Search results for "Nonsense"

showing 10 items of 140 documents

Mutational analysis of 105 mucopolysaccharidosis type VI patients

2007

Mucopolysaccharidosis type VI (MPS VI; Maroteaux-Lamy syndrome) is a lysosomal storage disorder caused by mutations in the N-acetylgalactosamine-4-sulfatase (arylsulfatase B, ARSB) gene. ARSB is a lysosomal enzyme involved in the degradation of the glycosaminoglycans (GAG) dermatan and chondroitin sulfate. ARSB mutations reduce enzyme function and GAG degradation, causing lysosomal storage and urinary excretion of these partially degraded substrates. Disease onset and rate of progression is variable, producing a spectrum of clinical presentation. In this study, 105 MPS VI patients—representing about 10% of the world MPS VI population—were studied for molecular genetic and biochemical parame…

AdultArylsulfatase BAdolescentN-Acetylgalactosamine-4-SulfataseMPS VIDNA Mutational AnalysisNonsense mutationMucopolysaccharidosis type VIBiologyPolymorphism Single NucleotideGenetic HeterogeneityAge DistributionGene FrequencyGenotypeGeneticsmedicineHumansMissense mutationGenetic TestingChildCells CulturedGenetics (clinical)mucopolysaccharidosis type VIGlycosaminoglycansGeneticsMucopolysaccharidosis VIGenetic heterogeneityMucopolysaccharidosis VIMiddle Agedmedicine.diseasearylsulfatase BMaroteaux–Lamy syndromeDisease ProgressionARSBMaroteaux-LamyHuman Mutation
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Association of Left Ventricular Systolic Dysfunction Among Carriers of Truncating Variants in Filamin C With Frequent Ventricular Arrhythmia and End-…

2021

Importance: Truncating variants in the gene encoding filamin C (FLNCtv) are associated with arrhythmogenic and dilated cardiomyopathies with a reportedly high risk of ventricular arrhythmia.Objective: To determine the frequency of and risk factors associated with adverse events among FLNCtv carriers compared with individuals carrying TTN truncating variants (TTNtv).Design, Setting, and Participants: This cohort study recruited 167 consecutive FLNCtv carriers and a control cohort of 244 patients with TTNtv matched for left ventricular ejection fraction (LVEF) from 19 European cardiomyopathy referral units between 1990 and 2018. Data analyses were conducted between June and October, 2020.Main…

AdultCardiomyopathy DilatedMalemedicine.medical_specialtyFilaminsCardiomyopathy030204 cardiovascular system & hematologySudden cardiac deathVentricular Dysfunction Left03 medical and health sciences0302 clinical medicineInterquartile rangeCardiac magnetic resonance imagingInternal medicinemedicineHumansConnectin030212 general & internal medicineHeart FailureEjection fractionmedicine.diagnostic_testbusiness.industryHazard ratioCorrectionStroke Volume[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismMiddle Agedmedicine.diseaseDefibrillators Implantable3. Good healthDeath Sudden CardiacCodon NonsenseHeart failureMutationCohortTachycardia VentricularCardiologyHeart TransplantationFemaleCardiology and Cardiovascular MedicinebusinessJAMA Cardiology
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Genomic analysis of the emergence and evolution of multidrug resistance during a Klebsiella pneumoniae outbreak including carbapenem and colistin res…

2014

et al.

AdultDNA BacterialMaleMicrobiology (medical)CarbapenemAntibiotic resistanceKlebsiella pneumoniaeMolecular Sequence DataNonsense mutationFosfomycinDisease OutbreaksMicrobiologyEvolution MolecularPlasmidAntibiotic resistanceMutation RateOutbreak genomicsmedicineHumansPharmacology (medical)AgedPharmacologyGeneticsbiologyColistinHypermutationSequence Analysis DNAMiddle Agedbiochemical phenomena metabolism and nutritionbiology.organism_classificationDrug Resistance MultipleAnti-Bacterial AgentsKlebsiella InfectionsMultiple drug resistanceKlebsiella pneumoniaeInfectious DiseasesCarbapenemsKlebsiella pneumoniae genomeColistinbacteriaFemaleGenome Bacterialmedicine.drugJournal of Antimicrobial Chemotherapy
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Homozygous variants in the gene SCAPER cause syndromic intellectual disability

2019

The S-Phase Cyclin A Associated Protein In The ER (SCAPER) gene is a ubiquitously expressed gene with unknown function in the brain. Recently, biallelic SCAPER variants were described in four patients from three families with retinitis pigmentosa (RP) and intellectual disability (ID). Here, we expand the spectrum of pathogenic variants in SCAPER and report on 10 further patients from four families with ID, RP, and additional dysmorphic features carrying homozygous variants in SCAPER. The variants found comprise frameshift, nonsense, and missense variants as well as an intragenic homozygous deletion, which spans SCAPER exons 15 and 16 and introduces a frameshift and a premature stop codon. A…

AdultMale0301 basic medicineAdolescentmedia_common.quotation_subjectCyclin ANonsenseGene Expression030105 genetics & heredityFrameshift mutationConsanguinityMice03 medical and health sciencesExonNeural Stem CellsIntellectual DisabilityRetinitis pigmentosaGene expressionGeneticsmedicineAnimalsHumansMissense mutationFamilyChildGeneGenetics (clinical)media_commonCerebral CortexNeuronsGeneticsbiologyHomozygoteSyndromemedicine.diseasePedigree030104 developmental biologyMutationbiology.proteinFemaleCarrier ProteinsRetinitis PigmentosaAmerican Journal of Medical Genetics Part A
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Identification of a novel LMF1 nonsense mutation responsible for severe hypertriglyceridemia by targeted next-generation sequencing

2016

Background Severe hypertriglyceridemia (HTG) may result from mutations in genes affecting the intravascular lipolysis of triglyceride (TG)-rich lipoproteins. Objective The aim of this study was to develop a targeted next-generation sequencing panel for the molecular diagnosis of disorders characterized by severe HTG. Methods We developed a targeted customized panel for next-generation sequencing Ion Torrent Personal Genome Machine to capture the coding exons and intron/exon boundaries of 18 genes affecting the main pathways of TG synthesis and metabolism. We sequenced 11 samples of patients with severe HTG (TG>885 mg/dL–10 mmol/L): 4 positive controls in whom pathogenic mutations had pre…

AdultMale0301 basic medicineCandidate geneEndocrinology Diabetes and MetabolismDNA Mutational AnalysisNonsense mutationPanel-based NGS sequencing030204 cardiovascular system & hematologyBiologymedicine.disease_causeDNA sequencing03 medical and health sciencessymbols.namesakeExon0302 clinical medicineNutrition and DieteticInternal MedicinemedicineHumansGeneHypertriglyceridemiaSanger sequencingGeneticsMutationNutrition and DieteticsLMF1 geneNonsense mutationHigh-Throughput Nucleotide SequencingInfantMembrane ProteinsIon semiconductor sequencingMiddle AgedIon torrent PGM sequencingPhenotype030104 developmental biologyChild PreschoolsymbolsFemaleCardiology and Cardiovascular MedicineJournal of Clinical Lipidology
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Mutation analysis in myophosphorylase deficiency (McArdle's disease).

1998

Inherited deficiency of myophosphorylase leads to glycogen storage disease type V (McArdle's disease). We performed mutation analysis in 9 patients of eight unrelated families from Germany with typical cliniclal presentation of myophos-phorylase deficiency. Beside previously described mutations we identified four novel mutations in the myophorsphorylase gene. Four patients were homozygous for a nonsense mutation Arg49Stop that has been reported to be the most common mutation in white patients. Two affected siblings were compound heterozygotes for a novel missense mutation Gly685Arg and the nonsense mutation Arg49Stop. One patient carried a novel nonsense mutation Arg575Stop and a previously…

AdultMaleAdolescentNonsense mutationDNA Mutational AnalysisBiologyCompound heterozygosityPolymerase Chain ReactionmedicineMissense mutationHumansAmino Acid SequenceChildCodonAgedGeneticsTransition (genetics)Base SequenceHomozygoteMiddle Agedmedicine.diseaseNeurologyMyophosphorylaseMutation (genetic algorithm)MutationMutation testingGlycogen Storage Disease Type VFemaleNeurology (clinical)Glycogen storage disease type VPolymorphism Restriction Fragment LengthAnnals of neurology
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Expanding the clinical phenotype of patients with a ZDHHC9 mutation.

2013

In 2007, 250 families with X-linked intellectual disability (XLID) were screened for mutations in genes on the X-chromosome, and in 4 of these families, mutations in the ZDHHC9 gene were identified. The ID was either isolated or associated with a marfanoid habitus. ZDHHC9 encodes a palmitoyl transferase that catalyzes the posttranslational modification of NRAS and HRAS. Since this first description, no additional patient with a ZDHHC9 mutation has been reported in the literature. Here, we describe a large family in which we identified a novel pathogenic ZDHHC9 nonsense mutation (p.Arg298*) by parallel sequencing of all X-chromosome exons. The mutation cosegregated with the clinical phenotyp…

AdultMaleAdolescentX-linked intellectual disabilityGenetic counselingNonsense mutationNeuropsychological TestsBioinformaticsYoung AdultFatal OutcomeGenes X-LinkedIntellectual DisabilityIntellectual disabilityGeneticsmedicineHumansHRASChildGenetics (clinical)GeneticsMassive parallel sequencingAcrocyanosisbusiness.industryBrainFaciesmedicine.diseaseMagnetic Resonance ImagingPedigreePhenotypeMutation (genetic algorithm)MutationbusinessAcyltransferasesAmerican journal of medical genetics. Part A
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Oligophrenin 1 mutations frequently cause X-linked mental retardation with cerebellar hypoplasia

2005

Background: Mutations of oligophrenin 1, one of the first genes identified in nonspecific X-linked mental retardation (MRX), have been described in patients with moderate to severe cognitive impairment and predominant cerebellar hypoplasia, in the vermis. Objective: To further delineate the phenotypic and mutational spectrum of the syndrome, by screening oligophrenin 1 in two cohorts of male patients with mental retardation (MR) with or without known posterior fossa anomalies. Methods: Clinical examination, cognitive testing, MRI studies, and mutational analysis (denaturing gradient gel electrophoresis and direct sequencing) on blood lymphocytes were performed in 213 unrelated affected indi…

AdultMaleCerebellumAdolescentGenotypeDNA Mutational AnalysisNonsense mutationNervous System Malformationsmedicine.disease_causeCohort StudiesExonCerebellar DiseasesCerebellummedicineHumansGenetic TestingChildCerebellar hypoplasiaGeneticsMutationSplice site mutationGTPase-Activating ProteinsNuclear Proteinsmedicine.diseaseMagnetic Resonance ImagingHypoplasiaPedigreeDevelopmental disorderAlternative SplicingCytoskeletal ProteinsPhenotypemedicine.anatomical_structureFacial AsymmetryCodon NonsenseChild PreschoolMutationMental Retardation X-LinkedRNA Splice SitesNeurology (clinical)PsychologyGene DeletionNeurology
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Auditory event-related potentials (ERP) reflect temporal changes in speech stimuli

1997

We studied the brain's reactions to deviations in the duration of a stop consonant using event-related potentials in an oddball paradigm. A naturally produced nonsense word was used as a frequent standard stimulus which differed from two infrequently presented deviant stimuli only by the duration of the silence period inside the stop, making the consonant sound longer. Evoked responses to the deviant stimuli showed sharply rising negativity after the unexpected prolongation of the silence and a later negativity, the duration of which was related to the timing of the beginning of the second part of the deviant sound. This later negativity is, at least partly, elicited by a mismatch process t…

AdultMaleConsonantmedicine.medical_specialtyTime Factorsmedicine.diagnostic_testAuditory eventGeneral NeuroscienceBrainMismatch negativityElectroencephalographyElectroencephalographyAudiologyAcoustic StimulationDuration (music)Stop consonantEvoked Potentials AuditorymedicineHumansSpeechFemaleNonsense wordPsychologyOddball paradigmNeuroReport
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Clinical and molecular genetic spectrum of autosomal dominant Emery-Dreifuss muscular dystrophy due to mutations of the lamin A/C gene.

2000

Emery-Dreifuss muscular dystrophy (EDMD) is characterized by early contractures of the elbows and Achilles tendons, slowly progressive muscle wasting and weakness, and life-threatening cardiomyopathy with conduction blocks. We recently identified LMNA encoding two nuclear envelope proteins, lamins A and C, to be implicated in the autosomal dominant form of EDMD. Here, we report on the variability of the phenotype and spectrum of LMNA mutations in 53 autosomal dominant EDMD patients (36 members of 6 families and 17 sporadic cases). Twelve of the 53 patients showed cardiac involvement exclusively, although the remaining 41 all showed muscle weakness and contractures. We were able to identify …

AdultMaleContractureAdolescentGenotypeBiopsyNonsense mutationDNA Mutational AnalysisEmerinMutation MissenseLaminopathyBiologyLMNACardiovascular Physiological PhenomenamedicineMissense mutationHumansEmery–Dreifuss muscular dystrophyMuscular dystrophyAge of OnsetChildCreatine KinasePhysical ExaminationMuscle contractureAgedGenes DominantGeneticsMuscle WeaknessMyocardiumNuclear ProteinsHeartMiddle Agedmedicine.diseaseLamin Type ALaminsMuscular Dystrophy Emery-DreifussPedigreeMuscular AtrophyPhenotypeNeurologyDisease ProgressionFemaleNeurology (clinical)Gene DeletionAnnals of neurology
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