Search results for "Mesh"

showing 10 items of 885 documents

A Novel Role for CSRP1 in a Lebanese Family with Congenital Cardiac Defects

2017

Despite an obvious role for consanguinity in congenital heart disease (CHD), most studies fail to document a monogenic model of inheritance except for few cases. We hereby describe a first-degree cousins consanguineous Lebanese family with 7 conceived children: 2 died in utero of unknown causes, 3 have CHD, and 4 have polydactyly. The aim of the study is to unveil the genetic variant(s) causing these phenotypes using next generation sequencing (NGS) technology. Targeted exome sequencing identified a heterozygous duplication in CSRP1 which leads to a potential frameshift mutation at position 154 of the protein. This mutation is inherited from the father, and segregates only with the CHD phen…

0301 basic medicineGeneticsPolydactylylcsh:QH426-470ConsanguinityBiologypolydactylymedicine.diseasecongenital heart diseaseFrameshift mutation03 medical and health scienceslcsh:Genetics030104 developmental biologyTRPS1Gene duplicationMutation (genetic algorithm)medicineGeneticsMolecular MedicineMissense mutationExomeGenetics (clinical)Exome sequencingOriginal ResearchCSRP1Frontiers in Genetics
researchProduct

Disentangling the effect of host genetics and gut microbiota on resistance to an intestinal parasite

2019

11 pages; International audience; Resistance to infection is a multifactorial trait, and recent work has suggested that the gut microbiota can also contribute to resistance. Here, we performed a fecal microbiota transplant to disentangle the contribution of the gut microbiota and host genetics as drivers of resistance to the intestinal nematode Heligmosomoides polygyrus. We transplanted the microbiota of a strain of mice (SJL), resistant to H. polygyrus, into a susceptible strain (CBA) and vice-versa. We predicted that if the microbiota shapes resistance to H. polygyrus, the FMT should reverse the pattern of resistance between the two host strains. The two host strains had different microbi…

0301 basic medicineHeligmosomoides polygyrusGut floramedicine.disease_causeFecal microbiota transplant0302 clinical medicinefluids and secretionsMESH: Fecal Microbiota TransplantationParasite hostingColonizationMESH: AnimalsMESH: Strongylida InfectionsDisease ResistanceGeneticsNematospiroides dubiusbiology[SDV.BA]Life Sciences [q-bio]/Animal biologyFecal Microbiota Transplantation3. Good healthInfectious DiseasesMESH: Nematospiroides dubiusGenetic Background030231 tropical medicineIntestinal parasiteHeterologousMice Inbred StrainsMESH: Disease ResistanceMESH: Host-Parasite InteractionsMESH: Mice Inbred Strainsdigestive systemMESH: Gastrointestinal MicrobiomeHost-Parasite Interactions03 medical and health sciencesImmunityparasitic diseasesmedicineAnimals[SDV.MP.PAR]Life Sciences [q-bio]/Microbiology and Parasitology/ParasitologyStrongylida InfectionsHost (biology)ImmunityLife history traitsMESH: Genetic Backgroundbiology.organism_classificationGastrointestinal MicrobiomeDisease Models Animalstomatognathic diseases030104 developmental biologyParasitologyHeligmosomoides polygyrusMESH: Disease Models Animal[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
researchProduct

Wiedemann-Steiner syndrome as a major cause of syndromic intellectual disability: A study of 33 French cases.

2018

International audience; Wiedemann-Steiner syndrome (WSS) is a rare syndromic condition in which intellectual disability (ID) is associated with hypertrichosis cubiti, short stature, and characteristic facies. Following the identification of the causative gene (KMT2A) in 2012, only 31 cases of WSS have been described precisely in the literature. We report on 33 French individuals with a KMT2A mutation confirmed by targeted gene sequencing, high-throughput sequencing or exome sequencing. Patients' molecular and clinical features were recorded and compared with the literature data. On the molecular level, we found 29 novel mutations. We observed autosomal dominant transmission of WSS in 3 fami…

0301 basic medicineHypertrichosisMalePediatrics[SDV]Life Sciences [q-bio]MESH: Magnetic Resonance ImagingPathognomonicMESH: ChildIntellectual disabilityMESH: SyndromeChildMESH: High-Throughput Nucleotide SequencingGenetics (clinical)Exome sequencingComputingMilieux_MISCELLANEOUSbiologyWiedemann-Steiner syndromeHigh-Throughput Nucleotide SequencingSyndromeKMT2AMESH: Amino Acid SubstitutionMagnetic Resonance Imaginghypertrichosis3. Good healthhairinessKMT2APhenotypeWiedemann-Steiner syndromeChild Preschoolcardiovascular systemFemaleDisease SusceptibilityFrancemedicine.symptomMESH: Tomography X-Ray ComputedMyeloid-Lymphoid Leukemia Proteinmedicine.medical_specialtyMESH: MutationAdolescentMESH: Disease SusceptibilityMESH: PhenotypeShort statureMESH: Intellectual Disability03 medical and health sciencesHypertrichosis cubitiIntellectual DisabilityGeneticsmedicineHumanshistone methylationMESH: Adolescent[SDV.GEN]Life Sciences [q-bio]/GeneticsMESH: Humansbusiness.industryMESH: Child PreschoolMESH: Histone-Lysine N-MethyltransferaseHistone-Lysine N-Methyltransferasemedicine.diseaseMESH: MaleMESH: France030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAmino Acid SubstitutionMESH: Myeloid-Lymphoid Leukemia ProteinMutationbiology.proteinbusinessTomography X-Ray ComputedMESH: FemaleClinical genetics
researchProduct

AMPK phosphorylation modulates pain by activation of NLRP3 inflammasome

2016

et al.

0301 basic medicineMESH : Carrier Proteins/geneticsMaleMESH: Fibromyalgia/geneticsFibromyalgiaIndolesPhysiologyInflammasomesClinical BiochemistryInterleukin-1betaInjuryAMP-Activated Protein KinasesNeuropathic painBiochemistryPyrin domainMice0302 clinical medicineAMP-activated protein kinaseRestrictionSunitinibDiseasePhosphorylationGeneral Environmental Sciencebiologyintegumentary systemChemistryInterleukin-18InflammasomePain Perception[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismMiddle AgedMetforminCell biologyOriginal Research CommunicationsMESH : Fibromyalgia/geneticsHyperalgesiaPhosphorylationFemalemedicine.symptommedicine.drugMESH : Inflammasomes/metabolismAdultmedicine.medical_specialtyPain03 medical and health sciencesMESH: Carrier Proteins/geneticsInternal medicineNLR Family Pyrin Domain-Containing 3 ProteinmedicineAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyPyrrolesProtein kinase AMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Inflammasomes/metabolismFibromialgia patientsAMPK ; fibromyalgia ; NLRP3 InflammasomeDangerAMPKCell BiologyAdenosineMESH: AMP-Activated Protein Kinases/genetics030104 developmental biologyEndocrinologyMetabolismProtein-Kinase AMPKbiology.proteinGeneral Earth and Planetary SciencesMESH : AMP-Activated Protein Kinases/geneticsAnalgesiaCarrier Proteins030217 neurology & neurosurgery
researchProduct

Trends of extended-spectrum β-lactamase-producing Escherichia coli sequence type 131 and its H30 subclone in a French hospital over a 15-year period.

2016

International audience; Sequence type 131 (ST131) is a predominant lineage among extraintestinal pathogenic Escherichia coli. It plays a major role in the worldwide dissemination of E. coli producing extended-spectrum β-lactamases (ESBLs). Here we describe the long-term epidemiology of this clonal group in a French university hospital, where the incidence of ESBL-producing E. coli has increased from 0.018 case per 1000 patient-days in the year 2000 to 0.50 case per 1000 patient-days in 2014. The first of the 141 ST131 isolates was recovered in 2006, and the ST131 clonal group accounted for 18.1% of total ESBL-producing E. coli over the whole period (2000-2014). Subclonal typing showed that …

0301 basic medicineMESH : Escherichia coliMESH : Retrospective StudiesMESH : Multilocus Sequence TypingMESH: beta-LactamasesMESH : GenotypeMultidrug resistancemedicine.disease_causeHospitals UniversityMESH: Genotype[ SDV.MP ] Life Sciences [q-bio]/Microbiology and ParasitologyPharmacology (medical)MESH: IncidenceMESH: Genetic VariationEscherichia coli InfectionsComputingMilieux_MISCELLANEOUSCross InfectionMolecular EpidemiologyExtraintestinal Pathogenic Escherichia coliMESH: Escherichia coliIncidenceIncidence (epidemiology)MESH : beta-LactamasesGeneral MedicinePFGEMESH : IncidenceElectrophoresis Gel Pulsed-Field3. Good healthInfectious DiseasesMESH: Electrophoresis Gel Pulsed-FieldMESH: Multilocus Sequence Typing[SDV.MP]Life Sciences [q-bio]/Microbiology and ParasitologyMESH : Escherichia coli Infections[SDE]Environmental SciencesFranceMESH : Cross InfectionMicrobiology (medical)clone (Java method)Lineage (genetic)GenotypeMESH : Molecular Epidemiology030106 microbiologyBiologybeta-LactamasesMicrobiology03 medical and health sciencesExtended-spectrum β-lactamaseMESH : Genetic VariationEscherichia coliPulsed-field gel electrophoresismedicineHumansMESH: Molecular EpidemiologyTypingMESH : FranceEscherichia coliMESH : Hospitals UniversityRetrospective StudiesMESH : Electrophoresis Gel Pulsed-FieldMESH: Escherichia coli InfectionsMESH: Hospitals UniversityMESH: HumansMESH : HumansGenetic VariationMESH: Cross InfectionMESH: Retrospective Studiesbacterial infections and mycosesMultiple drug resistanceMESH: FranceESBLMultilocus Sequence Typing
researchProduct

De novo mutations in the X-linked TFE3 gene cause intellectual disability with pigmentary mosaicism and storage disorder-like features

2020

IntroductionPigmentary mosaicism (PM) manifests by pigmentation anomalies along Blaschko’s lines and represents a clue toward the molecular diagnosis of syndromic intellectual disability (ID). Together with new insights on the role for lysosomal signalling in embryonic stem cell differentiation, mutations in the X-linked transcription factor 3 (TFE3) have recently been reported in five patients. Functional analysis suggested these mutations to result in ectopic nuclear gain of functions.Materials and methodsSubsequent data sharing allowed the clustering of de novo TFE3 variants identified by exome sequencing on DNA extracted from leucocytes in patients referred for syndromic ID with or with…

0301 basic medicineMESH: Basic Helix-Loop-Helix Leucine Zipper Transcription Factors[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyIntellectual disabilityTFE3Biology[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsMESH: Intellectual Disability03 medical and health sciencesExon0302 clinical medicineMESH: Whole Exome SequencingMESH: ChildIntellectual disabilityGeneticsmedicineMissense mutationGeneGenetics (clinical)Exome sequencingPigmentary mosaicismMESH: Pathology MolecularGeneticsMESH: AdolescentMESH: HumansAlternative splicingLysosomal metabolismMESH: Child Preschool[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyMESH: Adultmedicine.diseasePhenotypeMESH: InfantMESH: MaleTFE3Storage disorder030104 developmental biologyMESH: Genes X-Linked[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMESH: Young AdultMESH: EpilepsyMESH: MosaicismMESH: Pigmentation DisordersMESH: Female030217 neurology & neurosurgery
researchProduct

Peroxisome proliferator-activated receptor alpha deficiency impairs regulatory T cell functions: Possible application in the inhibition of melanoma t…

2016

International audience; Regulatory T (Treg) cells are important to induce and maintain immunological self-tolerance. Although the progress accomplished in understanding the functional mechanism of Treg cells, intracellular molecules that control the mechanisms of their suppressive capacity are still on investigation. The present study showed that peroxisome proliferator-activated receptor-alpha deficiency impaired the suppressive activity of Treg cells on CD4(+)CD25(-) and CD8(+) T cell proliferation. In Treg cells, PPARα gene deletion also induced a decrease of migratory abilities, and downregulated the expression of chemokine receptors (CCR-4, CCR-8 and CXCR-4) and p27(KIP1) mRNA. Treg ce…

0301 basic medicineMaleAdoptive cell transferMESH: Tumor BurdenB16 melanoma tumorMelanoma ExperimentalMESH: T-Lymphocyte SubsetsCD4(+)CD25(+) regulatory T cellsBiochemistryMESH: Mice KnockoutImmunotherapy AdoptiveT-Lymphocytes RegulatoryPPARαMESH : T-Lymphocytes RegulatoryCell MovementT-Lymphocyte SubsetsMESH: Reverse Transcriptase Polymerase Chain ReactionMESH : Cell ProliferationMESH : Cell MovementMESH: AnimalsIL-2 receptorMESH: PPAR alphaMESH: Cell MovementCells CulturedMice KnockoutMESH : Melanoma ExperimentalbiologyMESH : Tumor BurdenReverse Transcriptase Polymerase Chain ReactionMESH : Reverse Transcriptase Polymerase Chain ReactionFOXP3hemic and immune systemsGeneral MedicineMESH: Gene Expression Regulation Neoplastic3. Good healthTumor BurdenMESH: Melanoma ExperimentalDNA-Binding ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureMESH: Immunotherapy AdoptiveReceptors ChemokineMESH : DNA-Binding ProteinsMESH: Cells Culturedmedicine.medical_specialtyMESH : Receptors ChemokineMESH: Cell Line TumorRegulatory T cellMESH : Gene Expression Regulation NeoplasticT cellMESH : MaleMESH : PPAR alphachemical and pharmacologic phenomenaMESH : Mice Inbred C57BLMESH : Clonal Anergy03 medical and health sciencesMESH: Mice Inbred C57BLInternal medicineMESH: Cell ProliferationCell Line TumorMESH : Cells CulturedmedicineAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyPPAR alpha[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCell ProliferationClonal AnergyPerforinMESH : Cell Line TumorMESH: T-Lymphocytes RegulatoryMolecular biologyMESH: MaleMESH : T-Lymphocyte SubsetsGranzyme BMice Inbred C57BL030104 developmental biologyEndocrinologyPerforinMESH: Clonal Anergybiology.proteinMESH : Mice KnockoutMESH : AnimalsMESH: Receptors ChemokineCD8MESH: DNA-Binding ProteinsMESH : Immunotherapy Adoptive
researchProduct

Shared DNA methylation signatures in childhood allergy: The MeDALL study

2021

Contains fulltext : 232514.pdf (Publisher’s version ) (Open Access) BACKGROUND: Differential DNA methylation associated with allergy might provide novel insights into the shared or unique etiology of asthma, rhinitis, and eczema. OBJECTIVE: We sought to identify DNA methylation profiles associated with childhood allergy. METHODS: Within the European Mechanisms of the Development of Allergy (MeDALL) consortium, we performed an epigenome-wide association study of whole blood DNA methylation by using a cross-sectional design. Allergy was defined as having symptoms from at least 1 allergic disease (asthma, rhinitis, or eczema) and positive serum-specific IgE to common aeroallergens. The discove…

0301 basic medicineMaleAllergyMESH: Asthmalnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]EczemaImmunoglobulin EEpigenesis GeneticCohort Studies0302 clinical medicineMESH: DNA MethylationMESH: ChildImmunology and AllergyMedicineMESH: Epigenesis GeneticChildMESH: CpG IslandsMESH: Cohort StudiesDNA methylationbiologyMESH: Immunoglobulin EEpigeneticMethylation3. Good healthCpG site030220 oncology & carcinogenesisChild PreschoolDNA methylationMESH: Rhinitis AllergicFemaleEpigeneticsIgEAdolescentMESH: HypersensitivityImmunologyeducationSingle-nucleotide polymorphismArticle03 medical and health sciencesMESH: Cross-Sectional StudieschildrenHypersensitivityHumansEpigeneticsAsthmaMESH: AdolescentMESH: Humansbusiness.industryMESH: TranscriptomeMESH: Child PreschoolImmunoglobulin Emedicine.diseaseallergyRhinitis AllergicAsthmaMESH: Male030104 developmental biologyCross-Sectional StudiesMESH: Eczema3121 General medicine internal medicine and other clinical medicineImmunologybiology.proteinCpG IslandsbusinessTranscriptomeMESH: Female[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
researchProduct

Exome-wide somatic mutation characterization of small bowel adenocarcinoma

2018

Small bowel adenocarcinoma (SBA) is an aggressive disease with limited treatment options. Despite previous studies, its molecular genetic background has remained somewhat elusive. To comprehensively characterize the mutational landscape of this tumor type, and to identify possible targets of treatment, we conducted the first large exome sequencing study on a population-based set of SBA samples from all three small bowel segments. Archival tissue from 106 primary tumors with appropriate clinical information were available for exome sequencing from a patient series consisting of a majority of confirmed SBA cases diagnosed in Finland between the years 2003–2011. Paired-end exome sequencing was…

0301 basic medicineMaleCancer ResearchMICROSATELLITE INSTABILITYColorectal canceroncogenesReceptor ErbB-2medicine.disease_causeCOLORECTAL-CANCERACTIVATIONCohort Studies0302 clinical medicineAnimal CellsAdenocarcinomasMedicine and Health SciencesExomeFrameshift MutationExomeGenetics (clinical)Exome sequencingAged 80 and overSMALL-INTESTINEeducation.field_of_study1184 Genetics developmental biology physiologyCELIAC-DISEASENonsense MutationMiddle Aged3. Good healthsyöpägeenitOncology030220 oncology & carcinogenesissyöpätauditFemaleSIGNALING PATHWAYKRASCellular TypesResearch ArticleAdultProto-Oncogene Proteins B-raflcsh:QH426-470SEQUENCING DATAImmune CellsNonsense mutationPopulationImmunologyAntigen-Presenting CellsComputational biologysuolistosyövätBiologyAdenocarcinomata3111CarcinomasFrameshift mutation03 medical and health sciencesGermline mutationQUALITY-CONTROLGenetiikka kehitysbiologia fysiologia - Genetics developmental biology physiologySyöpätaudit - CancersIntestinal NeoplasmsmedicineGeneticsPoint MutationHumanseducationMolecular BiologyEcology Evolution Behavior and SystematicsAgedColorectal CancerBiology and Life SciencesCancers and Neoplasmscancerous diseasesCell Biologymedicine.diseaseta3122mutationsCOMPREHENSIVE MOLECULAR CHARACTERIZATIONlcsh:Genetics030104 developmental biologyMutationSomatic Mutationbowel cancer3111 BiomedicinemutaatiotHIGH-RESOLUTIONPLoS Genetics
researchProduct

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
researchProduct