Search results for "Hypotonia"

showing 10 items of 49 documents

Neonatal hyperinsulinemic hypoglycemia: case report of kabuki syndrome due to a novel KMT2D splicing-site mutation

2020

Abstract Background Persistent neonatal hypoglycemia, owing to the possibility of severe neurodevelopmental consequences, is a leading cause of neonatal care admission. Hyperinsulinemic hypoglycemia is often resistant to dextrose infusion and needs rapid diagnosis and treatment. Several congenital conditions, from single gene defects to genetic syndromes should be considered in the diagnostic approach. Kabuki syndrome type 1 (MIM# 147920) and Kabuki syndrome type 2 (MIM# 300867), can be associated with neonatal hyperinsulinemic hypoglycemia. Patient presentation We report a female Italian (Sicilian) child, born preterm at 35 weeks gestation, with persistent hypoglycemia. Peculiar facial dys…

0301 basic medicineHeterozygotePediatricsmedicine.medical_specialtyFacial dysmorphismNeonatal hypotoniaCase ReportHypoglycemiamedicine.disease_causeDiagnosis DifferentialNervous system malformation03 medical and health sciences0302 clinical medicineHyperinsulinismmedicineHumansAbnormalities MultipleHyperinsulinemic hypoglycemiaPathologicalbusiness.industryNeonatal hypoglycemiaInfant Newbornlcsh:RJ1-570lcsh:Pediatricsmedicine.diseaseHematologic DiseasesNeoplasm ProteinsDNA-Binding ProteinsPhenotype030104 developmental biologyNeonatal hypotoniaItalyVestibular DiseasesFaceMutationGestationFemalebusinessHyperinsulinismKabuki syndromeInfant PrematureNeonatal hypoglycemia030217 neurology & neurosurgeryItalian Journal of Pediatrics
researchProduct

Large national series of patients with Xq28 duplication involving MECP2: Delineation of brain MRI abnormalities in 30 affected patients.

2016

International audience; Xq28 duplications encompassing MECP2 have been described in male patients with a severe neurodevelopmental disorder associated with hypotonia and spasticity, severe learning disability, stereotyped movements, and recurrent pulmonary infections. We report on standardized brain magnetic resonance imaging (MRI) data of 30 affected patients carrying an Xq28 duplication involving MECP2 of various sizes (228 kb to 11.7 Mb). The aim of this study was to seek recurrent malformations and attempt to determine whether variations in imaging features could be explained by differences in the size of the duplications. We showed that 93% of patients had brain MRI abnormalities such …

0301 basic medicineMalePathologyMethyl-CpG-Binding Protein 2[SDV]Life Sciences [q-bio]030105 genetics & heredityCorpus callosumLateral ventricles0302 clinical medicineGene DuplicationIKBKGFLNAChildGenetics (clinical)GeneticsBrain Diseasesmedicine.diagnostic_testMiddle AgedPrognosisMagnetic Resonance ImagingHypotonia3. Good healthPedigree[SDV] Life Sciences [q-bio]medicine.anatomical_structurePhenotypeXq28 duplicationChild PreschoolFemalemedicine.symptomAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesAdolescentGenotypeBiologygenotype-phenotype correlationWhite matter03 medical and health sciencesYoung AdultGeneticsmedicineHumansGenetic Association StudiesChromosomes Human X[ SDV ] Life Sciences [q-bio]Infant NewbornInfantMagnetic resonance imagingHyperintensitynervous system diseasesMental Retardation X-LinkedMECP2 gene030217 neurology & neurosurgeryAmerican journal of medical genetics. Part A
researchProduct

The broad phenotypic spectrum of PPP2R1A -related neurodevelopmental disorders correlates with the degree of biochemical dysfunction

2021

PURPOSE: Neurodevelopmental disorders (NDD) caused by protein phosphatase 2A (PP2A) dysfunction have mainly been associated with de novo variants in PPP2R5D and PPP2CA, and more rarely in PPP2R1A. Here, we aimed to better understand the latter by characterizing 30 individuals with de novo and often recurrent variants in this PP2A scaffolding Aα subunit. METHODS: Most cases were identified through routine clinical diagnostics. Variants were biochemically characterized for phosphatase activity and interaction with other PP2A subunits. RESULTS: We describe 30 individuals with 16 different variants in PPP2R1A, 21 of whom had variants not previously reported. The severity of developmental delay …

0301 basic medicineMicrocephaly[SDV]Life Sciences [q-bio]Intellectual disability030105 genetics & heredityBioinformaticsEpilepsyNeurodevelopmental disorderIntellectual disabilityCOREProtein Phosphatase 2SPECIFICITYGenetics (clinical)PROTEIN PHOSPHATASE 2APhenotypeHypotoniaFAMILY3. Good healthPP2A[SDV] Life Sciences [q-bio]PPP2R1APPP2R5DINSIGHTSintellectual disabilityMicrocephalyMuscle Hypotoniamedicine.symptomLanguage delay[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsArticle03 medical and health sciencesNeurodevelopmental disorder[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologymedicineHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyEpilepsybusiness.industryMacrocephalyDEPHOSPHORYLATIONmedicine.diseaseneurodevelopmental disorder030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsNeurodevelopmental DisordersSUBUNITepilepsyHuman medicineTAUbusinessTranscription Factors
researchProduct

Microcephaly/Trigonocephaly, Intellectual Disability, Autism Spectrum Disorder, and Atypical Dysmorphic Features in a Boy with Xp22.31 Duplication

2019

The Xp22.31 segment of the short arm of the human X chromosome is a region of high instability with frequent rearrangement. The duplication of this region has been found in healthy people as well as in individuals with varying degrees of neurological impairment. The incidence has been reported in a range of 0.4-0.44% of the patients with neurological impairment. Moreover, there is evidence that Xp22.31 duplication may cause a common phenotype including developmental delay, intellectual disability, feeding difficulty, autistic spectrum disorders, hypotonia, seizures, and talipes. We report on a patient with microcephaly and trigonocephaly, moderate intellectual disability, speech and languag…

0301 basic medicinePediatricsmedicine.medical_specialtyMicrocephalyLanguage delayDevelopmental delayTrigonocephaly030105 genetics & heredityTooth anomaliesXp22.31 duplication03 medical and health sciencesGene duplicationIntellectual disabilityGeneticsmedicineTrigonocephalyTooth anomaliePathologicalGenetics (clinical)business.industrymedicine.diseaseHypotoniaAutism spectrum disorderNovel Insights from Clinical PracticeMicrocephalymedicine.symptombusiness
researchProduct

SPEN haploinsufficiency causes a neurodevelopmental disorder overlapping proximal 1p36 deletion syndrome with an episignature of X chromosomes in fem…

2021

Contains fulltext : 231702.pdf (Publisher’s version ) (Closed access) Deletion 1p36 (del1p36) syndrome is the most common human disorder resulting from a terminal autosomal deletion. This condition is molecularly and clinically heterogeneous. Deletions involving two non-overlapping regions, known as the distal (telomeric) and proximal (centromeric) critical regions, are sufficient to cause the majority of the recurrent clinical features, although with different facial features and dysmorphisms. SPEN encodes a transcriptional repressor commonly deleted in proximal del1p36 syndrome and is located centromeric to the proximal 1p36 critical region. Here, we used clinical data from 34 individuals…

0301 basic medicineSHARPMaleobesitygenotype-phenotype correlationsAutism Spectrum DisorderPROTEINChromosome DisordersHaploinsufficiencyRNA-Binding ProteinPHENOTYPE CORRELATIONS1p36; distal 1p36 deletion syndrome; DNA methylome analysis; episignature; genotype-phenotype correlations; neurodevelopmental disorder; obesity; proximal 1p36 deletion syndrome; SPEN; X chromosome; Adolescent; Autism Spectrum Disorder; Child; Child Preschool; Chromosome Deletion; Chromosome Disorders; Chromosomes Human Pair 1; Chromosomes Human X; DNA Methylation; DNA-Binding Proteins; Epigenesis Genetic; Female; Haploinsufficiency; Humans; Intellectual Disability; Male; Neurodevelopmental Disorders; Phenotype; RNA-Binding Proteins; Young AdultEpigenesis GeneticX chromosome0302 clinical medicineNeurodevelopmental disorderNeurodevelopmental DisorderIntellectual disabilityMOLECULAR CHARACTERIZATIONdistal 1p36 deletion syndromeChildGenetics (clinical)X chromosomeGeneticsXDNA methylome analysiRNA-Binding ProteinsSPLIT-ENDSHypotoniaDNA-Binding ProteinsPhenotypeAutism spectrum disorderChromosomes Human Pair 1Child PreschoolDNA methylome analysisMONOSOMY 1P36Pair 1SPENFemalemedicine.symptomChromosome DeletionHaploinsufficiencyRare cancers Radboud Institute for Health Sciences [Radboudumc 9]HumanAdolescentDNA-Binding ProteinBiologygenotype-phenotype correlationChromosomes03 medical and health sciencesYoung AdultGeneticSDG 3 - Good Health and Well-beingReportIntellectual DisabilityREVEALSGeneticsmedicineHumansEpigeneticsPreschoolChromosomes Human XNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]1p361p36 deletion syndromeIDENTIFICATIONMUTATIONSproximal 1p36 deletion syndromeDNA Methylationmedicine.diseaseneurodevelopmental disorderGENEepisignature030104 developmental biologyChromosome DisorderNeurodevelopmental Disorders030217 neurology & neurosurgeryEpigenesis
researchProduct

New insights into the clinical and molecular spectrum of the novel CYFIP2-related neurodevelopmental disorder and impairment of the WRC-mediated acti…

2021

International audience; Purpose: A few de novo missense variants in the cytoplasmic FMRP-interacting protein 2 (CYFIP2) gene have recently been described as a novel cause of severe intellectual disability, seizures, and hypotonia in 18 individuals, with p.Arg87 substitutions in the majority.Methods: We assembled data from 19 newly identified and all 18 previously published individuals with CYFIP2 variants. By structural modeling and investigation of WAVE-regulatory complex (WRC)-mediated actin polymerization in six patient fibroblast lines we assessed the impact of CYFIP2 variants on the WRC.Results: Sixteen of 19 individuals harbor two previously described and 11 novel (likely) disease-ass…

0301 basic medicine[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyWAVEregulatory complex (WRC)030105 genetics & heredityBiologyArticleIntellectual disability; Epilepsy; CYFIP2; WAVE-regulatory complex (WRC); WASF03 medical and health sciencesNeurodevelopmental disorderSeizuresWAVE-regulatory complex (WRC)medicineCYFIP2Missense mutationHumansGenetics(clinical)WASFGeneGenetics (clinical)ActinAdaptor Proteins Signal TransducingGenetics/dk/atira/pure/subjectarea/asjc/2700/2716medicine.diseaseActin cytoskeletonPhenotypeHypotoniaActins3. Good healthddc:030104 developmental biology[SDV.BDD.EO]Life Sciences [q-bio]/Development Biology/Embryology and OrganogenesisNeurodevelopmental Disordersintellectual disabilityCYFIP2epilepsymedicine.symptom
researchProduct

Cohen Syndrome-Associated Cataract Is Explained by VPS13B Functions in Lens Homeostasis and Is Modified by Additional Genetic Factors

2020

International audience; Purpose: Cohen syndrome (CS) is a rare genetic disorder caused by variants of the VPS13B gene. CS patients are affected with a severe form of retinal dystrophy, and in several cases cataracts also develop. The purpose of this study was to investigate the mechanisms and risk factors for cataract in CS, as well as to report on cataract surgeries in CS patients.Methods: To understand how VPS13B is associated with visual impairments in CS, we generated the Vps13b∆Ex3/∆Ex3 mouse model. Mice from 1 to 3 months of age were followed by ophthalmoscopy and slit-lamp examinations. Phenotypes were investigated by histology, immunohistochemistry, and western blot. Literature anal…

0301 basic medicinegenetic structuresDevelopmental DisabilitiesVesicular Transport Proteins030105 genetics & hereditysurgerygenetic backgroundchemistry.chemical_compoundLensMyopiaHomeostasisMice KnockoutCohen syndrome[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologymedicine.diagnostic_testRetinal DegenerationGenetic disorderinflamma- tionVPS13BcataractKnockout mouseMicrocephalyMuscle Hypotoniamedicine.medical_specialtymouse modelBlotting WesternRetinitisFingersOphthalmoscopy03 medical and health sciencesCataractsIntellectual DisabilityOphthalmologyVPS13BLens CrystallinemedicineAnimalsObesityCohen syndromebusiness.industryfibrosisRetinalgenetic modifiersmedicine.diseaseeye diseasesMice Inbred C57BLDisease Models Animalophthalmology030104 developmental biologyGene Expression RegulationchemistryinflammationRNAsense organsbusiness[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyInvestigative Ophthalmology & Visual Science
researchProduct

NDST1 missense mutations in autosomal recessive intellectual disability.

2014

NDST1 was recently proposed as a candidate gene for autosomal recessive intellectual disability in two families. It encodes a bifunctional GlcNAc N-deacetylase/N-sulfotransferase with important functions in heparan sulfate biosynthesis. In mice, Ndst1 is crucial for embryonic development and homozygous null mutations are perinatally lethal. We now report on two additional unrelated families with homozygous missense NDST1 mutations. All mutations described to date predict the substitution of conserved amino acids in the sulfotransferase domain, and mutation modeling predicts drastic alterations in the local protein conformation. Comparing the four families, we noticed significant overlap in …

AdultMaleModels MolecularCandidate geneAdolescentGenotypeProtein ConformationDNA Mutational AnalysisMutation MissenseGenes RecessiveBiologyBioinformaticsPolymorphism Single NucleotideAnimals Genetically ModifiedEpilepsyConsanguinityYoung AdultProtein structureIntellectual DisabilityIntellectual disabilityGeneticsmedicineMissense mutationAnimalsHumansChildGenetics (clinical)GeneticsGene knockdownMuscular hypotoniaBehavior AnimalComputational BiologyFaciesHigh-Throughput Nucleotide Sequencingmedicine.diseasePhenotypePedigreePhenotypeChild PreschoolGene Knockdown TechniquesDrosophilaFemaleSulfotransferasesGenome-Wide Association StudyAmerican journal of medical genetics. Part A
researchProduct

Hearing impairment as an early sign of alpha-mannosidosis in children with a mild phenotype: Report of seven new cases.

2019

Alpha-mannosidosis (AM) is a very rare (prevalence: 1/500000 births) autosomal recessive lysosomal storage disorder. It is characterized by multi-systemic involvement associated with progressive intellectual disability, hearing loss, skeletal anomalies, and coarse facial features. The spectrum is wide, from very severe and lethal to a milder phenotype that usually progresses slowly. AM is caused by a deficiency of lysosomal alpha-mannosidase. A diagnosis can be established by measuring the activity of lysosomal alpha-mannosidase in leucocytes and screening for abnormal urinary excretion of mannose-rich oligosaccharides. Genetic confirmation is obtained with the identification of MAN2B1 muta…

AdultMalePediatricsmedicine.medical_specialtyAdolescentHearing lossAlpha-mannosidosisUrinary systemYoung Adultalpha-MannosidaseIntellectual DisabilityIntellectual disabilityExome SequencingGeneticsmedicineHumansChildHearing LossGenetics (clinical)Exome sequencingCoarse facial featuresbusiness.industrySiblingsEnzyme replacement therapymedicine.diseaseHypotoniaPhenotypeChild Preschoolalpha-MannosidosisFemalemedicine.symptombusinessLysosomesAmerican journal of medical genetics. Part A
researchProduct

Epimutation at human chromosome 14q32.2 in a boy with a upd(14)mat-like clinical phenotype.

2009

Recently, three reports described deletions and epimutations affecting the imprinted region at chromosome 14q32.2 in individuals with a phenotype typical for maternal uniparental disomy of chromosome 14 [upd(14)mat]. In this study, we describe another patient with upd(14)mat-like phenotype including low birth weight, neonatal feeding problems, muscular hypotonia, motor and developmental delay, small hands and feet, and truncal obesity. Conventional cytogenetic analyses, fluorescence in situ hybridization subtelomere screening, multiplex ligation-dependent probe amplification analysis of common microdeletion and microduplication syndromes, and methylation analysis of SNRPN all gave normal re…

AdultMalecongenital hereditary and neonatal diseases and abnormalitiesMolecular Sequence DataMothersBiologyMethylationPolymorphism Single NucleotideEpigenesis GeneticGenomic ImprintingIntergenic regionGeneticsmedicineHumansAbnormalities MultipleEpigeneticsChildGenetics (clinical)GeneticsChromosomes Human Pair 14Muscular hypotoniamedicine.diagnostic_testBase SequenceChromosomeUniparental DisomySubtelomerePhenotypeDifferentially methylated regionsPhenotypeMutationFemaleFluorescence in situ hybridizationClinical genetics
researchProduct