Search results for "Heredity"

showing 10 items of 247 documents

Clinical and molecular spectrum of renal malformations in Kabuki syndrome.

2013

International audience; OBJECTIVE: To determine the frequency and types of renal malformations, and to evaluate renal function in a cohort of patients with Kabuki syndrome (KS). STUDY DESIGN: Renal ultrasound scans and plasma creatinine measurements were collected from a French cohort of 94 patients with genotyped KS. Renal function was evaluated based on the estimated glomerular filtration rate. A genotype-phenotype study was conducted for renal and urinary tract malformations. RESULTS: Renal malformations were present in 22% of cases, and urinary tract anomalies were present in 15%. Renal malformations were observed in 28% of the MLL2 mutation-positive group and in 0% of the MLL2 mutation…

MalePathologyGenotyping Techniquesurologic and male genital diseasesKidneyCohort Studieschemistry.chemical_compoundChildUltrasonographyHistone Demethylases0303 health sciencesKidney030305 genetics & heredityNuclear ProteinsHypoplasia3. Good healthNeoplasm ProteinsDNA-Binding Proteinsmedicine.anatomical_structureVestibular DiseasesChild PreschoolCreatinineBiological MarkersFemaleFranceAbnormalitiesMultipleCohort studyGlomerular Filtration RateAdultGenetic Markersmedicine.medical_specialtyAdolescentUrinary systemUrologyRenal function03 medical and health sciencesYoung AdultmedicineHumansAbnormalities MultiplePreschoolGenetic Association Studies030304 developmental biologyRetrospective StudiesCreatinine[SDV.GEN]Life Sciences [q-bio]/Geneticsbusiness.industryInfantRetrospective cohort studymedicine.diseaseHematologic DiseaseschemistryFacePediatrics Perinatology and Child Healthbusiness[ SDV.GEN ] Life Sciences [q-bio]/GeneticsKabuki syndromeBiomarkersThe Journal of pediatrics
researchProduct

A Paucisymptomatic Neuromuscular Disease Mimicking Type III 5q-SMA With Complex Rearrangements in the SMN Gene

2013

Spinal muscular atrophy is an autosomal-recessive neuromuscular disorder, causing progressive proximal weakness and atrophy of the voluntary muscles. More than 96% of the spinal muscular atrophy patients show a homozygous absence of exons 7 and 8, or exon 7 only, in SMN1, the telomeric copy of the SMN gene. We report a young male patient with neurogenic symptoms and sparse muscle fiber atrophy, suggestive of a mild form of type III spinal muscular atrophy. He was found to be a carrier of intragenic mutations in both copies of the SMN gene, exhibiting a homozygous duplication of exons 7 and 8 in SMN1 and a homozygous deletion of exon 8 as well as a heterozygous deletion of exon 7 in SMN2. H…

MalePathologymedicine.medical_specialtyNeuromuscular diseaseBiopsyDNA Mutational AnalysisSMN1Spinal Muscular Atrophies of ChildhoodBiologyQuadriceps MuscleDiagnosis DifferentialMice03 medical and health sciencesExonAtrophyGene duplicationmedicineAnimalsHumansChildSequence Deletion030304 developmental biology0303 health sciences030305 genetics & heredityNeuromuscular DiseasesSpinal muscular atrophymedicine.diseaseSMA*ImmunohistochemistrySurvival of Motor Neuron 1 ProteinMolecular biologynervous system diseasesSmn geneSurvival of Motor Neuron 2 ProteinMuscular AtrophyPhenotypeMutationPediatrics Perinatology and Child HealthNeurology (clinical)Journal of Child Neurology
researchProduct

Newborn screening and disease variants predict neurological outcome in isovaleric aciduria.

2021

Isovaleric aciduria (IVA), a metabolic disease with severe (classic IVA) or attenuated phenotype (mild IVA), is included in newborn screening (NBS) programs worldwide. The long-term clinical benefit of screened individuals, however, is still rarely investigated. A national, prospective, observational, multi-center study of individuals with confirmed IVA identified by NBS between 1998 and 2018 was conducted. Long-term clinical outcomes of 94 individuals with IVA were evaluated, representing 73.4% (for classic IVA: 92.3%) of the German NBS cohort. In classic IVA (N = 24), NBS prevented untimely death except in one individual with lethal neonatal sepsis (3.8%) but did not completely prevent si…

MalePediatricsmedicine.medical_specialtyAdolescentNeurocognitive DisordersDisease03 medical and health sciencesYoung AdultCognitionNeonatal ScreeningMaintenance therapyGermanyGeneticsmedicineHumansProspective StudiesMetabolic diseaseChildAmino Acid Metabolism Inborn ErrorsGenetics (clinical)030304 developmental biology0303 health sciencesNewborn screeningNeonatal sepsisIsovaleryl-CoA Dehydrogenasebusiness.industry030305 genetics & heredityInfant NewbornInfantmedicine.diseasePrognosisIsovaleric AcidemiaPhenotypeChild PreschoolCohortFemalesense organsbusinessNeurocognitiveJournal of inherited metabolic diseaseREFERENCES
researchProduct

Disruption of the ASTN2 / TRIM32 locus at 9q33.1 is a risk factor in males for Autism Spectrum Disorders, ADHD and other neurodevelopmental phenotypes

2014

Rare copy number variants (CNVs) disrupting ASTN2 or both ASTN2 and TRIM32 have been reported at 9q33.1 by genome-wide studies in a few individuals with neurodevelopmental disorders (NDDs). The vertebrate-specific astrotactins, ASTN2 and its paralog ASTN1, have key roles in glial-guided neuronal migration during brain development. To determine the prevalence of astrotactin mutations and delineate their associated phenotypic spectrum, we screened ASTN2/TRIM32 and ASTN1 (1q25.2) for exonic CNVs in clinical microarray data from 89 985 individuals across 10 sites, including 64 114 NDD subjects. In this clinical dataset, we identified 46 deletions and 12 duplications affecting ASTN2. Deletions o…

MaleReceptors Cell Surface/geneticsAutismChild Development Disorders Pervasive/geneticsGene ExpressionGenome-wide association studyMedical and Health SciencesTripartite Motif ProteinsRisk FactorsReceptors2.1 Biological and endogenous factorsProtein IsoformsNerve Tissue Proteins/geneticsCopy-number variationAetiologyChildGenetics (clinical)Sequence DeletionPediatricGenetics & HeredityGeneticseducation.field_of_studySingle NucleotideArticlesGeneral MedicineExonsBiological SciencesMental HealthPhenotypeAutism spectrum disorderOrgan SpecificityCerebellar cortexChild PreschoolCell SurfaceSpeech delayFemalemedicine.symptomTranscription Initiation SiteAttention Deficit Disorder with Hyperactivity/geneticsChromosomes Human Pair 9HumanPair 9AdultPediatric Research InitiativeChild Development DisordersAdolescentDNA Copy Number VariationsIntellectual and Developmental Disabilities (IDD)Ubiquitin-Protein LigasesPopulationTranscription Factors/geneticsNerve Tissue ProteinsReceptors Cell SurfaceBiologyPolymorphism Single NucleotideChromosomesYoung AdultClinical ResearchProtein Isoforms/geneticsBehavioral and Social ScienceGeneticsmedicineAttention deficit hyperactivity disorderHumansGenetic Predisposition to DiseasePolymorphismPreschooleducationMolecular BiologyGenetic Association StudiesPervasiveGlycoproteinsHuman GenomeNeurosciencesInfant NewbornGlycoproteins/geneticsInfantNewbornmedicine.diseaseBrain DisordersAttention Deficit Disorder with HyperactivityChild Development Disorders PervasiveCase-Control StudiesAutismTranscription Factors
researchProduct

Genetic variation in neuromuscular performance.

1973

Using a simple cumulative model of heredity plus environment, based on intrapair differences observed in monozygous (MZ) and dizygous (DZ) twins, the relative contribution of heredity to the interindividual variance in several neuromuscular parameters was determined with 15 pairs of male (8 MZ and 7 DZ) and 14 pairs of female (7 MZ and 7 DZ) twins ranging in age from 10 to 14 years. The data disclosed that in boys the variability in maximal mechanical (anaerobic) power was 99.2% genetically determined under the environmental conditions of the study. The corresponding heritability estimate values for the patellar reflex time and reaction time were 97.5% and 85.7%, respectively. In girls the …

MaleReflex StretchAdolescentPhysiologyPhysical ExertionNeuromuscular JunctionTwinsPhysiologyBiologymedicine.disease_causePregnancyPhysiology (medical)Genetic variationHereditymedicineReaction TimeHumansOrthopedics and Sports MedicineGenetic variabilityChildGeneticsmedicine.diagnostic_testBody WeightPublic Health Environmental and Occupational HealthPatellar reflexGeneral MedicineHuman physiologyPatellaHeritabilityBody HeightGenetic TechniquesGenetic CodeFemaleInternationale Zeitschrift fur angewandte Physiologie, einschliesslich Arbeitsphysiologie
researchProduct

Mandibular-pelvic-patellar syndrome (mpp) is a novel pitx1-related disorder due to alteration of pitx1 transactivation ability

2020

International audience; PITX1 is a homeobox transcription factor essential for hindlimb morphogenesis. Two PITX1-related human disorders have been reported to date: PITX1 ectopic expression causes Liebenberg syndrome, characterized by malformation of upper limbs showing a "lower limb" appearance; PITX1 deletions or missense variation cause a syndromic picture including clubfoot, tibial hemimelia, and preaxial polydactyly. We report two novel PITX1 missense variants, altering PITX1 transactivation ability, in three individuals from two unrelated families showing a distinct recognizable autosomal dominant syndrome, including first branchial arch, pelvic, patellar, and male genital abnormaliti…

MaleTranscriptional ActivationPathologymedicine.medical_specialtyHindlimb morphogenesis[SDV]Life Sciences [q-bio]Mutation MissensepelvisBiologyPierre-Robin03 medical and health sciencesTransactivationGeneticsmedicineMissense mutationAnimalsHumansPaired Box Transcription FactorsChildPITX1Genetics (clinical)030304 developmental biologyMice Knockoutcleft palate0303 health sciencesBone Diseases Developmental030305 genetics & heredityPreaxial polydactylyInfant NewbornLiebenberg syndromemedicine.disease3. Good healthgenitalpatella[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsChild PreschoolHomeoboxEctopic expressionHaploinsufficiency
researchProduct

Loss‐of‐function variants in ARHGEF9 are associated with an X‐linked intellectual disability dominant disorder

2021

ARHGEF9 defects lead to an X-linked intellectual disability disorder related to inhibitory synaptic dysfunction. This condition is more frequent in males, with a few affected females reported. Up to now, sequence variants and gross deletions have been identified in males, while only chromosomal aberrations have been reported in affected females who showed a skewed pattern of X-chromosome inactivation (XCI), suggesting an X-linked recessive (XLR) disorder. We report three novel loss-of-function (LoF) variants in ARHGEF9: A de novo synonymous variant affecting splicing (NM_015185.2: c.1056G>A, p.(Lys352=)) in one female; a nonsense variant in another female (c.865C>T, p.(Arg289*)), that is, a…

MaleX-linked intellectual disabilitymedia_common.quotation_subjectNonsenseMutation MissenseBiology03 medical and health sciencesGenes X-LinkedX Chromosome InactivationIntellectual DisabilityIntellectual disabilityGeneticsmedicineHumansMissense mutationGenetics (clinical)Loss function030304 developmental biologymedia_commonGenetics0303 health sciences030305 genetics & hereditymedicine.diseaseCodon NonsenseRNA splicingFemaleRho Guanine Nucleotide Exchange FactorsHuman Mutation
researchProduct

Treatment of Fabry Disease management with migalastat-outcome from a prospective 24 months observational multicenter study (FAMOUS).

2020

Abstract Aims Fabry disease (FD) is an X-linked lysosomal storage disorder caused by a deficiency of the lysosomal enzyme α-galactosidase A (GLA/AGAL), resulting in the lysosomal accumulation of globotriaosylceramide (Gb3). Patients with amenable GLA mutations can be treated with migalastat, an oral pharmacological chaperone increasing endogenous AGAL activity. In this prospective observational multicentre study, safety as well as cardiovascular, renal, and patient-reported outcomes and disease biomarkers were assessed after 12 and 24 months of migalastat treatment under ‘real-world’ conditions. Methods and results A total of 54 patients (26 females) (33 of these [61.1%] pre-treated with en…

Malemedicine.medical_specialty1-DeoxynojirimycinGlobotriaosylceramideRenal functionDiseaseGastroenterology03 medical and health scienceschemistry.chemical_compoundInternal medicineMigalastatmedicineHumansPharmacology (medical)Prospective Studies030304 developmental biology0303 health sciencesbusiness.industry030305 genetics & heredityDisease ManagementEnzyme replacement therapymedicine.diseaseFabry diseaseMulticenter studychemistryFabry DiseaseObservational studyFemaleCardiology and Cardiovascular MedicinebusinessEuropean heart journal. Cardiovascular pharmacotherapy
researchProduct

Overlapping phenotypes between SHORT and Noonan syndromes in patients with PTPN11 pathogenic variants

2020

Overlapping syndromes such as Noonan, Cardio-Facio-Cutaneous, Noonan syndrome (NS) with multiple lentigines and Costello syndromes are genetically heterogeneous conditions sharing a dysregulation of the RAS/mitogen-activated protein kinase (MAPK) pathway and are known collectively as the RASopathies. PTPN11 was the first disease-causing gene identified in NS and remains the more prevalent. We report seven patients from three families presenting heterozygous missense variants in PTPN11 probably responsible for a disease phenotype distinct from the classical Noonan syndrome. The clinical presentation and common features of these seven cases overlap with the SHORT syndrome. The latter is the c…

Malemusculoskeletal diseases0301 basic medicineMAPK/ERK pathwaycongenital hereditary and neonatal diseases and abnormalitiesMAP Kinase Signaling SystemProtein Tyrosine Phosphatase Non-Receptor Type 11030105 genetics & heredityBiologyGene productPhosphatidylinositol 3-Kinases03 medical and health sciencesMetabolic DiseasesGeneticsmedicineHumansMissense mutationskin and connective tissue diseasesProtein kinase BGrowth DisordersGenetics (clinical)GeneticsGenetic heterogeneityNoonan SyndromeGenetic Variationmedicine.diseasePTPN11NephrocalcinosisPhenotype030104 developmental biologySHORT syndromeHypercalcemiaNoonan syndromeFemaleMitogen-Activated Protein KinasesSignal TransductionClinical Genetics
researchProduct

What do French patients and geneticists think about prenatal and preimplantation diagnoses in Marfan syndrome?

2012

Objectives Marfan syndrome (MFS) is an autosomal dominant connective tissue disorder with manifestations mainly involving the skeletal, ocular, and cardiovascular systems. The phenotypic variability observed in MFS makes genetic counselling difficult. Prenatal diagnosis (PND) and preimplantation genetic diagnosis are technically feasible when a causal mutation is identified, but both raise many ethical questions in this condition. Little is known about opinions and practices in such reproductive issues in MFS. The goal of this study was to report on patients' points of view and geneticists' standard practices. Methods Two different questionnaires were produced. Results Fifty geneticists fil…

Marfan syndrome0303 health sciencesPediatricsmedicine.medical_specialty030219 obstetrics & reproductive medicinebusiness.industryGenetic counseling030305 genetics & heredityObstetrics and GynecologyPrenatal diagnosisDiseasePreimplantation genetic diagnosismedicine.disease3. Good health03 medical and health sciencesReproductive Issues0302 clinical medicineMedicineMedical diagnosisbusinessGenetics (clinical)Prenatal Diagnosis
researchProduct