Search results for "ADULT"

showing 10 items of 17453 documents

CD19 Isoforms Enabling Resistance to CART-19 Immunotherapy Are Expressed in B-ALL Patients at Initial Diagnosis.

2017

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0301 basic medicineMaleCancer Researchmedicine.medical_treatmentT-LymphocytesEpitopes T-LymphocyteT-Cell Antigen Receptor SpecificityImmunotherapy AdoptiveEpitopeCohort StudiesExon0302 clinical medicineimmune system diseasesImmunology and AllergyMedicineProtein IsoformsChildAged 80 and overbiologyCD19CART-19B-ALLMiddle AgedPrecursor Cell Lymphoblastic Leukemia-Lymphomaepitope-lossmedicine.anatomical_structureTreatment Outcome030220 oncology & carcinogenesisChild PreschoolComputingMethodologies_DOCUMENTANDTEXTPROCESSINGFemaleClone (B-cell biology)Gene isoformAdultAdolescentRecombinant Fusion ProteinsImmunologyAntigens CD19Receptors Antigen T-CellCancer VaccinesCD1903 medical and health sciencesYoung AdultAntigenHumansAgedPharmacologybusiness.industryInfant NewbornisoformsInfantImmunotherapy030104 developmental biologyImmunologybiology.proteinClinical StudyTumor EscapeBone marrowbusinessJournal of immunotherapy (Hagerstown, Md. : 1997)
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Exome sequencing in congenital ataxia identifies two new candidate genes and highlights a pathophysiological link between some congenital ataxias and…

2019

To investigate the genetic basis of congenital ataxias (CAs), a unique group of cerebellar ataxias with a nonprogressive course, in 20 patients from consanguineous families, and to identify new CA genes. Singleton -exome sequencing on these 20 well-clinically characterized CA patients. We first checked for rare homozygous pathogenic variants, then, for variants from a list of genes known to be associated with CA or very early-onset ataxia, regardless of their mode of inheritance. Our replication cohort of 180 CA patients was used to validate the new CA genes. We identified a causal gene in 16/20 families: six known CA genes (7 patients); four genes previously implicated in another neurologi…

0301 basic medicineMaleCandidate geneAtaxiaAdolescentCerebellar AtaxiaGenotype[SDV]Life Sciences [q-bio]Consanguinity030105 genetics & heredityBiologyPathophysiologyCohort Studies03 medical and health sciencesGenetic HeterogeneityYoung AdultmedicineSTXBP1HumansExomeGenetic Predisposition to DiseaseChildGenetics (clinical)Exome sequencingGeneticsEarly infantile epileptic encephalopathies[SDV.GEN]Life Sciences [q-bio]/GeneticsBRAT1Genetic heterogeneityPhenotype3. Good health030104 developmental biologyPhenotype[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsChild PreschoolMutationCerebellar atrophyCongenital ataxiaAtaxiaFemaleFrancemedicine.symptomSpasms Infantileexome sequencing
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Transcriptome-Wide Analysis Identifies Novel Associations With Blood Pressure.

2017

Hypertension represents a major cardiovascular risk factor. The pathophysiology of increased blood pressure (BP) is not yet completely understood. Transcriptome profiling offers possibilities to uncover genetics effects on BP. Based on 2 populations including 2549 individuals, a meta-analyses of monocytic transcriptome-wide profiles were performed to identify transcripts associated with BP. Replication was performed in 2 independent studies of whole-blood transcriptome data including 1990 individuals. For identified candidate genes, a direct link between long-term changes in BP and gene expression over time and by treatment with BP-lowering therapy was assessed. The predictive value of pro…

0301 basic medicineMaleCandidate geneGene ExpressionGenome-wide association studyBlood Pressure030204 cardiovascular system & hematologyCardiorespiratory Medicine and HaematologyCardiovascularLMNATranscriptome0302 clinical medicineRisk FactorsCEBPAGene expression2.1 Biological and endogenous factorsAetiologyGeneticsMyelin and Lymphocyte-Associated Proteolipid ProteinsBlood Pressure ; Gene Expression ; Genome-wide Association Study ; Hypertension ; Transcriptomeblood pressureGenomicsSingle NucleotideLIM Domain Proteinsblood pressure; gene expression; genome-wide association study; hypertension; transcriptomeStrokeHeart DiseaseHypertensionPublic Health and Health ServicesBiomarker (medicine)FemaleEssential HypertensionPoly(ADP-ribose) PolymerasesBiotechnologyAdulthypertensionClinical SciencesNucleoside Transport ProteinsBiologyPolymorphism Single NucleotideArticle03 medical and health sciencesClinical ResearchInternal MedicineGeneticsHumansPolymorphismgenome-wide association studyGene Expression ProfilingHuman GenomeBlood Pressure DeterminationGene expression profiling030104 developmental biologyGood Health and Well BeingCardiovascular System & Hematologygene expressionCCAAT-Enhancer-Binding ProteinsCarrier ProteinstranscriptomeTranscription Factors
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Genome-wide association scan identifies new variants associated with a cognitive predictor of dyslexia

2019

Developmental dyslexia (DD) is one of the most prevalent learning disorders, with high impact on school and psychosocial development and high comorbidity with conditions like attention-deficit hyperactivity disorder (ADHD), depression, and anxiety. DD is characterized by deficits in different cognitive skills, including word reading, spelling, rapid naming, and phonology. To investigate the genetic basis of DD, we conducted a genome-wide association study (GWAS) of these skills within one of the largest studies available, including nine cohorts of reading-impaired and typically developing children of European ancestry (N = 2562–3468). We observed a genome-wide significant effect (p < 1 × 10…

0301 basic medicineMaleCandidate geneMultifactorial InheritanceImaging geneticsQH301 BiologyLANGUAGEGenome-wide association study3124 Neurology and psychiatryCANDIDATE GENESDyslexiaCohort StudiesREADING-DISABILITYMOLECULAR-GENETICS0302 clinical medicineCognitionAUTOMATIZED NAMING RANChildSUSCEPTIBILITY LOCUSRapid automatized namingR2CSHORT-TERM-MEMORY~DC~IMAGING-GENETICSRJ Pediatrics[SDV.NEU.SC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive SciencesPsychiatry and Mental healthDyslexia/geneticsAnxietyFemalemedicine.symptomBDCRC0321 Neuroscience. Biological psychiatry. NeuropsychiatryClinical psychologyNeuroinformaticsAdultReading disabilityAdolescentGenotypeRJPolymorphism Single NucleotideArticlelcsh:RC321-571ENVIRONMENTAL-INFLUENCES03 medical and health sciencesCellular and Molecular NeuroscienceQH301Young AdultmedicinedysleksiaHumansGenetic Predisposition to Diseaselcsh:Neurosciences. Biological psychiatry. NeuropsychiatryBiological Psychiatrygeenitbusiness.industryDyslexiaDASmedicine.diseaseComorbiditypredictors030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsRC0321DEVELOPMENTAL DYSLEXIAbusiness030217 neurology & neurosurgeryGenome-Wide Association Study
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Heterozygous deletion of the LRFN2 gene is associated with working memory deficits

2016

International audience; Learning disabilities (LDs) are a clinically and genetically heterogeneous group of diseases. Array-CGH and high-throughput sequencing have dramatically expanded the number of genes implicated in isolated intellectual disabilities and LDs, highlighting the implication of neuron-specific post-mitotic transcription factors and synaptic proteins as candidate genes. We report a unique family diagnosed with autosomal dominant learning disability and a 6p21 microdeletion segregating in three patients. The 870 kb microdeletion encompassed the brain-expressed gene LRFN2, which encodes for a synaptic cell adhesion molecule. Neuropsychological assessment identified selective w…

0301 basic medicineMaleCandidate genefamilyspeechHippocampal formationRats Sprague-Dawley0302 clinical medicineBorderline intellectual functioningNeuropsychological assessmentChilddisordersGenetics (clinical)Cells Culturedadhesion-like moleculesMembrane Glycoproteinsmedicine.diagnostic_testLearning DisabilitiesBrainMagnetic Resonance Imaging3. Good healthPedigreeMemory Short-TermBrain sizeFemaleAdultHeterozygotenmda receptorautismNerve Tissue ProteinsBiologyReceptors N-Methyl-D-AspartateArticle03 medical and health sciencesFluorodeoxyglucose F18[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyexpressionGeneticsmedicineAnimalsHumansMemory DisorderslanguageGenetic heterogeneityWorking memoryMembrane Proteinsdown-syndromeRats030104 developmental biologyEndophenotypePositron-Emission TomographySynapsesshort-termRadiopharmaceuticalsNeuroscience030217 neurology & neurosurgeryGene Deletion[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Cannabinoid receptor expression in non-small cell lung cancer. Effectiveness of tetrahydrocannabinol and cannabidiol inhibiting cell proliferation an…

2020

Background/Objective Patients with non-small cell lung cancer (NSCLC) develop resistance to antitumor agents by mechanisms that involve the epithelial-to-mesenchymal transition (EMT). This necessitates the development of new complementary drugs, e.g., cannabinoid receptors (CB1 and CB2) agonists including tetrahydrocannabinol (THC) and cannabidiol (CBD). The combined use of THC and CBD confers greater benefits, as CBD enhances the effects of THC and reduces its psychotropic activity. We assessed the relationship between the expression levels of CB1 and CB2 to the clinical features of a cohort of patients with NSCLC, and the effect of THC and CBD (individually and in combination) on prolifer…

0301 basic medicineMaleCannabinoid receptorLung NeoplasmsPulmonologymedicine.medical_treatmentGene ExpressionBiochemistryLung and Intrathoracic TumorsReceptor Cannabinoid CB20302 clinical medicineContractile ProteinsReceptor Cannabinoid CB1Epidermal growth factorCarcinoma Non-Small-Cell LungMedicine and Health SciencesCannabidiolDronabinolAged 80 and overMultidisciplinaryChemistryQRDrugsMiddle AgedCancer Cell MigrationCell MotilityOncologyCell Processes030220 oncology & carcinogenesisMedicinelipids (amino acids peptides and proteins)Femalemedicine.drugResearch ArticleAdultEpithelial-Mesenchymal TransitionScienceChronic Obstructive Pulmonary DiseaseCell Migration03 medical and health sciencesCell Line Tumormental disordersmedicineGeneticsHumansEpithelial–mesenchymal transitionTetrahydrocannabinolCell ProliferationAgedA549 cellPharmacologyCannabinoid Receptor AgonistsPsychotropic DrugsCell growthCannabinoidsorganic chemicalsCancers and NeoplasmsBiology and Life SciencesProteinsCell Biologydigestive system diseasesActinsrespiratory tract diseasesNon-Small Cell Lung CancerCytoskeletal Proteins030104 developmental biologyA549 CellsCancer researchCannabinoidCannabidiolDevelopmental BiologyPLoS ONE
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CD16+ Macrophages Mediate Fibrosis in Inflammatory Bowel Disease.

2017

Background and Aims Fibrosis is a common complication of Crohn's disease [CD], and is related to dysregulated tissular repair following inflammation, in which macrophages play a central role. We have previously observed that STAT6-/- mice present delayed mucosal recovery after 2,4,6-trinitrobenzenesulfonic acid [TNBS]-induced colitis due to a deficiency in reparatory interleukin-4 [IL4]/STAT6-dependent M2 macrophages, which can be reverted by the exogenous transfer of this cell type. In the present study, we analyse the role of STAT6-dependent macrophages in intestinal fibrosis. Methods Colitis was induced by weekly intra-rectal administration of TNBS [6 weeks] to STAT6-/- mice and wild-typ…

0301 basic medicineMaleCell CountInflammatory bowel diseaseMiceCrohn DiseaseFibrosisMacrophageIntestinal MucosaCells CulturedMice Knockouteducation.field_of_studyMice Inbred BALB Cintegumentary systemGastroenterologyGeneral MedicineColitisColonic NeoplasmsFemalemedicine.symptomMannose ReceptorAdultAdolescentColonPopulationInflammationReceptors Cell SurfaceCD1603 medical and health sciencesYoung AdultProto-Oncogene Proteinsparasitic diseasesmedicineAnimalsHumansLectins C-TypeColitiseducationInterleukin 4business.industryMacrophagesReceptors IgGmedicine.diseaseFibrosisWnt Proteins030104 developmental biologyMannose-Binding LectinsTrinitrobenzenesulfonic AcidImmunologyInterleukin-4businessSTAT6 Transcription FactorJournal of Crohn'scolitis
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Intranasal Administration of Extracellular Vesicles Derived from Human Teeth Stem Cells Improves Motor Symptoms and Normalizes Tyrosine Hydroxylase E…

2018

Abstract Parkinson's disease (PD) is the second most common neurodegenerative disorder affecting millions of people worldwide. At present, there is no effective cure for PD; treatments are symptomatic and do not halt progression of neurodegeneration. Extracellular vesicles (EVs) can cross the blood–brain barrier and represent promising alternative to the classical treatment strategies. In the present study, we examined therapeutic effects of intranasal administration of EVs derived from human exfoliated deciduous teeth stem cells (SHEDs) on unilateral 6-hydroxydopamine (6-OHDA) medial forebrain bundle (MFB) rat model of PD. CatWalk gait tests revealed that EVs effectively suppressed 6-OHDA-…

0301 basic medicineMaleCell signalingParkinson's diseaseParkinson's diseaseStriatumPharmacology0302 clinical medicineMedicineMedial forebrain bundleAdult stem cellsStem CellsNeurodegenerationParkinson DiseaseGeneral MedicineAnimal modelsSubstantia NigraDifferentiationmedicine.symptom:MEDICINE::Physiology and pharmacology::Pharmacological research [Research Subject Categories]Tyrosine 3-MonooxygenaseCellular therapySubstantia nigraLesion03 medical and health sciencesExtracellular VesiclesMicroscopy Electron TransmissionTissue Engineering and Regenerative MedicineAnimalsHumansRats WistarOxidopamineAdministration IntranasalAgedHydroxydopamineTyrosine hydroxylasebusiness.industryCell Biologymedicine.diseaseCorpus StriatumRatsDisease Models Animal030104 developmental biologynervous systemMesenchymal stem cellsbusinessTooth030217 neurology & neurosurgeryDevelopmental BiologyStem cells translational medicine
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Regulation of PDE5 expression in human aorta and thoracic aortic aneurysms

2019

AbstractAneurysms and dissections affecting thoracic aorta are associated with smooth muscle cell (SMC) dysfunction. NO/cGMP signaling pathway in smooth muscle cells has been shown to be affected in sporadic thoracic aortic aneurysms. We analyzed the mRNA levels of PDE5, a cGMP-hydrolyzing enzyme highly expressed in aortic SMCs, that regulates arterious vascular tone by lowering cGMP levels. We found that aortic tissue obtained from Marfan, tricuspid and bicuspid thoracic aneurysms expressed lower levels of PDE5 mRNA compared to control aortas. In particular, we found that affected aortas showed lower levels of all the PDE5A isoforms, compared to control aortas. Transfection of vascular SMC…

0301 basic medicineMaleCelllcsh:MedicineStimulationMuscle Smooth VascularAortic aneurysmchemistry.chemical_compound0302 clinical medicinePDE5 expression human aorta and thoracic aortic aneurysmsMyocyteThoracic aortalcsh:ScienceSettore BIO/16MultidisciplinaryTransfectionMiddle AgedIsoenzymesmedicine.anatomical_structurecardiovascular systemFemaleGene isoformAdultmedicine.medical_specialtyMyocytes Smooth MuscleArticleGene Expression Regulation EnzymologicNitric oxide03 medical and health sciencesmedicine.arteryInternal medicinemedicineHumansSettore MED/05 - Patologia ClinicaAgedCyclic Nucleotide Phosphodiesterases Type 5Aortic Aneurysm Thoracicbusiness.industrylcsh:Rmedicine.disease030104 developmental biologyEndocrinologychemistryRisk factorsthoracic aortic aneurysmslcsh:QAngiogenesisPDE5business030217 neurology & neurosurgery
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Bi-allelic JAM2 Variants Lead to Early-Onset Recessive Primary Familial Brain Calcification

2020

International audience; Primary familial brain calcification (PFBC) is a rare neurodegenerative disorder characterized by a combination of neurological, psychiatric, and cognitive decline associated with calcium deposition on brain imaging. To date, mutations in five genes have been linked to PFBC. However, more than 50% of individuals affected by PFBC have no molecular diagnosis. We report four unrelated families presenting with initial learning difficulties and seizures and later psychiatric symptoms, cerebellar ataxia, extrapyramidal signs, and extensive calcifications on brain imaging. Through a combination of homozygosity mapping and exome sequencing, we mapped this phenotype to chromo…

0301 basic medicineMaleCerebellumPathology[SDV]Life Sciences [q-bio]recessive brain calcificationMice0302 clinical medicineCognitive declineAge of OnsetChildGenetics (clinical)Exome sequencingComputingMilieux_MISCELLANEOUSBrain Diseasesprimary familial brain calcificationMalalties neurodegenerativesBrainFahr diseaseCalcinosisOCLNNeurodegenerative DiseasesHuman brainMiddle AgedPedigree[SDV] Life Sciences [q-bio]medicine.anatomical_structureKnockout mouseFemalemedicine.symptomAdultmedicine.medical_specialtyAdolescentGenes RecessiveNeuropathologyBiologyCalcificacióCalcification03 medical and health sciencesBasal Ganglia DiseasesReportGeneticsmedicineAnimalsHumansAllelesSLC20A2Cerebellar ataxiaknock out mouse modelmedicine.diseaseJAM2030104 developmental biologyFahr disease; familial idiopathic basal ganglia calcification; JAM2; JAM3; knock out mouse model; MYORG; OCLN; primary familial brain calcification; recessive brain calcification; SLC20A2familial idiopathic basal ganglia calcificationJAM3MYORGXenotropic and Polytropic Retrovirus ReceptorCell Adhesion Molecules030217 neurology & neurosurgeryCalcification
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