Search results for "Loin"

showing 10 items of 294 documents

Exploring by whole exome sequencing patients with initial diagnosis of Rubinstein-Taybi syndrome: the interconnections of epigenetic machinery disord…

2019

Rubinstein–Taybi syndrome (RSTS) is an autosomal-dominant neurodevelopmental disease affecting 1:125,000 newborns characterized by intellectual disability, growth retardation, facial dysmorphisms and skeletal abnormalities. RSTS is caused by mutations in genes encoding for writers of the epigenetic machinery: CREBBP (~ 60%) or its homologous EP300 (~ 10%). No causative mutation is identified in up to 30% of patients. We performed whole-exome sequencing (WES) on eight RSTS-like individuals who had normal high-resolution array CGH testing and were CREBBP- and EP300-mutation -negative, to identify the molecular cause. In four cases, we identified putatively causal variants in three genes (ASXL…

MaleGenetic Association StudieCompound heterozygosityWhole Exome SequencingArticleEpigenesis Genetic03 medical and health scienceswhole exome sequencing Rubinstein–Taybi syndrome epigenetic mutationsExome SequencingGeneticsmedicineHumansEpigeneticsEP300ChildGenetics (clinical)Exome sequencingGenetic Association Studies030304 developmental biologyGeneticsRubinstein-Taybi Syndrome0303 health sciencesComparative Genomic HybridizationbiologyRubinstein–Taybi syndrome030305 genetics & heredityInfant NewbornFaciesInfantmedicine.diseaseFacieCREB-Binding ProteinHuman geneticsRSTSKMT2APhenotypeChild PreschoolMutationbiology.proteinNeurodegenerative disordersFemaleHaploinsufficiencyE1A-Associated p300 ProteinHumanHuman genetics
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Variable phenotype in 17q12 microdeletions: Clinical and molecular characterization of a new case

2014

Microdeletions of 17q12 including the hepatocyte nuclear factor 1 beta (HNF1B) gene, as well as point mutations of this gene, are associated with the Renal Cysts and Diabetes syndrome (RCAD, OMIM 137920) and genitourinary alterations. Also, microdeletions encompassing HNF1B were identified as a cause of Mayer-Rokitansky-Kuster-Hauser Syndrome (MRKH, OMIM 277000) in females and, recently, were associated with intellectual disability, autistic features, cerebral anomaly and facial dysmorphisms. In this report, we describe a boy with a deletion in 17q12 region detected by SNP array, encompassing the HNF1B gene, that showed dysmorphic features, intellectual disability (ID), serious speech delay…

MaleLIM-Homeodomain ProteinsSingle-nucleotide polymorphismHaploinsufficiencyBiologyBioinformaticsPolymorphism Single NucleotideIntellectual DisabilityIntellectual disabilityGeneticsmedicineHumansAbnormalities MultipleLanguage Development DisordersAutistic DisorderChildHNF1B 17q12 SNP array Renal Cysts and Diabetes syndrome Intellectual disabilityHepatocyte Nuclear Factor 1-betaGeneticsHaplotypeForkhead Transcription FactorsGeneral Medicinemedicine.diseaseHNF1BPenetrancePhenotypeHaplotypesSpeech delayFemalemedicine.symptomChromosome DeletionHaploinsufficiencySNP arrayAcetyl-CoA CarboxylaseChromosomes Human Pair 17Transcription Factors
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Widening of the genetic and clinical spectrum of Lamb-Shaffer syndrome, a neurodevelopmental disorder due to SOX5 haploinsufficiency

2020

International audience; PURPOSE: Lamb-Shaffer syndrome (LAMSHF) is a neurodevelopmental disorder described in just over two dozen patients with heterozygous genetic alterations involving SOX5, a gene encoding a transcription factor regulating cell fate and differentiation in neurogenesis and other discrete developmental processes. The genetic alterations described so far are mainly microdeletions. The present study was aimed at increasing our understanding of LAMSHF, its clinical and genetic spectrum, and the pathophysiological mechanisms involved.METHODS: Clinical and genetic data were collected through GeneMatcher and clinical or genetic networks for 41 novel patients harboring various ty…

MaleMedizinHaploinsufficiencyL-SOX5VARIANTS0302 clinical medicineNeurodevelopmental disorderIntellectual disabilityMissense mutation2.1 Biological and endogenous factorsAetiologyChildGenetics (clinical)GeneticsPediatricGenetics & Heredity0303 health sciencesPedigreeFAMILYDNA-Binding Proteinsdevelopmental delayTRANSCRIPTION FACTORSPhenotypeintellectual disabilityChild Preschoolmissense variantsFemalemissense variants.HaploinsufficiencySOXD Transcription FactorsAdultEXPRESSIONAdolescentIntellectual and Developmental Disabilities (IDD)Clinical SciencesMutation MissenseautismCell fate determinationBiologyLONG FORMSEQUENCEArticle03 medical and health sciencesYoung AdultRare DiseasesClinical ResearchCARTILAGEIntellectual DisabilitymedicineGeneticsAnimalsHumansLanguage Development DisordersGenetic Predisposition to DiseasePreschoolTranscription factorGene030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsMUTATIONSHuman GenomeInfantmedicine.diseaseBrain DisordersNeurodevelopmental DisordersDeciphering Developmental Disorder StudyMutationAutismepilepsyMissense030217 neurology & neurosurgeryGENERATIONGenetics in Medicine
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EPHA7 haploinsufficiency is associated with a neurodevelopmental disorder

2021

International audience; Ephrin receptor and their ligands, the ephrins, are widely expressed in the developing brain. They are implicated in several developmental processes that are crucial for brain development. Deletions in genes encoding for members of the Eph/ephrin receptor family were reported in several neurodevelopmental disorders. The ephrin receptor A7 gene (EPHA7) encodes a member of ephrin receptor subfamily of the protein-tyrosine kinase family. EPHA7 plays a role in corticogenesis processes, determines brain size and shape, and is involved in development of the central nervous system. One patient only was reported so far with a de novo deletion encompassing EPHA7 in 6q16.1. We…

MaleMicrocephaly[SDV]Life Sciences [q-bio]6q161 microdeletionInheritance PatternsEPHA7HaploinsufficiencyBiologyspeech and language developmentNeurodevelopmental disorderExome SequencingGeneticsmedicineEphrinHumansGenetic Predisposition to DiseasemicrocephalyGenetics (clinical)Genetic Association StudiesIn Situ Hybridization FluorescenceGeneticsComparative Genomic Hybridization6q16.1 microdeletionErythropoietin-producing hepatocellular (Eph) receptorReceptor EphA7medicine.diseasePenetrancePhenotypeneurodevelopmental disorderPedigree[SDV] Life Sciences [q-bio]PhenotypeNeurodevelopmental Disordersintellectual disabilityEPHA7MutationChromosomes Human Pair 6FemaleHaploinsufficiencyClinical Genetics
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Haploinsufficiency of the NOTCH1 receptor as a cause of Adams-Oliver syndrome with variable cardiac anomalies

2015

Background— Adams–Oliver syndrome (AOS) is a rare disorder characterized by congenital limb defects and scalp cutis aplasia. In a proportion of cases, notable cardiac involvement is also apparent. Despite recent advances in the understanding of the genetic basis of AOS, for the majority of affected subjects, the underlying molecular defect remains unresolved. This study aimed to identify novel genetic determinants of AOS. Methods and Results— Whole-exome sequencing was performed for 12 probands, each with a clinical diagnosis of AOS. Analyses led to the identification of novel heterozygous truncating NOTCH1 mutations (c.1649dupA and c.6049_6050delTC) in 2 kindreds in which AOS was segregat…

MaleModels MolecularProbandreceptorGene ExpressionHaploinsufficiencyNOTCH1Ectodermal DysplasiaMissense mutationExomeReceptor Notch1ChildExomeGenetics (clinical)GeneticsReverse Transcriptase Polymerase Chain ReactionAutosomal dominant traitMiddle AgedPedigreeembryonic structuresheart defectscardiovascular systemFemaleCardiology and Cardiovascular MedicineHaploinsufficiencySignal TransductionAdultHeart Defects CongenitalAdolescentLimb Deformities CongenitalNotch signaling pathwayBiologyArticleYoung AdultAdams-Oliver syndromeGeneticsmedicineHumansGenetic Predisposition to DiseaseGeneFamily HealthBase SequencecongenitalAdams-Oliver syndrome; genetics; haploinsufficiency; heart defects; congenital; receptor; NOTCH1; Cardiology and Cardiovascular Medicine; Genetics (clinical); GeneticsSequence Analysis DNAmedicine.diseaseProtein Structure TertiaryScalp DermatosesHuman medicineAdams–Oliver syndromeCirculation. Cardiovascular genetics
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The effect of alertness and attention on the modulation of the beta rhythm to tactile stimulation

2021

Abstract Beta rhythm modulation has been used as a biomarker to reflect the functional state of the sensorimotor cortex in both healthy subjects and patients. Here, the effect of reduced alertness and active attention to the stimulus on beta rhythm modulation was investigated. Beta rhythm modulation to tactile stimulation of the index finger was recorded simultaneously with MEG and EEG in 23 healthy subjects (mean 23, range 19–35 years). The temporal spectral evolution method was used to obtain the peak amplitudes of beta suppression and rebound in three different conditions (neutral, snooze, and attention). Neither snooze nor attention to the stimulus affected significantly the strength of…

MalePhysiologyEvent related synchronization030204 cardiovascular system & hematology0302 clinical medicinevigilanceAttentionEEGkosketusevent-related synchronizationMEGneuropsykologiaEvent related desynchronization1184 Genetics developmental biology physiologyMagnetoencephalographyElectroencephalographyBAND OSCILLATIONSvireysstimulointiFemaleOriginal ArticleSensorimotor CortexPsychologyaivotArousalCORTICAL OSCILLATIONSevent‐related desynchronizationAdultFREQUENCY ACTIVITYMU RHYTHMMental fatigueELECTRICAL-ACTIVITYLibrary sciencesensomotoriikkatuntoaistibeta oscillation03 medical and health sciencesMOVEMENTYoung Adultevent‐related synchronizationSPACE SEPARATION METHODPhysiology (medical)Physical StimulationHumansMENTAL FATIGUEtarkkaavaisuusFunding AgencyPRIMARY MOTOR CORTEXOriginal ArticlesAlertnessaivokuoriTouchCortical oscillationsBeta Rhythm030217 neurology & neurosurgeryevent-related desynchronization
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Proteomic signature of the Dravet syndrome in the genetic Scn1a-A1783V mouse model.

2021

Abstract Background Dravet syndrome is a rare, severe pediatric epileptic encephalopathy associated with intellectual and motor disabilities. Proteomic profiling in a mouse model of Dravet syndrome can provide information about the molecular consequences of the genetic deficiency and about pathophysiological mechanisms developing during the disease course. Methods A knock-in mouse model of Dravet syndrome with Scn1a haploinsufficiency was used for whole proteome, seizure, and behavioral analysis. Hippocampal tissue was dissected from two- (prior to epilepsy manifestation) and four- (following epilepsy manifestation) week-old male mice and analyzed using LC-MS/MS with label-free quantificati…

MaleProteomics0301 basic medicineProteomeHippocampusEpilepsies MyoclonicHaploinsufficiencyScn1aHippocampusSynaptic TransmissionElevated Plus Maze TestEpilepsyMice0302 clinical medicineTandem Mass Spectrometry11-beta-Hydroxysteroid Dehydrogenase Type 1Genetic epilepsyCarbon-Nitrogen LigasesGene Knock-In TechniquesGliosisNeuronal PlasticityBehavior AnimalEpileptic encephalopathyImmunohistochemistryAstrogliosisNeurologyProteomeDisease ProgressionFemaleHaploinsufficiencySignal TransductionRC321-571Dopamine and cAMP-Regulated Phosphoprotein 32Neovascularization PhysiologicNeurosciences. Biological psychiatry. NeuropsychiatryBiologyNitric Oxide03 medical and health sciencesDravet syndromemedicineAnimalsHyperthermiaSocial Behaviorras-GRF1Proteomic Profilingmedicine.diseaseVascular Endothelial Growth Factor Receptor-2NAV1.1 Voltage-Gated Sodium ChannelDisease Models Animal030104 developmental biologyRotarod Performance TestSynaptic plasticityEpileptic Encephalopathy ; Genetic Epilepsy ; Mice ; Proteome ; Scn1aCalcium-Calmodulin-Dependent Protein Kinase Type 2Open Field TestNeuroscience030217 neurology & neurosurgeryChromatography Liquid
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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
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Umbilical cord blood transplantation from unrelated donors in patients with Philadelphia chromosome-positive acute lymphoblastic leukemia

2014

Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't; There are very few disease-specific studies focusing on outcomes of umbilical cord blood transplantation for Philadelphia chromosome-positive acute lymphoblastic leukemia. We report the outcome of 45 patients with Philadelphia chromosome-positive acute lymphoblastic leukemia who underwent myeloablative single unit cord blood transplantation from unrelated donors within the GETH/GITMO cooperative group. Conditioning regimens were based on combinations of thiotepa, busulfan, cyclophospamide or fludarabine, and antithymocyte globulin. At the time of transplantation, 35 patients (78%) were in first complete remission, four (8%) …

MaleTransplantation Conditioning:Analytical Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Epidemiologic Study Characteristics as Topic::Epidemiologic Studies::Case-Control Studies::Retrospective Studies [Medical Subject Headings]Leucemia-linfoma linfoblástico de células precursorasGraft vs Host Disease:Named Groups::Persons::Age Groups::Adult::Middle Aged [Medical Subject Headings]Supervivencia sin EnfermedadGastroenterology:Anatomy::Body Regions::Transplants::Allografts [Medical Subject Headings]:Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Therapeutic Uses::Antineoplastic Agents::Myeloablative Agonists [Medical Subject Headings]:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings]hemic and lymphatic diseasesMedicineCumulative incidenceTasa de SupervivenciaPhiladelphia ChromosomeChildCromosoma Filadelfia:Diseases::Pathological Conditions Signs and Symptoms::Pathologic Processes::Disease Attributes::Chronic Disease [Medical Subject Headings]:Named Groups::Persons::Age Groups::Child::Child Preschool [Medical Subject Headings]ArticlesHematologyMiddle AgedPrecursor Cell Lymphoblastic Leukemia-LymphomaAllografts:Analytical Diagnostic and Therapeutic Techniques and Equipment::Therapeutics::Biological Therapy::Immunomodulation::Immunotherapy::Immunosuppression::Transplantation Conditioning [Medical Subject Headings]FludarabineSurvival RateChild Preschool:Named Groups::Persons::Age Groups::Adolescent [Medical Subject Headings]:Diseases::Pathological Conditions Signs and Symptoms::Pathologic Processes::Chromosome Aberrations::Translocation Genetic::Philadelphia Chromosome [Medical Subject Headings]:Analytical Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Statistics as Topic::Survival Analysis::Disease-Free Survival [Medical Subject Headings]FemaleAcondicionamiento para el trasplanteCord Blood Stem Cell TransplantationTrasplante de células madre de la sangre del cordónmedicine.drugAloinjertosAdultmedicine.medical_specialtyAdolescent:Check Tags::Male [Medical Subject Headings]Cord Blood Stem Cell TransplantationPhiladelphia chromosomeEnfermedad injerto contra huéspedDisease-Free SurvivalEstudios retrospectivosInternal medicine:Analytical Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Epidemiologic Study Characteristics as Topic::Epidemiologic Studies::Cohort Studies::Longitudinal Studies::Follow-Up Studies [Medical Subject Headings]:Named Groups::Persons::Age Groups::Adult [Medical Subject Headings]HumansPreschoolSurvival rate:Named Groups::Persons::Age Groups::Child [Medical Subject Headings]Retrospective Studies:Analytical Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Data Collection::Vital Statistics::Mortality::Survival Rate [Medical Subject Headings]business.industryUmbilical Cord Blood TransplantationEnfermedad crónicaAgonistas mieloablativosMyeloablative Agonistsmedicine.diseaseSettore MED/15SurgeryTransplantation:Diseases::Immune System Diseases::Graft vs Host Disease [Medical Subject Headings]:Diseases::Hemic and Lymphatic Diseases::Lymphatic Diseases::Lymphoproliferative Disorders::Leukemia Lymphoid::Precursor Cell Lymphoblastic Leukemia-Lymphoma [Medical Subject Headings]:Check Tags::Female [Medical Subject Headings]Estudios de SeguimientoChronic Disease:Analytical Diagnostic and Therapeutic Techniques and Equipment::Surgical Procedures Operative::Transplantation::Cell Transplantation::Stem Cell Transplantation::Cord Blood Stem Cell Transplantation [Medical Subject Headings]Adolescent; Adult; Allografts; Child; Child Preschool; Chronic Disease; Disease-Free Survival; Female; Follow-Up Studies; Graft vs Host Disease; Humans; Male; Middle Aged; Myeloablative Agonists; Retrospective Studies; Survival Rate; Cord Blood Stem Cell Transplantation; Philadelphia Chromosome; Precursor Cell Lymphoblastic Leukemia-Lymphoma; Transplantation ConditioningbusinessBusulfanFollow-Up Studies
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2p15-p16.1 microdeletions encompassing and proximal to BCL11A are associated with elevated HbF in addition to neurologic impairment.

2015

Elevated fetal hemoglobin (HbF) ameliorates the clinical severity of hemoglobinopathies such as β-thalassemia and sickle cell anemia. Currently, the only curative approach for individuals under chronic transfusion/chelation support therapy is allogeneic stem cell transplantation. However, recent analyses of heritable variations in HbF levels have provided a new therapeutic target for HbF reactivation: the transcriptional repressor BCL11A. Erythroid-specific BCL11A abrogation is now actively being sought as a therapeutic avenue, but the specific impact of such disruption in humans remains to be determined. Although single nucleotide polymorphisms in BCL11A erythroid regulatory elements have …

Malecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyAdolescentImmunologyBiologyBiochemistrySettore MED/38 - Pediatria Generale E SpecialisticaRed Cells Iron and ErythropoiesisInternal medicinehemic and lymphatic diseasesFetal hemoglobinmedicineGene silencingHumansChildNervous System DiseaseFetal HemoglobinNuclear ProteinHematologyNuclear ProteinsCell BiologyHematologymedicine.diseasePhenotypeSickle cell anemiaUp-RegulationTransplantationRepressor ProteinsSettore MED/03 - Genetica MedicaChromosomes Human Pair 22p15-p16.1 microdeletions BCL11A HbF neurologicImmunologyFemaleStem cellChromosome DeletionNervous System DiseasesCarrier ProteinHaploinsufficiencyCarrier ProteinsHumanBlood
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