Search results for "MUTATION"

showing 10 items of 2830 documents

Gene toxicity studies on titanium dioxide and zinc oxide nanomaterials used for UV-protection in cosmetic formulations

2010

Titanium dioxide and zinc oxide nanomaterials, used as UV protecting agents in sunscreens, were investigated for their potential genotoxicity in in vitro and in vivo test systems. Since standard OECD test methods are designed for soluble materials and genotoxicity testing for nanomaterials is still under revision, a battery of standard tests was used, covering different endpoints. Additionally, a procedure to disperse the nanomaterials in the test media and careful characterization of the dispersed test item was added to the testing methods. No genotoxicity was observed in vitro (Ames' Salmonella gene mutation test and V79 micronucleus chromosome mutation test) or in vivo (mouse bone marrow…

MaleMaterials scienceBiomedical EngineeringBone Marrow CellsNanotechnologyCosmeticsGene mutationToxicologymedicine.disease_causeCell LineNanomaterialsMicechemistry.chemical_compoundSalmonellaIn vivoCricetinaeAdministration InhalationMacrophages AlveolarmedicineAnimalsRats WistarMicronuclei Chromosome-DefectiveTitaniumChromatographyMutagenicity TestsBody WeightIn vitroNanostructuresRatschemistryData Interpretation StatisticalMicronucleus testTitanium dioxideZinc OxideMicronucleusSunscreening AgentsGenotoxicityNanotoxicology
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Widening of the genetic and clinical spectrum of Lamb-Shaffer syndrome, a neurodevelopmental disorder due to SOX5 haploinsufficiency

2020

International audience; PURPOSE: Lamb-Shaffer syndrome (LAMSHF) is a neurodevelopmental disorder described in just over two dozen patients with heterozygous genetic alterations involving SOX5, a gene encoding a transcription factor regulating cell fate and differentiation in neurogenesis and other discrete developmental processes. The genetic alterations described so far are mainly microdeletions. The present study was aimed at increasing our understanding of LAMSHF, its clinical and genetic spectrum, and the pathophysiological mechanisms involved.METHODS: Clinical and genetic data were collected through GeneMatcher and clinical or genetic networks for 41 novel patients harboring various ty…

MaleMedizinHaploinsufficiencyL-SOX5VARIANTS0302 clinical medicineNeurodevelopmental disorderIntellectual disabilityMissense mutation2.1 Biological and endogenous factorsAetiologyChildGenetics (clinical)GeneticsPediatricGenetics & Heredity0303 health sciencesPedigreeFAMILYDNA-Binding Proteinsdevelopmental delayTRANSCRIPTION FACTORSPhenotypeintellectual disabilityChild Preschoolmissense variantsFemalemissense variants.HaploinsufficiencySOXD Transcription FactorsAdultEXPRESSIONAdolescentIntellectual and Developmental Disabilities (IDD)Clinical SciencesMutation MissenseautismCell fate determinationBiologyLONG FORMSEQUENCEArticle03 medical and health sciencesYoung AdultRare DiseasesClinical ResearchCARTILAGEIntellectual DisabilitymedicineGeneticsAnimalsHumansLanguage Development DisordersGenetic Predisposition to DiseasePreschoolTranscription factorGene030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsMUTATIONSHuman GenomeInfantmedicine.diseaseBrain DisordersNeurodevelopmental DisordersDeciphering Developmental Disorder StudyMutationAutismepilepsyMissense030217 neurology & neurosurgeryGENERATIONGenetics in Medicine
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Age-Dependent Association of Human Mannose-Binding Lectin Mutations With Susceptibility to Invasive Meningococcal Disease in Childhood

2007

Mannose-binding lectin (MBL) is an important factor of the innate immune system, and MBL-initiated complement activation is an important early defense mechanism against various bacterial infections, including invasive meningococcal disease.In a pediatric cohort (ages 2-215 months) with invasive meningococcal disease, we investigated the overall and age-stratified frequency of 3 MBL exon 1 variations (C154T, G161A, G170A), previously shown to result in markedly decreased MBL plasma concentrations, by allele specific fluorescent hybridization probe real-time PCR assays and direct sequencing. Healthy age-matched volunteers with the same ethnic background and no history of meningococcal disease…

MaleMicrobiology (medical)AgingAdolescentMannosechemical and pharmacologic phenomenaMeningococcal diseasemedicine.disease_causeMannose-Binding Lectinchemistry.chemical_compoundPrevalencemedicineHumansGenetic Predisposition to DiseaseChildMannan-binding lectinMutationInnate immune systembiologybusiness.industryInfantLectinbacterial infections and mycosesmedicine.diseaseComplement systemMeningococcal InfectionsInfectious DiseaseschemistryChild PreschoolMutationPediatrics Perinatology and Child HealthImmunologyCohortbiology.proteinFemalebusinessPediatric Infectious Disease Journal
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HCV-1b intra-subtype variability: Impact on genetic barrier to protease inhibitors

2013

Abstract Due to error-prone RNA polymerase and the lack of proofreading mechanisms, to the spread worldwide and probable long-term presence in human population, HCV showed a high degree of inter- and intra-subtype genetic variability. Protease inhibitors (PIs), a new class of drugs, have been designed specifically on the HCV genotype 1 NS3 protease three-dimensional structure. The viral genetic barrier limits the efficacy of PIs, and fourteen loci in the HCV NS3 gene are involved in resistance to PIs. A sensitive method (15 UI/ml) for study the HCV genetic profile of 125 strains from patients naive to PIs, was developed through the use of new degenerate primers for subtype 1b. We observed t…

MaleMicrobiology (medical)Settore MED/07 - Microbiologia E Microbiologia Clinicamedicine.medical_treatmentPopulationLocus (genetics)HepacivirusIntra-subtype variabilityViral Nonstructural ProteinsBiologyMicrobiologyHCV genetic barrierNS3 sequencingDrug Resistance ViralGeneticsmedicineHumansGenetic variabilityTransversioneducationMolecular BiologyGenePhylogenyEcology Evolution Behavior and SystematicsAgedGeneticseducation.field_of_studyNS3ProteaseWild typeGenetic Variationvirus diseasesHepatitis C ChronicMiddle AgedProtease inhibitorsVirologyIFN-free therapyInfectious DiseasesMutationFemaleHCV genetic barrier; IFN-free therapy; Intra-subtype variability; NS3 sequencing; Protease inhibitors
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Key features and clinical variability of COG6-CDG

2015

The conserved oligomeric Golgi (COG) complex consists of eight subunits and plays a crucial role in Golgi trafficking and positioning of glycosylation enzymes. Mutations in all COG subunits, except subunit 3, have been detected in patients with congenital disorders of glycosylation (CDG) of variable severity. So far, 3 families with a total of 10 individuals with biallelic COG6 mutations have been described, showing a broad clinical spectrum. Here we present 7 additional patients with 4 novel COG6 mutations. In spite of clinical variability, we delineate the core features of COG6-CDG i.e. liver involvement (9/10), microcephaly (8/10), developmental disability (8/10), recurrent infections (7…

MaleMicrocephalyGlycosylationAdolescentEndocrinology Diabetes and MetabolismProtein subunitHyperkeratosisMolecular Sequence DataGolgi ApparatusCase ReportsResearch SupportBiochemistryConserved oligomeric Golgi complexYoung AdultEndocrinologyCogCongenital Disorders of GlycosylationGeneticsJournal ArticleMedicineHumansNon-U.S. Gov'tChildMolecular BiologyExome sequencingGenetic Association StudiesGeneticsbusiness.industryConserved oligomeric Golgi complexResearch Support Non-U.S. Gov'tHigh-Throughput Nucleotide SequencingInfantCongenital disorder of glycosylationmedicine.diseasePhenotypeAdaptor Proteins Vesicular TransportPhenotypeCOG6MutationMicrocephalyFemaleCDGbusinessCongenital disorder of glycosylation
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Baraitser-Winter cerebrofrontofacial syndrome : Delineation of the spectrum in 42 cases

2015

International audience; Baraitser-Winter, Fryns-Aftimos and cerebrofrontofacial syndrome types 1 and 3 have recently been associated with heterozygous gain-of-function mutations in one of the two ubiquitous cytoplasmic actin-encoding genes ACTB and ACTG1 that encode beta- and gamma-actins. We present detailed phenotypic descriptions and neuroimaging on 36 patients analyzed by our group and six cases from the literature with a molecularly proven actinopathy (9 ACTG1 and 33 ACTB). The major clinical anomalies are striking dysmorphic facial features with hypertelorism, broad nose with large tip and prominent root, congenital non-myopathic ptosis, ridged metopic suture and arched eyebrows. Iris…

MaleMicrocephalyPathologyCraniofacial abnormality[SDV]Life Sciences [q-bio]MedizinGYRAL MALFORMATIONSCraniofacial AbnormalitiesFUNCTIONAL DIVERSITY0302 clinical medicinePtosisGene OrderGenetics(clinical)HypertelorismNon-U.S. Gov'tChildGenetics (clinical)ArthrogryposisDystonia0303 health sciencesResearch Support Non-U.S. Gov'tAnatomy3. Good healthPhenotypeChild PreschoolFemalemedicine.symptomAbnormalitiesMultipleRare cancers Radboud Institute for Health Sciences [Radboudumc 9]Adultmedicine.medical_specialtyAPPARENTLY UNDESCRIBED SYNDROMEAdolescentLissencephalyBiologyResearch SupportArticle03 medical and health sciencesYoung AdultSDG 3 - Good Health and Well-beingmedicineGeneticsJournal ArticleHumansAbnormalities MultiplePreschool030304 developmental biologySHALLOW ORBITSNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]GAMMA-ACTINPachygyriaFaciesmedicine.diseaseIRIS COLOBOMAActinsBETA-ACTINAbnormalities Multiple; Actins; Adolescent; Adult; Amino Acid Substitution; Child; Child Preschool; Craniofacial Abnormalities; Facies; Female; Gene Order; Genetic Loci; Humans; Male; Mutation; Phenotype; Young AdultAmino Acid SubstitutionGenetic LociFACIAL SYNDROMEMutation030217 neurology & neurosurgeryMENTAL-RETARDATIONGROWTH-RETARDATION
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EPHA7 haploinsufficiency is associated with a neurodevelopmental disorder

2021

International audience; Ephrin receptor and their ligands, the ephrins, are widely expressed in the developing brain. They are implicated in several developmental processes that are crucial for brain development. Deletions in genes encoding for members of the Eph/ephrin receptor family were reported in several neurodevelopmental disorders. The ephrin receptor A7 gene (EPHA7) encodes a member of ephrin receptor subfamily of the protein-tyrosine kinase family. EPHA7 plays a role in corticogenesis processes, determines brain size and shape, and is involved in development of the central nervous system. One patient only was reported so far with a de novo deletion encompassing EPHA7 in 6q16.1. We…

MaleMicrocephaly[SDV]Life Sciences [q-bio]6q161 microdeletionInheritance PatternsEPHA7HaploinsufficiencyBiologyspeech and language developmentNeurodevelopmental disorderExome SequencingGeneticsmedicineEphrinHumansGenetic Predisposition to DiseasemicrocephalyGenetics (clinical)Genetic Association StudiesIn Situ Hybridization FluorescenceGeneticsComparative Genomic Hybridization6q16.1 microdeletionErythropoietin-producing hepatocellular (Eph) receptorReceptor EphA7medicine.diseasePenetrancePhenotypeneurodevelopmental disorderPedigree[SDV] Life Sciences [q-bio]PhenotypeNeurodevelopmental Disordersintellectual disabilityEPHA7MutationChromosomes Human Pair 6FemaleHaploinsufficiencyClinical Genetics
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<i>GJB2</i> Mutations and Genotype-Phenotype Correlation in 335 Patients from Germany with Nonsyndromic Sensorineural Hearing Loss: Evide…

2009

We report on 335 patients (319 families) with mild-to-profound nonsyndromic sensorineural hearing loss. We identified 178 mutated <i>GJB2</i> alleles representing 29 different sequence changes (including 3 novel mutations: Q7P, N14D, H100Q), and 2 alleles with the deletion del(GJB6-D13S1830) of the <i>GJB6</i> gene. Eleven <i>GJB2</i> mutations (119 mutated alleles) were truncating (T), and 18 mutations (59 alleles) were nontruncating (NT). Biallelic <i>GJB2</i> mutations were found in 71 patients (21.2%; 67 families; 25 different genotypes). Audiograms of 62 patients (56 families) with biallelic <i>GJB2</i> mutations typically ind…

MaleMild hearing impairmentPathologymedicine.medical_specialtyGenotypePhysiologyHearing lossHearing Loss SensorineuralGenes Recessivemedicine.disease_causePolymerase Chain ReactionConnexinsSpeech and HearingAudiometryGene FrequencyGermanyGenotypeotorhinolaryngologic diseasesmedicineHumansAlleleAllele frequencyAllelesGenetic Association StudiesGeneticsMutationbiologybusiness.industrymedicine.diseaseSensory SystemsConnexin 26PhenotypeOtorhinolaryngologyMutationbiology.proteinFemaleSensorineural hearing lossmedicine.symptombusinessGJB6Audiology and Neurotology
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Mitochondrial DNA effects on fitness in Drosophila subobscura

2011

We tested different fitness components on a series of conspecific mtDNA haplotypes, detected by RFLPs in Drosophila subobscura. Additionally, haplotype VIII, endemic to the Canary Islands, was tested upon its own native nuclear DNA background and upon that of the rest of mtDNAs tested herein. We found that both nuclear and mitochondrial DNA can have a significant effect upon their hosts' fitness, and that negative selection is one of the mechanisms that can intervene in this species' mtDNA haplotype pattern. We discuss the importance of this mechanism in relation to genetic drift, in the form of periodic population bottlenecks, and how the latter can enhance the former. We also detected a s…

MaleMitochondrial DNALongevityGenetic FitnessBiologyDNA MitochondrialGenetic driftGenetic variationHybrid VigorGeneticsAnimalsSelection GeneticGenetics (clinical)Cell NucleusGeneticsGenetic DriftHaplotypeGenetic VariationDrosophila subobscuraNuclear DNAFertilityHaplotypesSpainEvolutionary biologyMutationOriginal ArticleDrosophilaFemaleGenetic FitnessRestriction fragment length polymorphismWolbachiaHeredity
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Molecular oncology focus - is carcinogenesis a 'mitochondriopathy'?

2010

Abstract Mitochondria are sub-cellular organelles that produce adenosine triphosphate (ATP) through oxidative phosphorylation (OXPHOS). As suggested over 70 years ago by Otto Warburg and recently confirmed with molecular techniques, alterations in respiratory activity and in mitochondrial DNA (mtDNA) appear to be common features of malignant cells. Somatic mtDNA mutations have been reported in many types of cancer cells, and some reports document the prevalence of inherited mitochondrial DNA polymorphisms in cancer patients. Nevertheless, a careful reanalysis of methodological criteria and methodology applied in those reports has shown that numerous papers can't be used as relevant sources …

MaleMitochondrial DNAMitochondrial DiseasesEndocrinology Diabetes and MetabolismClinical BiochemistryMEDLINElcsh:MedicineComputational biologyReviewMitochondrionBiologymedicine.disease_causeMolecular oncologyDNA MitochondrialOxidative PhosphorylationNeoplasmsmedicineBiomarkers TumorHumansPharmacology (medical)Molecular BiologyBiomedicineGeneticsBiochemistry medicalbusiness.industryBiochemistry (medical)lcsh:RCancerGeneral MedicineCell BiologyDNA Neoplasmmedicine.diseaseMolecular medicineMitochondriaMutationFemaleCarcinogenesisbusinessJournal of biomedical science
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