Search results for "utis"

showing 10 items of 1091 documents

Autism spectrum disorders in children affected by Duchenne muscular dystrophy

2018

Background Duchenne muscular dystrophy (DMD) is the most frequent and severe form of the dystrophinopathies. The literature shows that about 30-40% of DMD subjects have intellectual disability. In males with Duchenne muscular dystrophy, neuropsychiatric disorders have also been observed: attention deficit disorder and hyperactivity, autism spectrum disorders, and obsessive-compulsive disorder. Duchenne muscular dystrophy is not just a muscle disorder, but also a disease that affects the brain. The aim of the present study was to describe a case series of children with Duchenne muscular dystrophy that have also the presence of autism spectrum disorders (ASDs). They have been assessed by mean…

0301 basic medicineDuchenne muscular dystrophyMalemedicine.medical_specialtyAutism Spectrum DisorderDuchenne muscular dystrophyMuscle disorderAudiologyAutism Diagnostic Observation Schedule03 medical and health sciences0302 clinical medicineIntellectual Disabilitymental disordersIntellectual disabilitymedicineHumansMuscular dystrophyChildbusiness.industryWechsler Adult Intelligence Scalemedicine.diseaseSettore MED/39 - Neuropsichiatria InfantileMuscular Dystrophy Duchenne030104 developmental biologyPediatrics Perinatology and Child HealthChildhood Autism Rating ScaleAutismAustism Spectrum Disorderbusiness030217 neurology & neurosurgeryHuman
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Autism is a prenatal disorder: Evidence from late gestation brain overgrowth

2018

This retrospective study aimed to specify the critical period for atypical brain development in individuals with autism spectrum disorder (ASD) using prenatal and postnatal head growth parameters. The sample consisted of 80 Caucasian, unrelated, idiopathic patients with ASD born after 1995. Fetal ultrasound parameters (head circumference [HC], abdominal circumference, and femur length) were obtained during the second and third trimesters of gestation. HC at birth and postnatal parameters at 12 and 24 months of age were also collected. Head overgrowth, assessed by HC, was highlighted during the second (20-26 weeks of amenorrhea) and third (28-36 weeks of amenorrhea) trimesters. Normal growth…

0301 basic medicineFetusPediatricsmedicine.medical_specialtybusiness.industryGeneral Neurosciencemedicine.disease03 medical and health sciences030104 developmental biology0302 clinical medicineNeurodevelopmental disorderAutism spectrum disorderIn uteromedicineGestationAutismAmenorrheaNeurology (clinical)medicine.symptombusinessPathological030217 neurology & neurosurgeryGenetics (clinical)Autism Research
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Specific mosaicKRASmutations affecting codon 146 cause oculoectodermal syndrome and encephalocraniocutaneous lipomatosis

2016

Oculoectodermal syndrome (OES) and encephalocraniocutaneous lipomatosis (ECCL) are rare disorders that share many common features, such as epibulbar dermoids, aplasia cutis congenita, pigmentary changes following Blaschko lines, bony tumor-like lesions, and others. About 20 cases with OES and more than 50 patients with ECCL have been reported. Both diseases were proposed to represent mosaic disorders, but only very recently whole-genome sequencing has led to the identification of somatic KRAS mutations, p.Leu19Phe and p.Gly13Asp, in affected tissue from two individuals with OES. Here we report the results of molecular genetic studies in three patients with OES and one with ECCL. In all four…

0301 basic medicineGeneticsSanger sequencingLipomatosis030105 genetics & heredityRASopathyBiologymedicine.diseasemedicine.disease_causeAplasia cutis congenita3. Good health03 medical and health sciencessymbols.namesake030104 developmental biologyGermline mutationGenotypeEncephalocraniocutaneous LipomatosisGeneticsmedicinesymbolsKRASmedicine.symptomGenetics (clinical)Clinical Genetics
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Shank3 Mice Carrying the Human Q321R Mutation Display Enhanced Self-Grooming, Abnormal Electroencephalogram Patterns, and Suppressed Neuronal Excitab…

2019

Shank3, a postsynaptic scaffolding protein involved in regulating excitatory synapse assembly and function, has been implicated in several brain disorders, including autism spectrum disorders (ASD), Phelan-McDermid syndrome, schizophrenia, intellectual disability, and mania. Here we generated and characterized a Shank3 knock-in mouse line carrying the Q321R mutation (Shank3Q321R mice) identified in a human individual with ASD that affects the ankyrin repeat region (ARR) domain of the Shank3 protein. Homozygous Shank3Q321R/Q321R mice show a selective decrease in the level of Shank3a, an ARR-containing protein variant, but not other variants. CA1 pyramidal neurons in the Shank3Q321R/Q321R hip…

0301 basic medicineHippocampusautism spectrum disorderBiologyNeurotransmissionElectroencephalographyInhibitory postsynaptic potentiallcsh:RC321-57103 medical and health sciencesCellular and Molecular NeuroscienceExcitatory synapse assembly0302 clinical medicinePostsynaptic potentialexcitabilitymedicineself-groomingEEGMolecular Biologylcsh:Neurosciences. Biological psychiatry. Neuropsychiatrypatient mutationsOriginal Researchmedicine.diagnostic_testanxiety-like behaviorseizure susceptibilitymedicine.disease030104 developmental biologyShank3SchizophreniaExcitatory postsynaptic potentialNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Molecular Neuroscience
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Clinical and hormonal characteristics in heterozygote carriers of congenital adrenal hyperplasia

2020

Abstract Non-classical congenital adrenal hyperplasia (NC-CAH) includes a group of genetic disorders due to a broad class of CYP21A2 variants identifying a disease-causing ‘C’ genotype. The heterozygous carriers of CYP21 mutations are at increased risk of developing clinically evident hyperandrogenism, even though clinical and laboratory characteristics are still underestimated. With the aim of obtaining a more accurate delineation of the phenotype of heterozygous carrier of CAH, we analyzed clinical, biochemical and molecular characteristics in a cohort of Sicilian subjects. Fifty-seven females with biallelic and monoallelic CYP21A2 variants classifying NC-CAH (24) and heterozygous carrier…

0301 basic medicineHirsutismHydrocortisoneendocrine system diseasesEndocrinology Diabetes and MetabolismClinical BiochemistryPhysiologyOverweighturologic and male genital diseasesBiochemistrySettore MED/13 - Endocrinologia0302 clinical medicineEndocrinologySettore BIO/10 - BiochimicaGenotypeMedicineChildhirsutismPolycystic ovaryfemale genital diseases and pregnancy complications030220 oncology & carcinogenesisCohortMolecular MedicineFemalemedicine.symptomAdultHeterozygotecongenital hereditary and neonatal diseases and abnormalitiesAdolescentYoung Adult03 medical and health sciencesHumansCongenital adrenal hyperplasiaMolecular BiologyHeterozygous carrierAdrenal Hyperplasia Congenitalbusiness.industryHyperandrogenismCongenital adrenal hyperplasianutritional and metabolic diseasesHeterozygote advantageCell BiologyOverweightmedicine.diseaseOligomenorrhea17OHProgesterone deficiency030104 developmental biologyMutationSteroid 21-HydroxylaseHyperandrogenismbusinessThe Journal of Steroid Biochemistry and Molecular Biology
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NEGR1 and FGFR2 cooperatively regulate cortical development and core behaviours related to autism disorders in mice.

2018

See Contreras and Hippenmeyer (doi:10.1093/brain/awy218) for a scientific commentary on this article. Autism spectrum disorders (ASDs) are complex conditions with diverse aetiologies. Szczurkowska et al. demonstrate that two ASD-related molecules – FGFR2 and Negr1 – physically interact to act on the same downstream pathway, and regulate cortical development and ASD-relevant behaviours in mice. Identifying common mechanisms in ASDs may reveal targets for pharmacological intervention.

0301 basic medicineMAPK/ERK pathwaygenetic structuresAutism Spectrum DisorderFGFR2 signalingFibroblast growth factorReceptor tyrosine kinaseMiceautism; development; cell adhesion; in utero electroporation; FGFR2 signaling0302 clinical medicineCell MovementCerebral CortexMice KnockoutbiologyBehavior AnimalKinaseCell adhesion moleculeCell biologyProtein TransportSignal Transductionmusculoskeletal diseasesMAP Kinase Signaling SystemCell Adhesion Molecules NeuronalDendritic SpinesNeurogenesisautismDown-Regulationbehavioral disciplines and activities03 medical and health sciencesmental disordersmedicineAnimalsHumansAutistic DisorderReceptor Fibroblast Growth Factor Type 2developmentProtein kinase BFibroblast growth factor receptor 2Cell Membranecell adhesionOriginal Articlesin utero electroporationmedicine.diseaseMice Inbred C57BLDisease Models Animal030104 developmental biologyHEK293 Cellsbiology.proteinAutismNeurology (clinical)030217 neurology & neurosurgeryBrain : a journal of neurology
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Heterozygous deletion of the LRFN2 gene is associated with working memory deficits

2016

International audience; Learning disabilities (LDs) are a clinically and genetically heterogeneous group of diseases. Array-CGH and high-throughput sequencing have dramatically expanded the number of genes implicated in isolated intellectual disabilities and LDs, highlighting the implication of neuron-specific post-mitotic transcription factors and synaptic proteins as candidate genes. We report a unique family diagnosed with autosomal dominant learning disability and a 6p21 microdeletion segregating in three patients. The 870 kb microdeletion encompassed the brain-expressed gene LRFN2, which encodes for a synaptic cell adhesion molecule. Neuropsychological assessment identified selective w…

0301 basic medicineMaleCandidate genefamilyspeechHippocampal formationRats Sprague-Dawley0302 clinical medicineBorderline intellectual functioningNeuropsychological assessmentChilddisordersGenetics (clinical)Cells Culturedadhesion-like moleculesMembrane Glycoproteinsmedicine.diagnostic_testLearning DisabilitiesBrainMagnetic Resonance Imaging3. Good healthPedigreeMemory Short-TermBrain sizeFemaleAdultHeterozygotenmda receptorautismNerve Tissue ProteinsBiologyReceptors N-Methyl-D-AspartateArticle03 medical and health sciencesFluorodeoxyglucose F18[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyexpressionGeneticsmedicineAnimalsHumansMemory DisorderslanguageGenetic heterogeneityWorking memoryMembrane Proteinsdown-syndromeRats030104 developmental biologyEndophenotypePositron-Emission TomographySynapsesshort-termRadiopharmaceuticalsNeuroscience030217 neurology & neurosurgeryGene Deletion[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Broad neurodevelopmental features and cortical anomalies associated with a novel de novo KMT2A variant in Wiedemann-Steiner syndrome.

2021

Abstract Wiedemann-Steiner syndrome (WDSTS) is a rare genetic disorder including developmental delay/intellectual disability (DD/ID), hypertrichosis cubiti, short stature, and distinctive facial features, caused by mutation in KMT2A gene, which encodes a histone methyltransferase (H3K4) that regulates chromatin-mediated transcription. Different neurodevelopmental phenotypes have been described within the WDSTS spectrum, including a peculiar Autism Spectrum Disorder (ASDs) subtype in some affected individuals. Here, we report a 9-year-old Caucasian male found by next-generation panel sequencing to carry a novel heterozygous de novo KMT2A frameshift variant (NM_001197104.2:c.4433delG; p. Arg1…

0301 basic medicineMaleDevelopmental Disabilities030105 genetics & heredityBiologyFocal cortical dysplasiaPalilaliaFrameshift mutation03 medical and health sciencesHypertrichosis cubitiIntellectual DisabilityGeneticsmedicineHumansChildFrameshift MutationGenetics (clinical)GeneticsCerebral CortexWiedemann-steiner syndrome.Genetic disorderHypertrichosis cubitiGeneral MedicineHistone-Lysine N-MethyltransferaseSyndromeKMT2ACortical dysplasiamedicine.diseasePalilaliaMalformations of Cortical Development030104 developmental biologyKMT2AWiedemann-Steiner syndromeAutism spectrum disorderbiology.proteinmedicine.symptomMyeloid-Lymphoid Leukemia ProteinEuropean journal of medical genetics
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Expanding the phenotype of reciprocal 1q21.1 deletions and duplications: a case series

2017

Abstract Background Recurrent reciprocal 1q21.1 deletions and duplications have been associated with variable phenotypes. Phenotypic features described in association with 1q21.1 microdeletions include developmental delay, craniofacial dysmorphism and congenital anomalies. The 1q21.1 reciprocal duplication has been associated with macrocephaly or relative macrocephaly, frontal bossing, hypertelorism, developmental delay, intellectual disability and autism spectrum disorder. Methods Our study describes seven patients, who were referred to us for developmental delay/intellectual disability, dysmorphic features and, in some cases, congenital anomalies, in whom we identified 1q21.1 CNVs by arra…

0301 basic medicineMalePediatricsmedicine.medical_specialtyArray-CGHDevelopmental delayTrigonocephaly03 medical and health sciencesFrontal BossingPregnancyPrenatal DiagnosisGene duplicationIntellectual disabilityMedicineHumansAbnormalities MultipleMegalencephalyHypertelorismChild1q21.1 deletionGeneticsbusiness.industryResearchMacrocephalylcsh:RJ1-570Infantlcsh:Pediatricsmedicine.diseaseMegalencephalyDysmorphism030104 developmental biologyPhenotypeAutism spectrum disorderChromosomes Human Pair 1Female1q21.1 duplicationmedicine.symptomChromosome DeletionbusinessItalian Journal of Pediatrics
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Proteomic Analysis of Brain Region and Sex-Specific Synaptic Protein Expression in the Adult Mouse Brain

2020

Genetic disruption of synaptic proteins results in a whole variety of human neuropsychiatric disorders including intellectual disability, schizophrenia or autism spectrum disorder (ASD). In a wide range of these so-called synaptopathies a sex bias in prevalence and clinical course has been reported. Using an unbiased proteomic approach, we analyzed the proteome at the interaction site of the pre- and postsynaptic compartment, in the prefrontal cortex, hippocampus, striatum and cerebellum of male and female adult C57BL/6J mice. We were able to reveal a specific repertoire of synaptic proteins in different brain areas as it has been implied before. Additionally, we found a region-specific set…

0301 basic medicineMaleProteomicsCerebellumAgingcerebellumProteomehippocampusstriatumHippocampusNerve Tissue ProteinsBiologyArticleSynapse03 medical and health sciences0302 clinical medicinePostsynaptic potentialsynapsemedicinesexAnimalsPrefrontal cortexlcsh:QH301-705.5prefrontal cortexSex CharacteristicsBrainGeneral Medicinemedicine.diseaseMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureGene Ontologylcsh:Biology (General)Autism spectrum disorderSchizophreniaProteomeSynapsesmass spectrometry-based proteomicsautism spectrum disorder (ASD)DDX3XFemaleNeuroscienceSET030217 neurology & neurosurgerySET ; cerebellum ; DDX3X ; striatum ; autism spectrum disorder (ASD) ; hippocampus ; synapse ; sex ; prefrontal cortexCells
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