Search results for "Normal"

showing 10 items of 2571 documents

A Typical Immune T/B Subset Profile Characterizes Bicuspid Aortic Valve: In an Old Status?

2018

Bicuspid valve disease is associated with the development of thoracic aortic aneurysm. The molecular mechanisms underlying this association still need to be clarified. Here, we evaluated the circulating levels of T and B lymphocyte subsets associated with the development of vascular diseases in patients with bicuspid aortic valve or tricuspid aortic valve with and without thoracic aortic aneurysm. We unveiled that the circulating levels of the MAIT, CD4+IL−17A+, and NKT T cell subsets were significantly reduced in bicuspid valve disease cases, when compared to tricuspid aortic valve cases in either the presence or the absence of thoracic aortic aneurysm. Among patients with tricuspid aortic…

Male0301 basic medicineAortic valveAgingT-LymphocytesLymphocyteHeart Valve Diseases030204 cardiovascular system & hematologyBiochemistryImmunoglobulin D0302 clinical medicineBicuspid aortic valveBicuspid Aortic Valve DiseaseBicuspid aortic valve aneurysm B cellsb-cellsnotch1Invariant t-cells; aneurysm formation; angiotensin-ii; signaling pathway; genetic-variants; apoptotic cells; b-cells; mechanisms; mutations; notch1B-Lymphocytesmechanismsbiologylcsh:Cytologyhemic and immune systemsGeneral MedicineMiddle Agedmedicine.anatomical_structureAortic ValveCardiologycardiovascular systemFemaleResearch Articlesignaling pathwaymedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesaneurysm formationInvariant t-cellsArticle SubjectBicuspid aortic valveT cellNaive B cellchemical and pharmacologic phenomenaThoracic aortic aneurysm03 medical and health sciencesBicuspid valveInternal medicinemedicineHumansSettore MED/05 - Patologia Clinicacardiovascular diseaseslcsh:QH573-671angiotensin-iigenetic-variantsB cellsbusiness.industrySettore MED/23 - Chirurgia Cardiacaapoptotic cellsCell Biologymutationsmedicine.disease030104 developmental biologybiology.proteinaneurysmbusinessA Typical Immune T/B Subset Profile Bicuspid Aortic Valve
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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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Mutation spectrum of NF1 gene in Italian patients with neurofibromatosis type 1 using Ion Torrent PGM™ platform

2017

Neurofibromatosis type 1 (NF1) is caused by mutations of the NF1 gene and is one of the most common human autosomal dominant disorders. The patient shows different signs on the skin and other organs from early childhood. The best known are six or more café au lait spots, axillary or inguinal freckling, increased risk of developing benign nerve sheath tumours and plexiform neurofibromas. Mutation detection is complex, due to the large gene size, the large variety of mutations and the presence of pseudogenes. Using Ion Torrent PGM™ Platform, 73 mutations were identified in 79 NF1 Italian patients, 51% of which turned out to be novel mutations. Pathogenic status of each variant was classifi…

Male0301 basic medicineDNA Mutational Analysismedicine.disease_causeChildGenetics (clinical)Sanger sequencingGeneticsMutationNeurofibromin 1biologyMosaicismCafe-au-Lait SpotsNeurofibromatosis type 1; Legius's syndrome; Next generation sequencingGeneral MedicineMiddle AgedItalyChild PreschoolsymbolsMedical geneticsFemalemedicine.symptomHumanAdultmedicine.medical_specialtyNeurofibromatosis 1AdolescentPseudogeneDNA Mutational Analysi03 medical and health sciencessymbols.namesakeGeneticNext generation sequencingCafé au lait spotSkin AbnormalitieGeneticsmedicineHumansCafe-au-Lait SpotNeurofibromatosisLegius's syndromeInfantSequence Analysis DNAIon semiconductor sequencingmedicine.diseaseNeurofibromin 1030104 developmental biologyMutationSkin Abnormalitiesbiology.proteinNeurofibromatosis type 1European Journal of Medical Genetics
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Early-infantile onset epilepsy and developmental delay caused by bi-allelic GAD1 variants

2020

Mice lacking GAD1 show neonatal mortality, but the human phenotype associated with GAD1 disruption is poorly characterized. Neuray et al. describe six patients with biallelic GAD1 mutations, presenting with early-infantile onset epilepsy, neurodevelopmental delay, muscle weakness and non-CNS manifestations.

Male0301 basic medicineGlutamate decarboxylaseMalalties cerebralsNeurotransmissorsNeurodevelopmental delayEpilepsy0302 clinical medicineMESH: ChildAge of OnsetChildcleft palateGAD1AcademicSubjects/SCI01870Glutamate DecarboxylaseGlutamate receptorMuscle weakness//purl.org/becyt/ford/3.1 [https]NeurotransmittersMESH: InfantHypotoniamuscle weakneCleft palateMESH: EpilepsyChild PreschoolMuscle Hypotonia[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]//purl.org/becyt/ford/3 [https]FemaleBrain diseasesAbnormalitiesmedicine.symptomMultiplemedicine.drugcleft palate; epilepsy; GAD1; muscle weakness; neurodevelopmental delayMESH: Glutamate Decarboxylasemedicine.medical_specialtyMESH: Abnormalities MultipleMESH: MutationMESH: Age of OnsetBiologyInhibitory postsynaptic potentialGAD1 cleft palate epilepsy muscle weakness neurodevelopmental delay.gamma-Aminobutyric acidGAD1neurodevelopmental delay03 medical and health sciencesExcitatory synapseInternal medicinemedicineHumansAbnormalities MultiplePreschoolAllelesMESH: Neurodevelopmental Disordersmuscle weaknessMESH: HumansEpilepsyMESH: Muscle HypotoniaMESH: AllelesMESH: Child PreschoolInfantmedicine.diseaseMESH: MaleEpilèpsiaEditor's Choice030104 developmental biologyEndocrinologyNeurodevelopmental DisordersMutationepilepsyAcademicSubjects/MED00310Neurology (clinical)Cleft palate; Epilepsy; GAD1; Muscle weakness; Neurodevelopmental delay; Abnormalities Multiple; Age of Onset; Alleles; Child; Child Preschool; Epilepsy; Female; Glutamate Decarboxylase; Humans; Infant; Male; Muscle Hypotonia; Mutation; Neurodevelopmental DisordersMESH: Female[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology030217 neurology & neurosurgeryReports
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Fifteen years of research on oral-facial-digital syndromes: from 1 to 16 causal genes

2017

Oral–facial–digital syndromes (OFDS) gather rare genetic disorders characterised by facial, oral and digital abnormalities associated with a wide range of additional features (polycystic kidney disease, cerebral malformations and several others) to delineate a growing list of OFDS subtypes. The most frequent, OFD type I, is caused by a heterozygous mutation in theOFD1gene encoding a centrosomal protein. The wide clinical heterogeneity of OFDS suggests the involvement of other ciliary genes. For 15 years, we have aimed to identify the molecular bases of OFDS. This effort has been greatly helped by the recent development of whole-exome sequencing (WES). Here, we present all our published and …

Male0301 basic medicineHeterozygoteciliopathieOral facial digital[SDV]Life Sciences [q-bio][ SDV.BBM.BM ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyBiologyCiliopathiesCentriole elongation03 medical and health sciencesIntraflagellar transportGenotypeGeneticsPolycystic kidney diseasemedicineHumansAbnormalities Multiple[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyFunctional studies[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyGene*oral-facial-digital syndromesGenetics (clinical)ComputingMilieux_MISCELLANEOUSEncephaloceleGeneticsPolycystic Kidney Diseases[ SDV ] Life Sciences [q-bio]*ciliopathiesProteinsMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6][SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyOrofaciodigital Syndromesmedicine.disease030104 developmental biologyFaceMutationciliopathiesoral-facial-digital syndromesFemaleRetinitis PigmentosaRare cancers Radboud Institute for Health Sciences [Radboudumc 9]Ciliary Motility Disorders
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The LepR-mediated leptin transport across brain barriers controls food reward

2018

Objective Leptin is a key hormone in the control of appetite and body weight. Predominantly produced by white adipose tissue, it acts on the brain to inhibit homeostatic feeding and food reward. Leptin has free access to circumventricular organs, such as the median eminence, but entry into other brain centers is restricted by the blood–brain and blood–CSF barriers. So far, it is unknown for which of its central effects leptin has to penetrate brain barriers. In addition, the mechanisms mediating the transport across barriers are unclear although high expression in brain barriers suggests an important role of the leptin receptor (LepR). Methods We selectively deleted LepR in brain endothelia…

Male0301 basic medicineLeptinHFD high-fat dietEndothelial cellsWhite adipose tissueCSF cerebrospinal fluidMice0302 clinical medicineCPP conditioned place preferenceBBB blood–brain barrierCells Culturedmedia_commonLeptindigestive oral and skin physiologyi.p. intraperitonealmedicine.anatomical_structureLepRBlood-Brain BarrierBlood–brain barrier; Endothelial cells; LepR; Leptin; Obesity; RewardMedian eminenceqPCR quantitative polymerase chain reactionReceptors LeptinOriginal ArticleChoroid plexusmedicine.medical_specialtylcsh:Internal medicinemedia_common.quotation_subjectHyperphagiaBiologyBlood–brain barrierVTA ventral tegmental areaBC bottle choice testCapillary PermeabilityBlood–brain barrierARC arcuate nucleus03 medical and health sciencesPBS phosphate buffered salineRewardInternal medicinemedicineAnimalsObesitylcsh:RC31-1245Molecular BiologyCircumventricular organsBlood-Nerve BarrierLeptin receptorNCD normal chow dietAppetiteCell Biology030104 developmental biologyEndocrinologyLepR leptin receptorChoroid PlexusBSA bovine serum albuminPFA paraformaldehyde030217 neurology & neurosurgeryDAPI 4′6-diamidino-2-phenylindoleMolecular Metabolism
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Removing Batch Effects from Longitudinal Gene Expression - Quantile Normalization Plus ComBat as Best Approach for Microarray Transcriptome Data

2016

International audience; Technical variation plays an important role in microarray-based gene expression studies, and batch effects explain a large proportion of this noise. It is therefore mandatory to eliminate technical variation while maintaining biological variability. Several strategies have been proposed for the removal of batch effects, although they have not been evaluated in large-scale longitudinal gene expression data. In this study, we aimed at identifying a suitable method for batch effect removal in a large study of microarray-based longitudinal gene expression. Monocytic gene expression was measured in 1092 participants of the Gutenberg Health Study at baseline and 5-year fol…

Male0301 basic medicineMolecular biologyMicroarrayslcsh:MedicineGene ExpressionPolynomialsMonocytesMathematical and Statistical Techniques0302 clinical medicineLongitudinal StudiesProspective Studieslcsh:ScienceOligonucleotide Array Sequence AnalysisGeneticsPrincipal Component Analysis[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyMultidisciplinaryGenomicsReplicateMiddle AgedRegressionRNA isolationBioassays and Physiological Analysis030220 oncology & carcinogenesisPhysical SciencesPrincipal component analysisFemaleRNA hybridizationDNA microarrayTranscriptome AnalysisStatistics (Mathematics)Research ArticleAdultComputational biologyBiologyBiomolecular isolationGeneralized linear mixed model03 medical and health sciencesDeming regressionExtraction techniquesGeneticsHumansStatistical MethodsAgedQuantile normalizationMolecular probe techniquesGene Expression Profilinglcsh:RBiology and Life SciencesComputational BiologyGenome AnalysisProbe hybridizationRNA extractionResearch and analysis methodsGene expression profilingMolecular biology techniquesAlgebra030104 developmental biologyNonlinear DynamicsMultivariate Analysislcsh:QMathematics[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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A standardization of the Novelty-Suppressed Feeding Test protocol in rats

2017

Tests based on hyponeophagia phenomena are the most widely used to check the efficacy and efficiency of new-generation chronic antidepressant treatments. Even so, these tests lack strict consensus about their methodology, which reduces their validity, reproducibility and makes translatability difficult. Therefore, after an extensive literature review on this subject, we propose a methodological protocol for the Novelty-Suppressed Feeding Test to normalize this situation. Animals were induced to a reserpine-induced depression model and were then chronically treated with duloxetine, desvenlafaxine or vehicle. After a 14-day treatment, a standardized Novelty-Suppressed Feeding Test was perform…

Male0301 basic medicineNormalization (statistics)medicine.medical_specialtyReserpineStandardizationDuloxetine HydrochlorideDuloxetine HydrochlorideRats Sprague-Dawley03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhysical medicine and rehabilitationmedicineAnimalsDuloxetinePsychiatryProtocol (science)Depressive DisorderDepressionGeneral NeuroscienceNoveltyReproducibility of ResultsAntidepressive AgentsTest (assessment)DesvenlafaxineDisease Models Animal030104 developmental biologychemistryExploratory BehaviorPsychology030217 neurology & neurosurgerymedicine.drugNeuroscience Letters
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Differential models of twin correlations in skew for body-mass index (BMI)

2018

Background Body Mass Index (BMI), like most human phenotypes, is substantially heritable. However, BMI is not normally distributed; the skew appears to be structural, and increases as a function of age. Moreover, twin correlations for BMI commonly violate the assumptions of the most common variety of the classical twin model, with the MZ twin correlation greater than twice the DZ correlation. This study aimed to decompose twin correlations for BMI using more general skew-t distributions. Methods Same sex MZ and DZ twin pairs (N = 7,086) from the community-based Washington State Twin Registry were included. We used latent profile analysis (LPA) to decompose twin correlations for BMI into mul…

Male0301 basic medicinePhysiologyEntropyTwinsNormal Distributionlcsh:MedicineOverweight01 natural sciencesBody Mass IndexCorrelation010104 statistics & probabilityStatisticsTwins DizygoticMedicine and Health SciencesMixture distributionRegistrieslcsh:Science10. No inequalityMathematics2. Zero hungerMultidisciplinaryPhysicsMiddle AgedPhenotypePhysiological ParametersPhysical SciencesThermodynamicsFemalemedicine.symptomResearch ArticleStatistical DistributionsAdultMaterials by StructureMaterials ScienceSkewnessNormal distribution03 medical and health sciencesmedicineHumansObesity0101 mathematicsModels Geneticlcsh:RBody WeightBiology and Life SciencesTwins MonozygoticOverweightProbability TheoryProbability DistributionMixture modelTwin study030104 developmental biologySkewnessMixtureslcsh:QBody mass indexMathematicsDevelopmental BiologyPLOS ONE
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Inhibition of histone deacetylation rescues phenotype in a mouse model of Birk-Barel intellectual disability syndrome

2020

Mutations in the actively expressed, maternal allele of the imprinted KCNK9 gene cause Birk-Barel intellectual disability syndrome (BBIDS). Using a BBIDS mouse model, we identify here a partial rescue of the BBIDS-like behavioral and neuronal phenotypes mediated via residual expression from the paternal Kcnk9 (Kcnk9pat) allele. We further demonstrate that the second-generation HDAC inhibitor CI-994 induces enhanced expression from the paternally silenced Kcnk9 allele and leads to a full rescue of the behavioral phenotype suggesting CI-994 as a promising molecule for BBIDS therapy. Thus, these findings suggest a potential approach to improve cognitive dysfunction in a mouse model of an impri…

Male0301 basic medicinePotassium Channels[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyGeneral Physics and AstronomyDiseasePhenylenediamines[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyCraniofacial AbnormalitiesHistonesMice0302 clinical medicineIntellectual disabilityImprinting (psychology)lcsh:ScienceMice KnockoutGeneticsMultidisciplinaryBehavior AnimalbiologyNeurodevelopmental disordersDevelopmental disordersQBrainPhenotypeUp-RegulationPhenotypeHistoneGene Knockdown TechniquesBenzamidesMuscle HypotoniaFemaleLocus CoeruleusEpigeneticsScienceArticleGeneral Biochemistry Genetics and Molecular BiologyGenomic Imprinting03 medical and health sciencesDevelopmental disorders ; Neurodevelopmental disorders ; EpigeneticsIntellectual DisabilitymedicineAnimalsHumansddc:610AlleleGene[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyGeneral Chemistrymedicine.diseaseHistone Deacetylase InhibitorsMice Inbred C57BLDisease Models Animal030104 developmental biologyAcetylationMutationbiology.proteinlcsh:Q030217 neurology & neurosurgery
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