Homozygosity mapping of a patient with isolated RP was followed by BBS1 sequence analysis. We performed restriction fragment length polymorphism analysis of the p.M390R allele in 2007 patients with isolated RP or autosomal recessive RP and in 1824 ethnically matched controls. Patients with 2 BBS1 variants underwent extensive clinical and ophthalmologic assessment. RESULTS: In an RP proband who did not fulfill the clinical criteria for BBS, we identified a large homozygous region encompassing the BBS1 gene, which carrie…

ProbandMaleBBS1Genetics and epigenetic pathways of disease [NCMLS 6]DNA Mutational AnalysisEvaluation of complex medical interventions Genomic disorders and inherited multi-system disorders [NCEBP 2]GenotypeEthnicityPrevalenceIsraelGeneticseducation.field_of_studyRetinitis Pigmentosa/diagnosisMiddle AgedDisease gene identificationPedigreeEuropePhenotypeFemaleMicrotubule-Associated ProteinsRetinitis PigmentosaAdultcongenital hereditary and neonatal diseases and abnormalitiesCanadaPopulationCanada/epidemiologyMicroscopy AcousticMutation MissenseEthnic GroupsDNA/geneticsBiologyEurope/epidemiologyGenomic disorders and inherited multi-system disorders [IGMD 3]Bardet-Biedl Syndrome/diagnosisBardet–Biedl syndromeRetinitis pigmentosamedicineElectroretinographyHumansAlleleeducationBardet-Biedl SyndromeIsrael/epidemiologyAllelesDNAMicrotubule-Associated Proteins/geneticsmedicine.diseaseOphthalmoscopyOphthalmologyGenetics and epigenetic pathways of disease Genomic disorders and inherited multi-system disorders [NCMLS 6]
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A homozygous mutation in the TUB gene associated with retinal dystrophy and obesity.

2013

Inherited retinal dystrophies are a major cause of childhood blindness. Here, we describe the identification of a homozygous frameshift mutation (c.1194_1195delAG, p.Arg398Serfs*9) in TUB in a child from a consanguineous UK Caucasian family investigated using autozygosity mapping and whole-exome sequencing. The proband presented with obesity, night blindness, decreased visual acuity, and electrophysiological features of a rod cone dystrophy. The mutation was also found in two of the proband's siblings with retinal dystrophy and resulted in mislocalization of the truncated protein. In contrast to known forms of retinal dystrophy, including those caused by mutations in the tubby-like protein …

ProbandMaleobesity030209 endocrinology & metabolismGenes RecessiveConsanguinityBiologymedicine.disease_causeWhite PeopleFrameshift mutation03 medical and health sciencesConsanguinity0302 clinical medicineRetinitis pigmentosaGeneticsRod-cone dystrophymedicineHomeostasisHumansretinal dystrophyTUBChildEye ProteinsFrameshift MutationGenetics (clinical)030304 developmental biologyAdaptor Proteins Signal TransducingGenetics0303 health sciencesMutationHomozygoteChildhood blindnessciliatubbyChromosome MappingProteinsmedicine.diseaseUnited Kingdom3. Good healthPedigreeBrief ReportsFemaleRetinal DystrophiesRetinitis Pigmentosa
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Interference by toxic metal ions with zinc-dependent proteins involved in maintaining genomic stability.

2002

Metal ions are essential components of biological systems; nevertheless, even essential elements may have toxic or carcinogenic properties. Thus, besides As(III) and Cd(II), also Ni(II) and Co(II) have been shown previously to disturb different types of DNA repair systems at low, non-cytotoxic concentrations. Since some metals exert high affinities for SH groups, we investigated whether zinc finger structures in DNA-binding motifs of DNA repair proteins are potential targets for toxic metal ions. The bacterial formamidopyrimidine-DNA glycosylase (Fpg protein) involved in base excision repair was inhibited by Cd(II), Cu(II) and Hg(II) with increasing efficiencies, whereas Co(II), As(III), Pb…

Protein FoldingDNA RepairDNA repairCations DivalentPoly ADP ribose polymeraseToxicologymedicine.disease_causechemistry.chemical_compoundMetals HeavymedicineMetallothioneinHumansN-Glycosyl HydrolasesChemistryRNA-Binding ProteinsZinc FingersGeneral MedicineBase excision repairXeroderma Pigmentosum Group A ProteinDNA-Binding ProteinsZincBiochemistryDNA glycosylaseZinc toxicityDNAFood ScienceNucleotide excision repairFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association
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Zebrafish as a Model to Evaluate a CRISPR/Cas9-Based Exon Excision Approach as a Future Treatment Option for EYS-Associated Retinitis Pigmentosa

2021

Retinitis pigmentosa (RP) is an inherited retinal disease (IRD) with an overall prevalence of 1 in 4000 individuals. Mutations in EYS (Eyes shut homolog) are among the most frequent causes of non-syndromic autosomal recessively inherited RP and act via a loss-of-function mechanism. In light of the recent successes for other IRDs, we investigated the therapeutic potential of exon skipping for EYS-associated RP. CRISPR/Cas9 was employed to generate zebrafish from which the region encompassing the orthologous exons 37-41 of human EYS (eys exons 40-44) was excised from the genome. The excision of these exons was predicted to maintain the open reading frame and to result in the removal of exactl…

QH301-705.5CatalysisSensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]ArticleInorganic ChemistryExonAll institutes and research themes of the Radboud University Medical CenterEYSProtein Domainsretinitis pigmentosaRetinitis pigmentosamedicineCRISPRCoding regionAnimals<i>EYS</i>Biology (General)Physical and Theoretical ChemistryOuter nuclear layerEye ProteinsQD1-999Molecular BiologyZebrafishCRISPR/Cas9SpectroscopyGeneticsexon skipping therapybiologyOrganic ChemistryphotoreceptorsGeneral MedicineExonsGenetic TherapyZebrafish Proteinsmedicine.diseasebiology.organism_classificationzebrafishExon skippingComputer Science ApplicationsChemistryOpen reading frameDisease Models Animalmedicine.anatomical_structurePhenotypeCRISPR-Cas Systemsantisense oligonucleotidesInternational Journal of Molecular Sciences
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