Search results for "Heterozygote"

showing 10 items of 240 documents

Benign nocturnal alternating hemiplegia of childhood

2018

Objective: To describe the clinical spectrum of benign nocturnal alternating hemiplegia of childhood (BNAHC) including long-term follow-up data of previously published cases and to propose an underlying genetic cause of this disorder. Methods: We studied the medical data of two novel patients, reviewed the literature on BNAHC, and gathered information of the most recent follow-up of published cases regarding the course of episodes, further development, attempted drugs, ancillary investigations, and sequelae. Results: All patients, i.e. two novel cases and twelve patients identified in the literature (13 boys, 1 girl, age at onset four months to three years), experienced episodes of hemipleg…

0301 basic medicineMaleExome sequencingPediatricsmedicine.medical_specialtyHeterozygoteHemiplegiaNerve Tissue ProteinsPATIENTSensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]03 medical and health sciences0302 clinical medicinePRRT2 MUTATIONSmedicineHumansIctalPAROXYSMAL KINESIGENIC DYSKINESIAFamily historyPRRT2 geneExome sequencingCryingbusiness.industryAlternating hemiplegia of childhoodInfantMembrane ProteinsGeneral MedicineParoxysmal dyskinesiamedicine.diseaseDisorders of movement Donders Center for Medical Neuroscience [Radboudumc 3]GENESleep deprivation030104 developmental biologyPhenotypeTreatment OutcomeSYNAPTIC-TRANSMISSIONMigraineMIGRAINEChild PreschoolPediatrics Perinatology and Child HealthDisease ProgressionNeurology (clinical)medicine.symptombusinessINFANTILE CONVULSIONS030217 neurology & neurosurgeryGene DeletionBenign nocturnal alternating hemiplegia of childhoodEuropean Journal of Paediatric Neurology
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Clinical and biochemical characteristics of individuals with low cholesterol syndromes: A comparison between familial hypobetalipoproteinemia and fam…

2017

Background The most frequent monogenic causes of low plasma cholesterol are familial hypobetalipoproteinemia (FHBL1) because of truncating mutations in apolipoprotein B coding gene (APOB) and familial combined hypolipidemia (FHBL2) due to loss-of-function mutations in ANGPTL3 gene. Objective A direct comparison of lipid phenotypes of these 2 conditions has never been carried out. In addition, although an increased prevalence of liver steatosis in FHBL1 has been consistently reported, the hepatic consequences of FHBL2 are not well established. Methods We investigated 350 subjects, 67 heterozygous carriers of APOB mutations, 63 carriers of the p.S17* mutation in ANGPTL3 (57 heterozygotes and …

0301 basic medicineMaleHepatic steatosisSettore MED/09 - Medicina InternaApolipoprotein BEndocrinology Diabetes and Metabolism030204 cardiovascular system & hematologymedicine.disease_causeANGPTL3 gene; APOB gene; Familial combined hypolipidemia; Familial hypobetalipoproteinemia; HDL cholesterol; Hepatic steatosis; Low cholesterol syndromesHypobetalipoproteinemiasExon0302 clinical medicineHDL cholesterolANGPTL3Nutrition and DieteticFamilial hypobetalipoproteinemiaGeneticsMutationNutrition and Dieteticsbiologyhepatic steatosisHomozygoteANGPTL3 geneMiddle AgedLow cholesterol syndromesPhenotypePhenotypelipids (amino acids peptides and proteins)FemaleCardiology and Cardiovascular MedicineANGPTL3 gene; APOB gene; familial combined hypolipidemia; familial hypobetalipoproteinemia; HDL cholesterol; hepatic steatosis; low cholesterol syndromesmedicine.medical_specialtyHeterozygoteLow cholesterol syndromeHepatic steatosi03 medical and health sciencesInternal medicineInternal MedicinemedicineHumansAPOB geneFamilial combined hypolipidemiaGeneAgedAngiopoietin-Like Protein 3Apolipoproteins Bbusiness.industryHeterozygote advantagemedicine.disease030104 developmental biologyEndocrinologyAngiopoietin-like ProteinsMutationbiology.proteinlow cholesterol syndromesSteatosisbusiness
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Generation of a disease-specific iPS cell line derived from a patient with Charcot-Marie-Tooth type 2K lacking functional GDAP1 gene

2016

Human CMT2-FiPS4F1 cell line was generated from fibroblasts of a patient with Charcot-Marie-Tooth disease harbouring the following mutations in the GDAP1 gene in heterozygosis: p.Q163X/p.T288NfsX3. This patient did not present mutations in the PM22, MPZ or GJB genes. Human reprogramming factors OCT3/4, KLF4, SOX2 and C-MYC were delivered using a non-integrative methodology that involves the use of Sendai virus.

0301 basic medicineMaleHeterozygoteCellular differentiationCèl·lulesDNA Mutational AnalysisGenetic VectorsInduced Pluripotent Stem CellsKaryotypeNerve Tissue ProteinsBiologyPolymorphism Single NucleotideSendai virusCell Line03 medical and health sciencesKruppel-Like Factor 4stomatognathic systemCharcot-Marie-Tooth DiseaseHumansInduced pluripotent stem cellGeneTranscription factorMedicine(all)GeneticsBase SequenceHeterozygote advantageCell DifferentiationCell BiologyGeneral MedicineFibroblastsbiology.organism_classificationCellular ReprogrammingSendai virus030104 developmental biologyMicroscopy FluorescenceKLF4embryonic structuresSistema nerviós MalaltiesReprogrammingDevelopmental BiologyTranscription Factors
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Heterozygous Variants in KDM4B Lead to Global Developmental Delay and Neuroanatomical Defects

2020

International audience; KDM4B is a lysine-specific demethylase with a preferential activity on H3K9 tri/di-methylation (H3K9me3/2)-modified histones. H3K9 tri/di-demethylation is an important epigenetic mechanism responsible for silencing of gene expression in animal development and cancer. However, the role of KDM4B on human development is still poorly characterized. Through international data sharing, we gathered a cohort of nine individuals with mono-allelic de novo or inherited variants in KDM4B. All individuals presented with dysmorphic features and global developmental delay (GDD) with language and motor skills most affected. Three individuals had a history of seizures, and four had a…

0301 basic medicineMaleJumonji Domain-Containing Histone Demethylases[SDV]Life Sciences [q-bio]Developmental DisabilitiesCorpus callosumHippocampusEpigenesis GeneticHistonesMice0302 clinical medicineNeurodevelopmental disorderPolymicrogyriaGlobal developmental delayAgenesis of the corpus callosumGenetics (clinical)BrainMagnetic Resonance Imaging[SDV] Life Sciences [q-bio]intellectual disabilityBrain sizeFemaledysmorphic hippocampiSignal TransductionHeterozygoteheterozygous variantglobal developmental delayBiologyNervous System MalformationsMethylation03 medical and health sciencesSeizuresReportKDM4BGeneticsmedicineAnimalsHumansneurodevelopmental disorder.Dentate gyrusGenetic VariationJMJD2Bmedicine.diseaseneurodevelopmental disorder030104 developmental biologyagenesis of the corpus callosumNeuroscienceProtein Processing Post-Translational030217 neurology & neurosurgeryVentriculomegalyAmerican journal of human genetics
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Characterization of the Clinical and Immunologic Phenotype and Management of 157 Individuals with 56 Distinct Heterozygous NFKB1 Mutations

2020

Contains fulltext : 229571.pdf (Publisher’s version ) (Closed access) BACKGROUND: An increasing number of NFKB1 variants are being identified in patients with heterogeneous immunologic phenotypes. OBJECTIVE: To characterize the clinical and cellular phenotype as well as the management of patients with heterozygous NFKB1 mutations. METHODS: In a worldwide collaborative effort, we evaluated 231 individuals harboring 105 distinct heterozygous NFKB1 variants. To provide evidence for pathogenicity, each variant was assessed in silico; in addition, 32 variants were assessed by functional in vitro testing of nuclear factor of kappa light polypeptide gene enhancer in B cells (NF-κB) signaling. RESU…

0301 basic medicineMaleNF-KAPPA-BMedizinlnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]Fluorescent Antibody TechniqueAutoimmunityDiseaseNUCLEAR-FACTORKaplan-Meier Estimatemedicine.disease_causeHypogammaglobulinemia0302 clinical medicineNFKB1 variants and mutations; autosomal dominant inheritance; common variable immunodeficiency; reduced penetrance; variable expressivityHDE PEDImmunology and Allergyvariants and mutationsNF-κB1-related phenotypeImmunodeficiencyIMMUNODEFICIENCY*NF-?B1-related phenotypeNFKB1 variants and mutations1184 Genetics developmental biology physiologycommon variable immunodeficiencyDisease ManagementMiddle AgedNF-kappa B1-related phenotypereduced penetrancePrognosisPenetranceImmunohistochemistryMagnetic Resonance Imaging3. Good healthPhenotypeNFKB1 variant*NFKB1 variant*common variable immunodeficiencyFemaleHaploinsufficiency*reduced penetranceNFKB1 mutationAdultHeterozygote*NFKB1 mutationImmunologyHAPLOINSUFFICIENCYArticle03 medical and health sciencesvariable expressivityautosomal dominantmedicineHumansGenetic Predisposition to DiseaseGenetic Association StudiesAgedbusiness.industryCommon variable immunodeficiencyNF-kappa B p50 SubunitNF-KAPPA-B1Immune dysregulationmedicine.diseaseautosomal dominant inheritance030104 developmental biologyBiological Variation PopulationImmunologyCELLSMutation*autosomal dominantPrimary immunodeficiency3111 BiomedicinebusinessTomography X-Ray ComputedBiomarkers030215 immunology
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Homocysteine concentration in coronary artery disease: Influence of three common single nucleotide polymorphisms.

2017

Whether single nucleotide polymorphisms (SNPs) of homocysteine metabolism enzymes influence the rate of cardiovascular (CV) events in coronary artery disease (CAD) patients remains controversial.In this analysis, 1126 subjects from the AtheroGene study with CAD and 332 control subjects without known CAD were included. The following SNPs were investigated: methylentetrahydrofolate reductase (MTHFR-C667T), methionin synthetase (MS-D919G), and cystathionin beta synthetase (CBS-I278T). The endpoint was the combination of cardiovascular death, stroke, and non-fatal myocardial infarction (N = 286). The median follow-up time was 6.4 years. Kaplan-Meier curve analysis showed an increasing event rat…

0301 basic medicineMaleTime FactorsHomocysteineEndocrinology Diabetes and MetabolismMyocardial InfarctionMedicine (miscellaneous)Coronary Artery DiseaseKaplan-Meier Estimate030204 cardiovascular system & hematologyReductaseGastroenterology5-Methyltetrahydrofolate-Homocysteine S-MethyltransferaseCoronary artery diseasechemistry.chemical_compound0302 clinical medicineGene FrequencyRisk FactorsMyocardial infarctionStrokeHomocysteineGeneticsNutrition and DieteticsbiologyHomozygoteMiddle AgedStrokePhenotypeArea Under CurveDisease ProgressionFemaleCardiology and Cardiovascular Medicinemedicine.medical_specialtyHeterozygoteCystathionine beta-SynthaseSingle-nucleotide polymorphismPolymorphism Single NucleotideRisk Assessment03 medical and health sciencesPredictive Value of TestsInternal medicinemedicineHumansGenetic Predisposition to DiseaseGenetic Association StudiesMethylenetetrahydrofolate Reductase (NADPH2)AgedProportional Hazards ModelsChi-Square DistributionCurve analysismedicine.disease030104 developmental biologychemistryROC CurveMethylenetetrahydrofolate reductaseCase-Control Studiesbiology.proteinBiomarkersNutrition, metabolism, and cardiovascular diseases : NMCD
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The neuroanatomy of Eml1 knockout mice, a model of subcortical heterotopia

2018

Symposium issue: Human Cortex Developmentidentifiant wos: 000482426800014; International audience; The cerebral cortex is a highly organized structure responsible for advanced cognitive functions. Its development relies on a series of steps including neural progenitor cell proliferation, neuronal migration, axonal outgrowth and brain wiring. Disruption of these steps leads to cortical malformations, often associated with intellectual disability and epilepsy. We have generated a new resource to shed further light on subcortical heterotopia, a malformation characterized by abnormal neuronal position. We describe here the generation and characterization of a knockout (KO) mouse model for Eml1,…

0301 basic medicineMale[SDV.MHEP.AHA] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]heterotopiaHistology[SDV.BA] Life Sciences [q-bio]/Animal biologyClassical Lissencephalies and Subcortical Band HeterotopiasBiologyCorpus callosum03 medical and health sciences0302 clinical medicinemedicine[SDV.MHEP.AHA]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]Animals[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Progenitor cellMolecular BiologyEcology Evolution Behavior and SystematicsMice Knockout[SDV.BA]Life Sciences [q-bio]/Animal biologyBrainHeterozygote advantageCell BiologyOriginal Articlesmouse model of developmental disordersmedicine.diseasecortical malformationsCorticogenesisDisease Models Animal030104 developmental biologymedicine.anatomical_structureHeterotopia (medicine)Cerebral cortexKnockout mouseFemale[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]AnatomyNeuroscienceMicrotubule-Associated Proteins030217 neurology & neurosurgeryDevelopmental BiologyNeuroanatomy
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Genome-wide diversity and runs of homozygosity in the “Braque Français, type Pyrénées” dog breed

2018

Objective Braque Français, type Pyrénées is a French hunting-dog breed whose origin is traced back to old pointing gun-dogs used to assist hunters in finding and retrieving game. This breed is popular in France, but seldom seen elsewhere. Despite the ancient background, the literature on its genetic characterization is surprisingly scarce. A recent study looked into the demography and inbreeding using pedigree records, but there is yet no report on the use of molecular markers in this breed. The aim of this work was to genotype a population of Braque Français, type Pyrénées dogs with the high-density SNP array to study the genomic diversity of the breed. Results The average observed (\docum…

0301 basic medicineMalelcsh:MedicineRuns of HomozygosityGenetic diversitySettore AGR/17 - Zootecnica Generale E Miglioramento Geneticotype PyrénéesSNPGenetic diversityMolecular markersInbreedingRuns of homozygosityHeterozygosityEffective population sizeDogInbreedingDogBraque Français type PyrénéesSNPGenetic diversityMolecular markersInbreedingRuns of homozygosityHeterozygositylcsh:QH301-705.5education.field_of_studyHeterozygosityGenomeHomozygote04 agricultural and veterinary sciencesGeneral Medicinetype PyrénéesBraque Français type PyrénéesBreedResearch NoteFemaleFranceInbreedingSNP arrayGenetic MarkersHeterozygotePopulationSNPBiologyRuns of homozygosityPolymorphism Single NucleotideGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesDogsAnimalsGenetic variabilityeducationlcsh:Science (General)Genetic diversityDogBraque Françaislcsh:R0402 animal and dairy sciencebraque françaisMolecular markersGenetic Variation040201 dairy & animal science030104 developmental biologylcsh:Biology (General)Evolutionary biologyDog Braque Français type Pyrénées SNP Genetic diversity Molecular markers Inbreeding Runs of homozygosity Heterozygositylcsh:Q1-390BMC Research Notes
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Neuronal Excitability And Spontaneous Synaptic Transmission In The Entorhinal Cortex Of Bdnf Heterozygous Mice

2018

Abstract Brain Derived Neurotropic Factor (BDNF) is a neutrophic factor that is required for the normal neuronal development and function. BDNF is involved in regulation of synapses as well as neuronal excitability. Entorhinal Cortex (EC) is a key brain area involved in many physiological and pathological processes. In this study we investigated the effects of chronically reduced BDNF levels on layer 3 pyramidal neurons of EC. We aimed to assess the effects of reduced levels of BDNF on firing properties, spontaneous synaptic currents and excitation/inhibition balance from acute brain slices. Patch clamp recordings were obtained from pyramidal neurons of Entorhinal Cortex Layer 3. Findings o…

0301 basic medicineMalemedicine.medical_specialtyHeterozygoteAction potentialAction PotentialsNeurotransmissionInhibitory postsynaptic potentialSynaptic Transmission03 medical and health sciencesMice0302 clinical medicineInternal medicinemedicinePremovement neuronal activityAnimalsEntorhinal CortexPatch clampChemistryGeneral NeuroscienceSpontaneous synaptic transmissionBrain-Derived Neurotrophic FactorExcitatory Postsynaptic PotentialsEntorhinal cortex030104 developmental biologyEndocrinologyInhibitory Postsynaptic Potentialsnervous systemGene Knockdown TechniquesExcitatory postsynaptic potentialFemale030217 neurology & neurosurgery
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Heterozygous carriage of the alpha1-antitrypsin Pi*Z variant increases the risk to develop liver cirrhosis.

2018

ObjectiveHomozygous alpha1-antitrypsin (AAT) deficiency increases the risk for developing cirrhosis, whereas the relevance of heterozygous carriage remains unclear. Hence, we evaluated the impact of the two most relevant AAT variants (‘Pi*Z’ and ‘Pi*S’), present in up to 10% of Caucasians, on subjects with non-alcoholic fatty liver disease (NAFLD) or alcohol misuse.DesignWe analysed multicentric case–control cohorts consisting of 1184 people with biopsy-proven NAFLD and of 2462 people with chronic alcohol misuse, both cohorts comprising cases with cirrhosis and controls without cirrhosis. Genotyping for the Pi*Z and Pi*S variants was performed.ResultsThe Pi*Z variant presented in 13.8% of p…

0301 basic medicineMalemedicine.medical_specialtyHeterozygoteCirrhosisMedizinSingle-nucleotide polymorphismDiseaseGastroenterologyPolymorphism Single NucleotideRisk Assessment03 medical and health sciences0302 clinical medicineAge DistributionLiver Cirrhosis AlcoholicNon-alcoholic Fatty Liver DiseaseInternal medicineGermanymedicinePiConfidence IntervalsOdds RatioHumansGenetic Predisposition to DiseaseRisk factorSex DistributionGenotypingLiver injurybusiness.industryGenetic Carrier ScreeningIncidenceFatty liverBiopsy NeedleGastroenterologyGenetic Variationmedicine.diseasePrognosisImmunohistochemistry030104 developmental biologyAustriaCase-Control Studiesalpha 1-Antitrypsin030211 gastroenterology & hepatologyFemalebusinessGut
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