Search results for " Delay"

showing 10 items of 442 documents

Heterozygous HMGB1 loss-of-function variants are associated with developmental delay and microcephaly

2021

International audience; 13q12.3 microdeletion syndrome is a rare cause of syndromic intellectual disability. Identification and genetic characterization of patients with 13q12.3 microdeletion syndrome continues to expand the phenotypic spectrum associated with it. Previous studies identified four genes within the approximately 300 Kb minimal critical region including two candidate protein coding genes: KATNAL1 and HMGB1. To date, no patients carrying a sequence-level variant or a single gene deletion in HMGB1 or KATNAL1 have been described. Here we report six patients with loss-of-function variants involving HMGB1 and who had phenotypic features similar to the previously described 13q12.3 m…

Male0301 basic medicineHeterozygoteMicrocephalyAdolescentDNA Copy Number VariationsLanguage delay[SDV]Life Sciences [q-bio]KaryotypeInheritance Patternschemical and pharmacologic phenomena030105 genetics & heredityBiologydysmorphic featuresloss of function mutation03 medical and health sciencesExome SequencingIntellectual disabilityGeneticsmedicineHumansGenetic Predisposition to DiseaseHMGB1 ProteinChildGeneGenetic Association StudiesIn Situ Hybridization FluorescenceGenetics (clinical)Loss functionGeneticsHMGB1FaciesExonsdevelopmental disabilitiesMicrodeletion syndromemedicine.diseasePhenotypePhenotype030104 developmental biologyChild PreschoolMicrocephalyFemaleHaploinsufficiency
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Microsomal triglyceride transfer protein gene mutations in Turkish children: A novel mutation and clinical follow up.

2016

Abetalipoproteinemia (ABL; OMIM 200100) is a rare autosomal recessive disease that affects the absorption of dietary fats and fat soluble vitamins. Here, we describe the clinical and genetic characteristics of three patients with ABL. Two patients (patients 1 and 2) who were carriers of the c.398-399delAA mutation (previously known mutation) had developmental delay and hepatic steatosis developed at the age of five in patient 1. Patient 3 was the carrier of a novel mutation (g.10886-10902delAAGgtaagtttgtgttg in intron 3 and c.506A>T exon 5) in microsomal triglyceride transfer protein (MTP) gene and had hepatic steatosis.

Male0301 basic medicineHeterozygotemedicine.medical_specialtySettore MED/09 - Medicina InternaTurkeyDevelopmental delayDevelopmental DisabilitiesTurkish030204 cardiovascular system & hematologyHepatic steatosimedicine.disease_causeMicrosomal triglyceride transfer protein03 medical and health sciencesExon0302 clinical medicineInternal medicineHumansMedicineGeneGenetic Association StudiesGeneticsMutationABLbiologyAbetalipoproteinemiaDevelopmental delayHepatic steatosisMicrosomal triglyceride transfer proteinTurkishbusiness.industryIntronGastroenterologyInfantAbetalipoproteinemiaMicrosomal triglyceride transfer proteinmedicine.diseaseIntronsAbetalipoproteinemiaFatty Liver030104 developmental biologyEndocrinologyMutationbiology.proteinFemaleSteatosisCarrier ProteinsbusinessFollow-Up Studies
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Obesogen effects after perinatal exposure of 4,4′-sulfonyldiphenol (Bisphenol S) in C57BL/6 mice

2016

International audience; Bisphenol A were removed from consumer products and replaced by chemical substitutes such as Bisphenol S (BPS). Based on their structural similarity, BPS may be obesogen like Bisphenol A in mice. Our objective was to determine the impact of BPS on lipid homeostasis in C57B1/6 mice after perinatal and chronic exposure. Pregnant mice were exposed to BPS via the drinking water (0.2; 1.5; 50 mu g/kg bw/d). Treatment began at gestational day 0 and continued in offspring up to 23-weeks old. Then, offspring mice were fed with a standard or high fat diet. The body weight, food consumption, fat mass and energy expenditure were measured. A lipid load test was performed to chec…

Male0301 basic medicineLeptinBisphenol S[ SDV.TOX ] Life Sciences [q-bio]/ToxicologyAdipose tissue010501 environmental sciencesToxicologyurologic and male genital diseases01 natural sciencesPolyethylene GlycolsMicechemistry.chemical_compoundPregnancyInduced ObesityHyperinsulinemiapériode perinataleObesogenSulfones2. Zero hungerLeptinHigh-Fat Dietsanté humaineLipidsEnergy-Balance3. Good healthSafe AlternativesobésitéAdipose TissuePrenatal Exposure Delayed Effects[SDV.TOX]Life Sciences [q-bio]/Toxicologybisphénol sFemalehormones hormone substitutes and hormone antagonistsmedicine.medical_specialtyOffspringDiet High-Fat03 medical and health sciencesInsulin resistancePhenolsInternal medicinemedicineAnimalshoméostasie lipidiqueObesityRNA MessengerTriglycerides0105 earth and related environmental sciencesDose-Response Relationship DrugAdiponectinTriglycerideInsulin-ResistanceBody WeightOverweightmedicine.diseasebisphenol S;food contaminant;perinatal exposure;low dose;obesogenPerinatal exposureMice Inbred C57BLFood contaminant030104 developmental biologyEndocrinologycontaminant chimiqueLow doseGlucoseMetabolismGene Expression RegulationchemistryIn-VitroObesogenAnalogs
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A Recurrent De Novo PACS2 Heterozygous Missense Variant Causes Neonatal-Onset Developmental Epileptic Encephalopathy, Facial Dysmorphism, and Cerebel…

2018

International audience; Developmental and epileptic encephalopathies (DEEs) represent a large clinical and genetic heterogeneous group of neurodevelopmental diseases. The identification of pathogenic genetic variants in DEEs remains crucial for deciphering this complex group and for accurately caring for affected individuals (clinical diagnosis, genetic counseling, impacting medical, precision therapy, clinical trials, etc.). Whole-exome sequencing and intensive data sharing identified a recurrent de novo PACS2 heterozygous missense variant in 14 unrelated individuals. Their phenotype was characterized by epilepsy, global developmental delay with or without autism, common cerebellar dysgene…

Male0301 basic medicinePathologyPACS-2Vesicular Transport ProteinsPHENOTYPEBioinformaticsDISEASESensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]Epilepsy0302 clinical medicineMissense mutationGlobal developmental delayAge of OnsetChildGenetics (clinical)Epileptic encephalopathyAPOPTOSIS3. Good healthcerebellar dysgenesisMutation Missense/geneticsintellectual disabilityChild PreschoolEpilepsy GeneralizedFemalePACS2CLINICAL EPILEPSYmedicine.medical_specialtyHeterozygoteGeneralized/geneticsPROTEINSGenetic counselingMutation MissenseMissense/geneticsNeonatal onsetBiologyDIAGNOSISVesicular Transport Proteins/geneticsFacial dysmorphism03 medical and health sciencesDysgenesisAll institutes and research themes of the Radboud University Medical CenterCerebellar DiseasesReportMENDELIAN DISORDERSGeneticsmedicineHumansGeneralized epilepsyPreschoolNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Cerebellar Diseases/geneticsbusiness.industryMUTATIONSInfant NewbornCorrectionInfantFaciesNewbornmedicine.disease030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMutationepilepsyAutismbusinessEpilepsy Generalized/genetics030217 neurology & neurosurgery
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NFIB Haploinsufficiency Is Associated with Intellectual Disability and Macrocephaly

2018

The nuclear factor I (NFI) family of transcription factors play an important role in normal development of multiple organs. Three NFI family members are highly expressed in the brain, and deletions or sequence variants in two of these, NFIA and NFIX, have been associated with intellectual disability (ID) and brain malformations. NFIB, however, has not previously been implicated in human disease. Here, we present a cohort of 18 individuals with mild ID and behavioral issues who are haploinsufficient for NFIB. Ten individuals harbored overlapping microdeletions of the chromosomal 9p23-p22.2 region, ranging in size from 225 kb to 4.3 Mb. Five additional subjects had point sequence variations c…

Male0301 basic medicinechromosome 9p23Medical and Health SciencesCorpus CallosumCohort StudiesMice2.1 Biological and endogenous factorsMegalencephalyAetiologyChildAgenesis of the corpus callosumGenetics (clinical)PediatricGenetics & HeredityCerebral CortexMice KnockoutGeneticsSingle Nucleotidenuclear factor IBiological SciencesNFIBNFIXdevelopmental delayMental HealthNFIBCodon NonsenseNFIAintellectual disabilityChild Preschoolchromosome 9p22.3NeurologicalSpeech delayFemalemedicine.symptomHaploinsufficiencyAdultAdolescentKnockoutIntellectual and Developmental Disabilities (IDD)[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsBiologymacrocephalyPolymorphism Single NucleotideArticleYoung Adult03 medical and health sciencesRare DiseasesBehavioral and Social ScienceGeneticsmedicinemegalencephalyAnimalsHumansPolymorphismCodonPreschoolNeurosciencesMacrocephalymedicine.diseaseBrain DisordershaploinsufficiencyNFI Transcription Factors030104 developmental biologyNonsense[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsbiology.proteinagenesis of the corpus callosumAmerican journal of human genetics
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A paradigmatic autistic phenotype associated with loss of PCDH11Y and NLGN4Y genes

2021

Abstract Background Most studies relative to Y chromosome abnormalities are focused on the sexual developmental disorders. Recently, a few studies suggest that some genes located on Y chromosome may be related to different neurodevelopment disorders. Case presentation We report a child with sexual developmental disorder associated with a peculiar phenotype characterized by severe language impairment and autistic behaviour associated with a mosaicism [45,X(11)/46,XY(89)] and a partial deletion of the short and long arm of Y chromosome (del Yp11.31q11.23) that also involves the loss of both PCDH11Y and NLGN4Y genes. To our knowledge no study has ever reported the occurrence of the lack of bot…

Male0301 basic medicinelcsh:Internal medicineMixed gonadal dysgenesilcsh:QH426-470Autism Spectrum DisorderCell Adhesion Molecules NeuronalNeuroliginProtocadherinCase ReportNeuroliginDevelopmental global delayBiologyY chromosome03 medical and health sciences0302 clinical medicineProtocadherinSettore M-PSI/08 - Psicologia ClinicaGeneticsmedicineHumanslcsh:RC31-1245ChildGenetics (clinical)GeneticsMosaicismMixed gonadal dysgenesismedicine.diseasePhenotypeSettore MED/39 - Neuropsichiatria InfantileHuman geneticsDevelopmental disorderlcsh:GeneticsPhenotype030104 developmental biologymedicine.anatomical_structureCerebral cortexAutism spectrum disorder030217 neurology & neurosurgeryBMC Medical Genomics
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Reversing behavioural abnormalities in mice exposed to maternal inflammation

2016

Viral infection during pregnancy is correlated with increased frequency of neurodevelopmental disorders, and this is studied in mice prenatally subjected to maternal immune activation (MIA). We previously showed that maternal T helper 17 cells promote the development of cortical and behavioural abnormalities in MIA-affected offspring. Here we show that cortical abnormalities are preferentially localized to a region encompassing the dysgranular zone of the primary somatosensory cortex (S1DZ). Moreover, activation of pyramidal neurons in this cortical region was sufficient to induce MIA-associated behavioural phenotypes in wild-type animals, whereas reduction in neural activity rescued the be…

Male0301 basic medicinemedicine.medical_specialtyOffspringEfferentMothersBiologySomatosensory systemArticleMaternal inflammationMice03 medical and health sciencesNeural activity0302 clinical medicinePregnancyCortical abnormalitiesInternal medicinemedicineAnimalsPregnancy Complications InfectiousSocial BehaviorInflammationPregnancyMultidisciplinaryBehavior AnimalMental DisordersPyramidal CellsSomatosensory Cortexmedicine.diseasePhenotypePhenotype030104 developmental biologyEndocrinologyPrenatal Exposure Delayed EffectsImmunologyTh17 CellsFemale030217 neurology & neurosurgeryNature
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Protein expression in submandibular glands of young rats is modified by a high-fat/high-sugar maternal diet

2018

International audience; OBJECTIVE: Maternal diet has consequences on many organs of the offspring, but salivary glands have received little attention despite the importance of the saliva secretory function in oral health and control of food intake. The objective of this work was therefore to document in rats the impact of maternal high-fat/high-sugar diet (Western Diet) on submandibular glands of the progeny. DESIGN: Sprague-Dawley rat dams were fed either a Western diet or control diet during gestation and lactation and their pups were sacrificed 25 days after birth. The pups' submandibular gland protein content was characterized by means of 2D-electrophoresis followed by LC-MS/MS. Data we…

Male0301 basic medicinemedicine.medical_specialtySalivaOffspringsalivary glandsproteomeSubmandibular Glandannexin a5BiologyRats Sprague-Dawley03 medical and health scienceschemistry.chemical_compoundPregnancyHeat shock proteinInternal medicineLactationmedicineAnimalsSalivary Proteins and PeptidesGeneral Dentistry2. Zero hungerimmunohistologyCell BiologyGeneral MedicineGlutathioneImmunohistochemistrySubmandibular glandwestern dietRatsOxidative Stress030104 developmental biologyEndocrinologymedicine.anatomical_structureOtorhinolaryngologychemistryDiet WesternPrenatal Exposure Delayed EffectsGestationFemaleAnnexin A5[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
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Intragenic FMR1 disease-causing variants: a significant mutational mechanism leading to Fragile-X syndrome

2017

International audience; Fragile-X syndrome (FXS) is a frequent genetic form of intellectual disability (ID). The main recurrent mutagenic mechanism causing FXS is the expansion of a CGG repeat sequence in the 5'-UTR of the FMR1 gene, therefore, routinely tested in ID patients. We report here three FMR1 intragenic pathogenic variants not affecting this sequence, identified using high-throughput sequencing (HTS): a previously reported hemizygous deletion encompassing the last exon of FMR1, too small to be detected by array-CGH and inducing decreased expression of a truncated form of FMRP protein, in three brothers with ID (family 1) and two splice variants in boys with sporadic ID: a de novo …

Male0301 basic medicinemedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesdiagnosisRNA SplicingBiologymedicine.disease_causePolymorphism Single NucleotideArticleFragile X Mental Retardation Protein03 medical and health sciencesExonGenetic linkageplacebo-controlled trial[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyMolecular geneticsGeneticsmedicineHumansgeneGenetics (clinical)GeneticsMutationintron 10SiblingsMiddle Agedmedicine.diseaseFMR1Human genetics3. Good healthFragile X syndromedevelopmental delayof-the-literature030104 developmental biologyintellectual disabilityFragile X SyndromeMutationmental-retardationMedical geneticsFemalepoint mutationdouble-blind[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Influences of prenatal and postnatal stress on adult hippocampal neurogenesis: The double neurogenic niche hypothesis

2015

International audience; Adult hippocampal neurogenesis (AHN) is involved in learning, memory, and stress, and plays a significant role in neurodegenerative and psychiatric disorders. As an age-dependent process, AHN is largely influenced by changes that occur during the pre- and postnatal stages of brain development, and constitutes an important field of research. This review examines the current knowledge regarding the regulators of AHN and the influence of prenatal and postnatal stress on later AHN. In addition, a hypothesis is presented suggesting that each kind of stress influences a specific neurogenic pool, developmental or postnatal, that later becomes a precursor with important repe…

MaleAgingBrain developmentprogenitor cellNeurogenesisNicheAdult hipocampal neurogenesis (AHN)neural stem-cellHippocampal formationgrowth-factorHippocampusHypothalamic-pituitary-adrenal (HPA)03 medical and health sciencesBehavioral Neuroscience0302 clinical medicinePregnancyRisk FactorsPrecursor cellPostnatal stressAnimalsHumanspattern separation030304 developmental biologyCell Proliferationrat dentate gyrus0303 health sciencesMental DisordersNeurogenesisStressorsubventricular zoneCell DifferentiationPrecursor cellsPostnatal stress (PTS)Neurogenic poolgenetic influencePrenatal Exposure Delayed Effectsolfactory-bulbPrenatal stress (PS)Female[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]decreases neurogenesisPsychologyNeuroscience030217 neurology & neurosurgeryStress Psychologicalbrain neurogenesis
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