Search results for "Phenotype"

showing 10 items of 1875 documents

Sex Differences in the Neuroadaptations of Reward-related Circuits in Response to Subchronic Variable Stress

2018

Women are twice as likely to be diagnosed with major depressive disorder. However, fewer studies in rodent models of depression have used female animals, leading to a relative lack of understanding of the female brain’s response to stress, especially at a neural circuit level. In this study, we utilized a 6-day subchronic variable stress (SCVS) mouse model and measured novelty suppressed feeding as behavioral criteria to evaluate susceptibility to SCVS in male and female mice. First, we showed that SCVS induced a decrease in latency to eat (susceptible phenotype) in female mice, but not in males (resilient phenotype). After determining behavioral phenotypes, we investigated the firing activ…

Male0301 basic medicineAction Potentialsneuronal activityTissue Culture Techniques0302 clinical medicinePremovement neuronal activitylocus coeruleuNeuronsSex CharacteristicsNeuronal Plasticitymusculoskeletal neural and ocular physiologyGeneral NeuroscienceBrainPhenotypeVentral tegmental areamedicine.anatomical_structureMajor depressive disorderFemaleDisease Susceptibilitylateral habenulamedicine.drugmedicine.medical_specialtyCell typesex differenceventral tegmental areaBiologyArticle03 medical and health sciencesRewardDopamineInternal medicinemedicineAnimalsAction PotentialDepressive DisorderAnimalNeuronmedicine.diseaseMice Inbred C57BLElectrophysiology030104 developmental biologyEndocrinologynervous systemSettore BIO/14 - FarmacologiaLocus coeruleusTissue Culture Techniquemajor depressionStress Psychological030217 neurology & neurosurgeryNeuroscience
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TBL1XR1 mutations in Pierpont syndrome are not restricted to the recurrent p.Tyr446Cys mutation

2018

IF 2.264; International audience; Pierpont syndrome is a rare and sporadic syndrome, including developmental delay, facial characteristics, and abnormal extremities. Recently, a recurrent de novo TBL1XR1 variant (c.1337A > G; p.Tyr446Cys) has been identified in eight patients by whole‐exome sequencing. A dominant‐negative effect of this mutation is strongly suspected, since patients with TBL1XR1 deletion and other variants predicting loss of function do not share the same phenotype. We report two patients with typical Pierpont‐like syndrome features. Exome sequencing allowed identifying a de novo heterozygous missense TBL1XR1 variant in both patients, different from those already reported: …

Male0301 basic medicineAdolescentGenotypeReceptors Cytoplasmic and NuclearBiology03 medical and health sciences0302 clinical medicinePIERPONT SYNDROMEGeneticsHumansTBL1XR1Missense mutationAbnormalities MultipleRecurrent mutationGenetic TestingAllelesGenetics (clinical)Exome sequencingLoss functionUltrasonographyGeneticsComparative Genomic Hybridization[SDV.GEN]Life Sciences [q-bio]/GeneticsBrainFaciesNuclear ProteinsSyndromeMagnetic Resonance ImagingPhenotype3. Good healthRepressor ProteinsPhenotype030104 developmental biologyAmino Acid Substitution030220 oncology & carcinogenesisMutationMutation (genetic algorithm)Pierpont syndromeAmerican Journal of Medical Genetics Part A
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Reduced firing rates of pyramidal cells in the frontal cortex of APP/PS1 can be restored by acute treatment with levetiracetam

2020

Contains fulltext : 229488.pdf (Publisher’s version ) (Open Access) Contains fulltext : 229488pre.pdf (Author’s version preprint ) (Open Access) In recent years, aberrant neural oscillations in various cortical areas have emerged as a common physiological hallmark across mouse models of amyloid pathology and patients with Alzheimer's disease. However, much less is known about the underlying effect of amyloid pathology on single cell activity. Here, we used high-density silicon probe recordings from frontal cortex area of 9-month-old APP/PS1 mice to show that local field potential power in the theta and beta band is increased in transgenic animals, whereas single-cell firing rates, specifica…

Male0301 basic medicineAgingAlzheimer`s disease Donders Center for Medical Neuroscience [Radboudumc 1]LevetiracetamAction PotentialsamyloidoosiLocal field potentialAlzheimerin tautiAmyloid beta-Protein Precursor0302 clinical medicineBeta RhythmChemistryPyramidal CellsGeneral Neuroscienceamyloidfood and beveragesAmyloidosisPhenotypePathophysiologyFrontal Lobesingle cellmedicine.anatomical_structureLevetiracetamPyramidal cellAlzheimer’s diseasemedicine.drugNeuroinformaticspatofysiologiaAmyloidmouse modelTransgeneMice Transgenic03 medical and health sciencesAlzheimer Diseasemental disordersPresenilin-1medicineAnimalslocal field potential (LFP)hermosolutDisease Models Animal030104 developmental biologynervous systemfiring rateNeurology (clinical)Geriatrics and GerontologyNeuroscience030217 neurology & neurosurgeryDevelopmental BiologyNeurobiology of Aging
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ATNX2 is not a regulatory gene in Italian amyotrophic lateral sclerosis patients with C9ORF72 GGGGCC expansion

2015

Abstract There are indications that both familial amyotrophic lateral sclerosis (ALS) and sporadic ALS phenotype and prognosis are partly regulated by genetic and environmental factors, supporting the theory that ALS is a multifactorial disease. The aim of this article was to assess the role of ATXN2 intermediate length repeats in a large series of Italian and Sardinian ALS patients and controls carrying a pathogenetic C9ORF72 GGGGCC hexanucleotide repeat. A total of 1972 ALS cases were identified through the database of the Italian ALS Genetic consortium, a collaborative effort including 18 ALS centers throughout Italy. The study population included: (1) 276 Italian and 57 Sardinian ALS ca…

Male0301 basic medicineAgingC9ORF72Genetic Association Studie030105 genetics & heredityBiologySettore MED/03 - GENETICA MEDICA03 medical and health sciences0302 clinical medicineC9orf72medicineAlleleAmyotrophic lateral sclerosisAmyotrophic lateral sclerosiAgedAtaxin-2Regulator geneAmyotrophic lateral sclerosis; ATXN2; C9ORF72; Phenotype; Neuroscience (all); Medicine (all); Aging; Developmental Biology; Geriatrics and Gerontology; Neurology (clinical)GeneticsDNA Repeat ExpansionNeuroscience (all)ProteinMedicine (all)General NeuroscienceATXN2Middle AgedDNA Repeat Expansionmedicine.diseaseAmyotrophic lateral sclerosis3. Good healthC9orf72 ProteinAmyotrophic lateral sclerosis; ATXN2; C9ORF72; Phenotype; Neurology (clinical); Neuroscience (all); Aging; Developmental Biology; Geriatrics and GerontologyPhenotypeItalyPopulation studyFemaleSettore MED/26 - NeurologiaNeurology (clinical)Geriatrics and GerontologyTrinucleotide repeat expansion030217 neurology & neurosurgeryHumanDevelopmental Biology
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DNA methylation in childhood asthma

2018

Background: DNA methylation profiles associated with childhood asthma might provide novel insights into disease pathogenesis. We did an epigenome-wide association study to assess methylation profiles associated with childhood asthma. Methods: We did a large-scale epigenome-wide association study (EWAS) within the Mechanisms of the Development of ALLergy (MeDALL) project. We examined epigenome-wide methylation using Illumina Infinium Human Methylation450 BeadChips (450K) in whole blood in 207 children with asthma and 610 controls at age 4–5 years, and 185 children with asthma and 546 controls at age 8 years using a cross-sectional case-control design. After identification of differentially m…

Male0301 basic medicineAllergyCytotoxicT-Lymphocytes[SDV]Life Sciences [q-bio]Respiratory Systemlnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]CHILDRENImmunoglobulin EEpigenesis GeneticChildPOPULATIONeducation.field_of_studybiologyMethylation3. Good healthCpG siteChild PreschoolDNA methylationFemaleBIOS ConsortiumLife Sciences & BiomedicinePulmonary and Respiratory MedicinePopulationPHENOTYPESIMMUNITY03 medical and health sciencesCritical Care MedicineGeneticGeneral & Internal MedicinemedicineHumansCOHORTEpigeneticsIGEEXPOSUREPreschooleducationAsthmaScience & Technologybusiness.industryRHINITISDNADNA Methylationmedicine.diseaseAsthmaEosinophils030104 developmental biology3121 General medicine internal medicine and other clinical medicineImmunologybiology.proteinGENOMEWIDE ASSOCIATIONCpG IslandsbusinessCOLLECTIONT-Lymphocytes CytotoxicEpigenesisGenome-Wide Association StudyThe Lancet. Respiratory Medicine
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Disruption of the ATXN1-CIC complex causes a spectrum of neurobehavioral phenotypes in mice and humans

2017

International audience; Gain-of-function mutations in some genes underlie neurodegenerative conditions, whereas loss-of-function mutations in the same genes have distinct phenotypes. This appears to be the case with the protein ataxin 1 (ATXN1), which forms a transcriptional repressor complex with capicua (CIC). Gain of function of the complex leads to neurodegeneration, but ATXN1-CIC is also essential for survival. We set out to understand the functions of the ATXN1-CIC complex in the developing forebrain and found that losing this complex results in hyperactivity, impaired learning and memory, and abnormal maturation and maintenance of upper-layer cortical neurons. We also found that CIC …

Male0301 basic medicineAutism Spectrum DisorderAtaxin 1neuronsautismNerve Tissue Proteinsattention-deficit/hyperactivity disorderAmygdalaArticleMice03 medical and health sciencesTranscriptional repressor complexataxin-1Cerebellum[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyGeneticsmedicineAnimalsHumansAttention deficit hyperactivity disorderInterpersonal Relationssca1 neuropathologybiologysocial-behaviorNeurodegenerationcag repeatNuclear ProteinsNeurodegenerative Diseasesmedicine.diseasePhenotypeRepressor ProteinsPhenotype030104 developmental biologymedicine.anatomical_structureAutism spectrum disorderintellectual disabilitybiology.proteinAutismFemaleNeurosciencetime pcr datarepressor capicua[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Infiltrating mast cell-mediated stimulation of estrogen receptor activity in breast cancer cells promotes the luminal phenotype

2019

Abstract Tumor growth and development is determined by both cancer cell–autonomous and microenvironmental mechanisms, including the contribution of infiltrating immune cells. Because the role of mast cells (MC) in this process is poorly characterized and even controversial, we investigated their part in breast cancer. Crossing C57BL/6 MMTV-PyMT mice, which spontaneously develop mammary carcinomas, with MC-deficient C57BL/6-KitW-sh/W-sh (Wsh) mice, showed that MCs promote tumor growth and prevent the development of basal CK5-positive areas in favor of a luminal gene program. When cocultured with breast cancer cells in vitro, MCs hindered activation of cMET, a master regulator of the basal pr…

Male0301 basic medicineCancer ResearchReceptor ErbB-2Estrogen receptorBreast NeoplasmsMice TransgenicCell CommunicationCell Growth ProcessesMice03 medical and health sciences0302 clinical medicineBreast cancerImmune systemCell Line TumormedicineAnimalsHumansMast CellsNeoplasm Metastasisskin and connective tissue diseasesEstrogen receptor activityMice Inbred BALB Cbusiness.industryMammary Neoplasms ExperimentalCancerProto-Oncogene Proteins c-metmedicine.diseaseMast cellPhenotypeErbB ReceptorsMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureReceptors EstrogenOncology030220 oncology & carcinogenesisCancer researchFemalebusinessmast cell estrogen receptor breast cancer luminal phenotypeEstrogen receptor alpha
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Variant recurrence in neurodevelopmental disorders: the use of publicly available genomic data identifies clinically relevant pathogenic missense var…

2019

Next-generation sequencing has revealed the major impact of de novo variants (DNVs) in developmental disorders (DD) such as intellectual disability, autism, and epilepsy. However, a substantial fraction of these predicted pathogenic DNVs remains challenging to distinguish from background DNVs, notably the missense variants acting via nonhaploinsufficient mechanisms on specific amino acid residues. We hypothesized that the detection of the same missense variation in at least two unrelated individuals presenting with a similar phenotype could be a powerful approach to reveal novel pathogenic variants. We looked for variations independently present in both our database of >1200 solo exomes and…

Male0301 basic medicineCandidate geneDevelopmental DisabilitiesMutation Missense030105 genetics & heredityBiology03 medical and health sciencesNeurodevelopmental disorderIntellectual DisabilityDatabases GeneticIntellectual disabilitymedicineHumansMissense mutationExomeGenetic Predisposition to DiseaseGenetic TestingAutistic DisorderGeneGenetics (clinical)Exome sequencingGeneticsComputational BiologyHigh-Throughput Nucleotide SequencingGenomicsSequence Analysis DNAmedicine.diseasePhenotype030104 developmental biologyNeurodevelopmental DisordersAutismFemaleTranscription FactorsGenetics in Medicine
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Novel Mutations in the NKX2.1 gene and the PAX8 gene in a Boy with Brain-Lung-Thyroid Syndrome

2017

Abstract Objective To elucidate the molecular mechanism which causes thyroid dysgenesis (TD) in a boy with brain-lung-thyroid syndrome. Design, patients, measurements We describe a patient with TD, respiratory disease and cerebral palsy who is heterozygous for mutations in two different genes, the PAX8 (p.E234K) and the NKX2.1 (p.A329GfsX108). In vitro studies were performed to functionally characterize these mutations. Congenital hypothyroidism (CH) was identified by neonatal screening associated with a hypoplastic thyroid gland. Postpartum he developed a brain-lung-thyroid syndrome with severe respiratory failure, symptomatic epilepsy and a considerable psychomotor retardation. The DNA-bi…

Male0301 basic medicineCandidate geneEndocrinology Diabetes and MetabolismThyroid Nuclear Factor 1030105 genetics & heredityBiologymedicine.disease_causeThyroid dysgenesisPAX8 Transcription Factor03 medical and health sciencesEndocrinologyChoreaCongenital HypothyroidismInternal MedicinemedicineHumansChildAthetosisGeneRespiratory Distress Syndrome NewbornMutationPsychomotor retardationGeneral Medicinemedicine.diseasePhenotypeCongenital hypothyroidismMutationCancer researchmedicine.symptomPAX8Experimental and Clinical Endocrinology & Diabetes
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WNT Signaling Perturbations Underlie the Genetic Heterogeneity of Robinow Syndrome

2018

International audience; Locus heterogeneity characterizes a variety of skeletal dysplasias often due to interacting or overlapping signaling pathways. Robinow syndrome is a skeletal disorder historically refractory to molecular diagnosis, potentially stemming from substantial genetic heterogeneity. All current known pathogenic variants reside in genes within the noncanonical Wnt signaling pathway including ROR2, WNT5A, and more recently, DVL1 and DVL3. However, ∼70% of autosomal-dominant Robinow syndrome cases remain molecularly unsolved. To investigate this missing heritability, we recruited 21 families with at least one family member clinically diagnosed with Robinow or Robinow-like pheno…

Male0301 basic medicineCandidate geneFrizzledGROWTH-PLATEDEP DOMAINlnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]PROTEINskeletal dysplasiaCraniofacial Abnormalities0302 clinical medicineLocus heterogeneityChromosome SegregationChild[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsWnt Signaling PathwayGenetics (clinical)Genes DominantGeneticsWnt signaling pathwayMiddle AgedRobinow syndromeMENDELIAN-INHERITANCEPhenotypeChild PreschoolFemaleNEURAL-TUBE DEFECTSVERTEBRATE GASTRULATIONhuman embryonic developmentRare cancers Radboud Institute for Health Sciences [Radboudumc 9]AdultAdolescentCELL POLARITYLimb Deformities CongenitalMutation MissenseDwarfismBiologyArticledual molecular diagnosisDiagnosis DifferentialGenetic Heterogeneity03 medical and health sciencesFrizzledAll institutes and research themes of the Radboud University Medical CenterSkeletal disorderGeneticsmedicineHumansGenetic Association StudiesNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Base SequenceGenetic heterogeneityMUTATIONSROR2medicine.diseaseDROSOPHILA TISSUE POLARITY030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsUrogenital AbnormalitiesAUTOSOMAL-DOMINANT030217 neurology & neurosurgery
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