Search results for "abnormal"

showing 10 items of 761 documents

Clinical and molecular characterization of 112 single-center patients with Neurofibromatosis type 1.

2018

Abstract Background The aim of this retrospective study was to define clinical and molecular characteristics of a large sample of neurofibromatosis type 1 (NF1) patients, as well as to evaluate mutational spectrum and genotype-phenotype correlation. NF1 is a relatively common neurogenetic disorder (1:2500–1:3000 individuals). It is caused by mutations of the NF1 gene on chromosome 17ql1.2, with autosomal dominant pattern of inheritance and wide phenotypical variability. Café-au-lait spots (CALs), cutaneous and/or subcutaneous neurofibromas (CNFs/SCNFs), skinfold freckling, skeletal abnormalities, Lisch nodules of the iris and increased risk of learning and intellectual disabilities, as well…

0301 basic medicineGenotype-phenotype correlation; New mutation; NF1 gene; NF1 microdeletion syndrome; Adolescent; Adult; Age Factors; Child; Child Preschool; Cohort Studies; DNA Mutational Analysis; Female; Genes Neurofibromatosis 1; Genetic Association Studies; Genetic Predisposition to Disease; Humans; Italy; Male; Middle Aged; Neurofibromatosis 1; Prevalence; Prognosis; Retrospective Studies; Risk Assessment; Sex Factors; Young Adult; Mutation MissenseMaleGenotype-phenotype correlationDNA Mutational AnalysisDiseaseCohort Studies0302 clinical medicineDNA Mutational AnalysisGenotypePrevalenceMedicineYoung adultChildNew mutationlcsh:RJ1-570Age FactorsMiddle AgedPrognosisItalyNF1 geneChild PreschoolCohortFemaleNF1 microdeletion syndromeCohort studyAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesNeurofibromatosis 1AdolescentMutation MissenseRisk Assessment03 medical and health sciencesYoung AdultSex FactorsGenes Neurofibromatosis 1HumansGenetic Predisposition to DiseaseNeurofibromatosisPreschoolGenetic Association StudiesRetrospective Studiesbusiness.industryResearchRetrospective cohort studylcsh:Pediatricsmedicine.diseaseDermatology030104 developmental biologyGenesPediatrics Perinatology and Child HealthMutationMissensebusiness030217 neurology & neurosurgeryItalian journal of pediatrics
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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
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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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A rare disease and education : Neurofibromatosis type 1 decreases educational attainment

2021

Rare heritable syndromes may affect educational attainment. Here, we study education in neurofibromatosis 1 (NF1) that is associated with multifaceted medical, social and cognitive consequences. Educational attainment in the Finnish population‐based cohort of 1408 individuals with verified NF1 was compared with matched controls using Cox proportional hazards model with delayed entry and competing risk for death. Moreover, models accounting for the effects of cancer at age 15–30 years, parental NF1 and developmental disorders were constructed. Overall, the attainment of secondary education was reduced in individuals with NF1 compared to controls (hazard ratio 0.83, 95%CI 0.74–0.92). History …

0301 basic medicineMale030105 genetics & heredityNeoplasmsneurofibromatosis 1ChildGenetics (clinical)FinlandLearning DisabilitiesHazard ratioCognitionVocational educationChild Preschooleducational attainmentCohortEducational StatusFemaleOriginal ArticleAdultopintomenestyscongenital hereditary and neonatal diseases and abnormalitiesNeurofibromatosis 1Adolescentrare diseaseneurofibromatoosiAffect (psychology)multiorgan syndromeschool performance03 medical and health sciencesRare DiseaseskoulutustasoGeneticsmedicineHumansEducation Graduateharvinaiset tauditNeurofibromatosisneoplasmsProportional Hazards ModelsVocational Educationperinnölliset tauditProportional hazards modelbusiness.industrySiblingsOriginal Articlesmedicine.diseaseEducational attainmenteye diseasesnervous system diseases030104 developmental biologybusinessDemographyFollow-Up Studies
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Molecular, clinical and neuropsychological study in 31 patients with Kabuki syndrome and KMT2D mutations

2017

IF 3.326; International audience; Kabuki syndrome (KS-OMIM 147920) is a rare developmental disease characterized by the association of multiple congenital anomalies and intellectual disability. This study aimed to investigate intellectual performance in children with KS and link the performance to several clinical features and molecular data. We recruited 31 children with KMT2D mutations who were 6 to 16 years old. They all completed the Weschler Intelligence Scale for Children, fourth edition. We calculated all indexes: the Full Scale Intellectual Quotient (FSIQ), Verbal Comprehension Index (VCI), Perceptive Reasoning Index (PRI), Processing Speed Index (PSI), and Working Memory Index (WMI…

0301 basic medicineMaleAdolescentVisual impairmentDNA Mutational AnalysisIntelligenceneuropsychologyDisease[SDV.GEN] Life Sciences [q-bio]/GeneticsNeuropsychological Testsgenotype-phenotype correlation03 medical and health sciencesIntensive careIntellectual disabilityGene OrderGeneticsmedicineHumansAbnormalities MultipleChildKMT2D mutationGenetics (clinical)AllelesGenetic Association Studies[SDV.GEN]Life Sciences [q-bio]/GeneticsKabuki syndromebusiness.industryWorking memoryNeuropsychologyWechsler Adult Intelligence Scalemedicine.diseaseHematologic Diseases3. Good healthNeoplasm ProteinsDNA-Binding Proteins030104 developmental biologyPhenotypeVestibular DiseasesGenetic LociFaceMutationFemalemedicine.symptombusinessKabuki syndromeClinical psychology
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Lifespan Changes of the human brain in Alzheimer's disease

2018

[EN] Brain imaging studies have shown that slow and progressive cerebral atrophy characterized the development of Alzheimer's Disease (AD). Despite a large number of studies dedicated to AD, key questions about the lifespan evolution of AD biomarkers remain open. When does the AD model diverge from the normal aging model? What is the lifespan trajectory of imaging biomarkers for AD? How do the trajectories of biomarkers in AD differ from normal aging? To answer these questions, we proposed an innovative way by inferring brain structure model across the entire lifespan using a massive number of MRI (N = 4329). We compared the normal model based on 2944 control subjects with the pathological …

0301 basic medicineMaleAgingLongevityHippocampuslcsh:MedicineTrastorns de la cognició en la vellesaAmygdalaArticle03 medical and health sciencesLateral ventricles0302 clinical medicineNeuroimagingmedicine[INFO.INFO-IM]Computer Science [cs]/Medical ImagingHumanslcsh:ScienceAgedCerebral atrophyAged 80 and overMultidisciplinarybusiness.industryNeurodegenerationlcsh:RBrainTrastorns de la memòriaHuman brainMiddle Agedmedicine.disease3. Good health030104 developmental biologymedicine.anatomical_structureFISICA APLICADADisease Progressionlcsh:QFemaleAbnormalitybusinessNeuroscience030217 neurology & neurosurgery
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Cardiac electrical defects in progeroid mice and Hutchinson-Gilford progeria syndrome patients with nuclear lamina alterations

2016

This work was supported by Spanish Ministry of Economy and Competitiveness (MINECO) Grants SAF2010-16044 and SAF2013-46663-R (to V.A.), SAF2011-30312 and SAF2014-58286-C2-1-R (to L.H.-M.), SAF2011-30088 (to E.D.), and SAF2014-52413-R (to C.L.-O.) and Fondo de Investigación Sanitaria del Instituto de Salud Carlos III Grants RD12/0042/0028 (to V.A.), RD12/0042/0011 (to J.T.), and RD12/0042/0002 (to L.H.-M.), with cofunding from the Fondo Europeo de Desarrollo Regional and the Progeria Research Foundation. J.A.G. is the recipient of a U-Mobility Grant from the Marie Curie cofunding of Regional, National and International Programme (Grant 246550). The Instituto Universitario de Oncología is sup…

0301 basic medicineMaleHutchinson–Gilford progeria syndrome calcium handling connexin43 prelamin A progerinElectrònica en cardiologia030204 cardiovascular system & hematologyPathogenesisCiencias Biomedicas0302 clinical medicineProgeriaCardiac Conduction System DiseasefisiologiapatologíaTecnología médicaChildCiencias médicasMice KnockoutProgeriaprelamin AMultidisciplinaryintegumentary systemMetalloendopeptidasesHeartProgerinHutchinson-Gilford progeria syndrome3. Good health:Enginyeria biomèdica::Electrònica biomèdica::Electrònica en cardiologia [Àrees temàtiques de la UPC]Sarcoplasmic Reticulummedicine.anatomical_structurePNAS PlusChild Preschoolcardiovascular systemNuclear laminaFemalemedicine.symptomBradycardiaAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesAdolescentBiology03 medical and health sciencesQRS complexYoung AdultElectrònica mèdicaInternal medicinemedicineAnimalsHumansPR intervalHutchinson–Gilford progeria syndromeNuclear LaminaMyocardiumMembrane Proteinsnutritional and metabolic diseasesArrhythmias Cardiacmedicine.diseaseMedical electronicsconnexin43Mice Inbred C57BL030104 developmental biologyEndocrinologyVentricleprogerinConnexin 43calcium handlingsistema cardiovascularCalcium
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The oculoauriculofrontonasal syndrome: Further clinical characterization and additional evidence suggesting a nontraditional mode of inheritance

2018

IF 2.264; International audience; The oculoauriculofrontonasal syndrome (OAFNS) is a rare disorder characterized by the association of frontonasal dysplasia (widely spaced eyes, facial cleft, and nose abnormalities) and oculo-auriculo-vertebral spectrum (OAVS)-associated features, such as preauricular ear tags, ear dysplasia, mandibular asymmetry, epibulbar dermoids, eyelid coloboma, and costovertebral anomalies. The etiology is unknown so far. This work aimed to identify molecular bases for the OAFNS. Among a cohort of 130 patients with frontonasal dysplasia, accurate phenotyping identified 18 individuals with OAFNS. We describe their clinical spectrum, including the report of new features…

0301 basic medicineMaleInheritance Patterns030105 genetics & heredityfrontonasal dysplasiawhole exome sequencingCraniofacial Abnormalities0302 clinical medicinePolymicrogyriaEye AbnormalitiesEar External10. No inequalityChildGenetics (clinical)Exome sequencingwhole genome sequencingThyroid agenesisHypoplasiaDNA-Binding ProteinsPhenotypeChild PreschoolFemaleRespiratory System Abnormalitiesmedicine.medical_specialtyAdolescentQuantitative Trait LociOculoauriculofrontonasal syndrome03 medical and health sciencesExome SequencingGeneticsmedicineHumansGenetic Predisposition to DiseaseFrontonasal dysplasiaGenetic Association StudiesWhole genome sequencingHomeodomain Proteinsbusiness.industryFacial cleftSkullInfant NewbornFaciesInfant030206 dentistrymedicine.diseaseDermatologySpine[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsDysplasiabusinessTomography Spiral ComputedTranscription Factors
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De Novo and Inherited Pathogenic Variants in KDM3B Cause Intellectual Disability, Short Stature, and Facial Dysmorphism

2019

Contains fulltext : 202646.pdf (Publisher’s version ) (Open Access) By using exome sequencing and a gene matching approach, we identified de novo and inherited pathogenic variants in KDM3B in 14 unrelated individuals and three affected parents with varying degrees of intellectual disability (ID) or developmental delay (DD) and short stature. The individuals share additional phenotypic features that include feeding difficulties in infancy, joint hypermobility, and characteristic facial features such as a wide mouth, a pointed chin, long ears, and a low columella. Notably, two individuals developed cancer, acute myeloid leukemia and Hodgkin lymphoma, in childhood. KDM3B encodes for a histone …

0301 basic medicineMaleJumonji Domain-Containing Histone DemethylasesDevelopmental DisabilitiesWEAVER SYNDROMEPROTEINHaploinsufficiencyCraniofacial AbnormalitiesHistones0302 clinical medicineIntellectual disabilityTumours of the digestive tract Radboud Institute for Molecular Life Sciences [Radboudumc 14]Missense mutationDEMETHYLASE KDM3BExomeChildGenetics (clinical)Exome sequencingGeneticsRUBINSTEIN-TAYBI SYNDROMEMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]Phenotype030220 oncology & carcinogenesisFemalemedicine.symptomHaploinsufficiencyRare cancers Radboud Institute for Health Sciences [Radboudumc 9]Joint hypermobilityGENETICSJMJD1CMutation MissenseDwarfismBiologyShort statureKdm3b ; Cancer Predisposition ; Developmental Delay ; Facial Recognition ; Intellectual Disability ; Leukemia ; Lymphoma ; Short Stature03 medical and health sciencesReportIntellectual DisabilitymedicineHumansMYELOID-LEUKEMIAGenetic Association StudiesGerm-Line MutationWeaver syndromeNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Rubinstein–Taybi syndromeMUTATIONSDELETIONGenetic Variationmedicine.diseaseBody HeightMusculoskeletal AbnormalitiesINDIVIDUALS030104 developmental biologyFaceNanomedicine Radboud Institute for Molecular Life Sciences [Radboudumc 19]American Journal of Human Genetics
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Mutation-specific pathophysiological mechanisms define different neurodevelopmental disorders associated with SATB1 dysfunction

2021

AbstractWhereas large-scale statistical analyses can robustly identify disease-gene relationships, they do not accurately capture genotype-phenotype correlations or disease mechanisms. We use multiple lines of independent evidence to show that different variant types in a single gene,SATB1, cause clinically overlapping but distinct neurodevelopmental disorders. Clinical evaluation of 42 individuals carryingSATB1variants identified overt genotype-phenotype relationships, associated with different pathophysiological mechanisms, established by functional assays. Missense variants in the CUT1 and CUT2 DNA-binding domains result in stronger chromatin binding, increased transcriptional repression…

0301 basic medicineMaleModels MolecularMISSENSE MUTATIONSCHROMATINTranscription GeneticCellMedizinDiseaseHaploinsufficiencymedicine.disease_cause0302 clinical medicineMissense mutationde novo variantsGenetics (clinical)INTERLEUKIN-2seizuresGenetics0303 health sciencesMutationChromatin bindingneurodevelopmental disordersMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]SATB1Phenotypemedicine.anatomical_structureintellectual disabilityFemaleHaploinsufficiencyteeth abnormalitiesProtein BindingNeuroinformaticsEXPRESSIONGENESMutation MissenseBiologyBINDING PROTEINREGION03 medical and health sciencesSATB1Protein DomainsReportGeneticsmedicineHPO-based analysisHumansGenetic Association StudiesHpo-based Analysis ; Satb1 ; Cell-based Functional Assays ; De Novo Variants ; Intellectual Disability ; Neurodevelopmental Disorders ; Seizures ; Teeth Abnormalities030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Matrix Attachment Region Binding Proteins030104 developmental biologyNeurodevelopmental DisordersMutationNanomedicine Radboud Institute for Molecular Life Sciences [Radboudumc 19]030217 neurology & neurosurgerycell-based functional assays
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