Search results for "spectrum [cosmic radiation]"

showing 10 items of 636 documents

Circulating exosomes deliver free fatty acids from the bloodstream to cardiac cells: Possible role of CD36

2019

Regulation of circulating free fatty acid (FFA) levels and delivery is crucial to maintain tissue homeostasis. Exosomes are nanomembranous vesicles that are released from diverse cell types and mediate intercellular communication by delivering bioactive molecules. Here, we sought to investigate the uptake of FFAs by circulating exosomes, the delivery of FFA-loaded exosomes to cardiac cells and the possible role of the FFA transporter CD36 in these processes. Circulating exosomes were purified from the serum of healthy donors after an overnight fast (F) or 20 minutes after a high caloric breakfast (postprandial, PP). Western blotting, Immunogold Electron Microscopy and FACS analysis of circu…

0301 basic medicineCD36 AntigensMaleLuminescenceCD36Mice SCIDFatty Acids NonesterifiedExosomesBiochemistryFatsMiceSpectrum Analysis TechniquesAnimal CellsMice Inbred NODMedicine and Health SciencesMyocytes CardiacTissue homeostasischemistry.chemical_classificationCardiomyocytesMultidisciplinarybiologymedicine.diagnostic_testPhysicsElectromagnetic RadiationQFatty AcidsRHeartFlow CytometryLipidsCell biologyBlotSpectrophotometryPhysical SciencesMedicinelipids (amino acids peptides and proteins)FemaleCytophotometryCellular Structures and OrganellesAnatomyCellular TypesResearch ArticleAdultScienceMuscle TissueResearch and Analysis MethodsFluorescenceFlow cytometryCell Line03 medical and health sciencesIn vivomedicineDiabetes MellitusAnimalsHumansVesiclesObesityRats WistarMuscle Cells030102 biochemistry & molecular biologyFatty acidBiology and Life SciencesCell BiologyAtherosclerosisMicrovesiclesDisease Models Animal030104 developmental biologyBiological Tissuechemistrybiology.proteinCardiovascular AnatomyEx vivoPLoS ONE
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Prediabetes is associated with the modulation of antigen-specific Th1/Tc1 and Th17/Tc17 responses in latent Mycobacterium tuberculosis infection.

2017

Type 2 diabetes mellitus (DM) is associated with the down modulation of Th1, Th2 and Th17 responses in latent Mycobacterium tuberculosis infection but the role of prediabetes (PDM) in this setting is not well understood. To examine the role of CD4+ and CD8+ T cell cytokines in latent tuberculosis (LTB) with coincident PDM, we studied the baseline, mycobacterial, control antigen and mitogen-stimulated T cell cytokine responses in LTB individuals with (LTB-PDM; n = 20) or without (LTB-NDM; n = 20) concomitant prediabetes. LTB-PDM is characterized by diminished frequencies of mono-and dual-functional CD4+ Th1 and Th17 cells and mono-functional Th2 cells at baseline and/or following mycobacteri…

0301 basic medicineCD4-Positive T-LymphocytesMaleBacterial DiseasesPhysiologymedicine.medical_treatmentlcsh:MedicineCD8-Positive T-LymphocytesWhite Blood Cells0302 clinical medicineSpectrum Analysis TechniquesEndocrinologyAnimal CellsImmune PhysiologyMedicine and Health SciencesMedicinePrediabeteslcsh:ScienceInnate Immune SystemMultidisciplinarybiologyLatent tuberculosisT CellsMiddle AgedFlow Cytometry3. Good healthActinobacteriaCytokinemedicine.anatomical_structureInfectious DiseasesSpectrophotometryCytokinesFemaleCytophotometryCellular TypesResearch ArticleAdultEndocrine DisordersT cellImmune CellsImmunologyCytotoxic T cellsResearch and Analysis MethodsMycobacterium tuberculosisPrediabetic State03 medical and health sciencesImmune systemTh2 CellsAntigenLatent TuberculosisDiabetes MellitusHumansTuberculosisT Helper CellsAgedAntigens BacterialBlood CellsBacteriabusiness.industrylcsh:ROrganismsBiology and Life SciencesMycobacterium tuberculosisCell BiologyTh1 CellsMolecular Developmentmedicine.diseasebiology.organism_classificationTropical Diseases030104 developmental biologyCase-Control StudiesImmune SystemMetabolic DisordersImmunologyTh17 Cellslcsh:QbusinessCD8030215 immunologyDevelopmental BiologyPloS one
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RBFOX1, encoding a splicing regulator, is a candidate gene for aggressive behavior

2020

The RBFOX1 gene (or A2BP1) encodes a splicing factor important for neuronal development that has been related to autism spectrum disorder and other neurodevelopmental phenotypes. Evidence from complementary sources suggests that this gene contributes to aggressive behavior. Suggestive associations with RBFOX1 have been identified in genome-wide association studies (GWAS) of anger, conduct disorder, and aggressive behavior. Nominal association signals in RBFOX1 were also found in an epigenome-wide association study (EWAS) of aggressive behavior. Also, variants in this gene affect temporal lobe volume, a brain area that is altered in several aggression-related phenotypes. In animals, this gen…

0301 basic medicineCandidate geneNeuroimagingRBFOX1Genome-wide association studyBiologyEpigenesis GeneticA2BP103 medical and health sciencesAll institutes and research themes of the Radboud University Medical Center0302 clinical medicineGeneticsmedicineAnimalsHumansPharmacology (medical)TranscriptomicsRBFOX1Genetic Association StudiesBiological PsychiatryRegulator genePharmacologyGeneticsNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]AggressionGenetic Variationmedicine.diseasePhenotypeAnimal modelsAggressionPsychiatry and Mental health030104 developmental biologyNeurologyAutism spectrum disorderEpigeneticsRBFOX1 GeneRNA Splicing FactorsNeurology (clinical)medicine.symptom030217 neurology & neurosurgeryGenome-Wide Association Study
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Alterations in Tau Protein Level and Phosphorylation State in the Brain of the Autistic-Like Rats Induced by Prenatal Exposure to Valproic Acid

2021

Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by deficient social interaction and communication besides repetitive, stereotyped behaviours. A characteristic feature of ASD is altered dendritic spine density and morphology associated with synaptic plasticity disturbances. Since microtubules (MTs) regulate dendritic spine morphology and play an important role in spine development and plasticity the aim of the present study was to investigate the alterations in the content of neuronal α/β-tubulin and Tau protein level as well as phosphorylation state in the valproic acid (VPA)-induced rat model of autism. Our results indicated that maternal exposure to VPA indu…

0301 basic medicineDendritic spineHippocampuslcsh:Chemistry0302 clinical medicinePregnancyTubulinPhosphorylationlcsh:QH301-705.5SpectroscopyValproic AcidbiologyERK1/2Chemistryautism spectrum disorders (ASD)valproic acid (VPA)BrainGeneral MedicineImmunohistochemistryComputer Science Applicationsmedicine.anatomical_structureCerebral cortexMaternal ExposurePrenatal Exposure Delayed EffectsFemaleDisease Susceptibilitymedicine.drugSignal Transductionmedicine.medical_specialtyCDK5Tau proteintau ProteinsCatalysisArticleInorganic Chemistry03 medical and health sciencesInternal medicinemental disordersmedicineAnimalsPhysical and Theoretical ChemistryAutistic DisorderMolecular BiologyCyclin-dependent kinase 5GSK-3βValproic AcidOrganic Chemistryα/β-tubulinRatsEnzyme Activation030104 developmental biologyEndocrinologylcsh:Biology (General)lcsh:QD1-999MAP-TauChromatolysisSynaptic plasticitybiology.proteinAkt/mTOR signalling030217 neurology & neurosurgeryBiomarkersInternational Journal of Molecular Sciences
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Autism spectrum disorders in children affected by Duchenne muscular dystrophy

2018

Background Duchenne muscular dystrophy (DMD) is the most frequent and severe form of the dystrophinopathies. The literature shows that about 30-40% of DMD subjects have intellectual disability. In males with Duchenne muscular dystrophy, neuropsychiatric disorders have also been observed: attention deficit disorder and hyperactivity, autism spectrum disorders, and obsessive-compulsive disorder. Duchenne muscular dystrophy is not just a muscle disorder, but also a disease that affects the brain. The aim of the present study was to describe a case series of children with Duchenne muscular dystrophy that have also the presence of autism spectrum disorders (ASDs). They have been assessed by mean…

0301 basic medicineDuchenne muscular dystrophyMalemedicine.medical_specialtyAutism Spectrum DisorderDuchenne muscular dystrophyMuscle disorderAudiologyAutism Diagnostic Observation Schedule03 medical and health sciences0302 clinical medicineIntellectual Disabilitymental disordersIntellectual disabilitymedicineHumansMuscular dystrophyChildbusiness.industryWechsler Adult Intelligence Scalemedicine.diseaseSettore MED/39 - Neuropsichiatria InfantileMuscular Dystrophy Duchenne030104 developmental biologyPediatrics Perinatology and Child HealthChildhood Autism Rating ScaleAutismAustism Spectrum Disorderbusiness030217 neurology & neurosurgeryHuman
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Autism is a prenatal disorder: Evidence from late gestation brain overgrowth

2018

This retrospective study aimed to specify the critical period for atypical brain development in individuals with autism spectrum disorder (ASD) using prenatal and postnatal head growth parameters. The sample consisted of 80 Caucasian, unrelated, idiopathic patients with ASD born after 1995. Fetal ultrasound parameters (head circumference [HC], abdominal circumference, and femur length) were obtained during the second and third trimesters of gestation. HC at birth and postnatal parameters at 12 and 24 months of age were also collected. Head overgrowth, assessed by HC, was highlighted during the second (20-26 weeks of amenorrhea) and third (28-36 weeks of amenorrhea) trimesters. Normal growth…

0301 basic medicineFetusPediatricsmedicine.medical_specialtybusiness.industryGeneral Neurosciencemedicine.disease03 medical and health sciences030104 developmental biology0302 clinical medicineNeurodevelopmental disorderAutism spectrum disorderIn uteromedicineGestationAutismAmenorrheaNeurology (clinical)medicine.symptombusinessPathological030217 neurology & neurosurgeryGenetics (clinical)Autism Research
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Shank3 Mice Carrying the Human Q321R Mutation Display Enhanced Self-Grooming, Abnormal Electroencephalogram Patterns, and Suppressed Neuronal Excitab…

2019

Shank3, a postsynaptic scaffolding protein involved in regulating excitatory synapse assembly and function, has been implicated in several brain disorders, including autism spectrum disorders (ASD), Phelan-McDermid syndrome, schizophrenia, intellectual disability, and mania. Here we generated and characterized a Shank3 knock-in mouse line carrying the Q321R mutation (Shank3Q321R mice) identified in a human individual with ASD that affects the ankyrin repeat region (ARR) domain of the Shank3 protein. Homozygous Shank3Q321R/Q321R mice show a selective decrease in the level of Shank3a, an ARR-containing protein variant, but not other variants. CA1 pyramidal neurons in the Shank3Q321R/Q321R hip…

0301 basic medicineHippocampusautism spectrum disorderBiologyNeurotransmissionElectroencephalographyInhibitory postsynaptic potentiallcsh:RC321-57103 medical and health sciencesCellular and Molecular NeuroscienceExcitatory synapse assembly0302 clinical medicinePostsynaptic potentialexcitabilitymedicineself-groomingEEGMolecular Biologylcsh:Neurosciences. Biological psychiatry. Neuropsychiatrypatient mutationsOriginal Researchmedicine.diagnostic_testanxiety-like behaviorseizure susceptibilitymedicine.disease030104 developmental biologyShank3SchizophreniaExcitatory postsynaptic potentialNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Molecular Neuroscience
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MET-EGFR dimerization in lung adenocarcinoma is dependent on EGFR mtations and altered by MET kinase inhibition

2017

Advanced lung cancer has poor survival with few therapies. EGFR tyrosine kinase inhibitors (TKIs) have high response rates in patients with activating EGFR mutations, but acquired resistance is inevitable. Acquisition of the EGFR T790M mutation causes over 50% of resistance; MET amplification is also common. Preclinical data suggest synergy between MET and EGFR inhibitors. We hypothesized that EGFR-MET dimerization determines response to MET inhibition, depending on EGFR mutation status, independently of MET copy number. We tested this hypothesis by generating isogenic cell lines from NCI-H1975 cells, which co-express L858R and T790M EGFR mutations, namely H1975L858R/T790M (EGFR TKI resista…

0301 basic medicineLung NeoplasmsKinase InhibitorsCancer Treatmentlcsh:MedicinePhysical ChemistryBiochemistryFluorophotometryT790MSpectrum Analysis Techniques0302 clinical medicineFluorescence Resonance Energy TransferMedicine and Health SciencesPhosphorylationEnzyme Inhibitorslcsh:ScienceExtracellular Signal-Regulated MAP KinasesEGFR inhibitorsStainingMice Inbred BALB CMultidisciplinaryFluorescent in Situ HybridizationPhysicsCell StainingProto-Oncogene Proteins c-metPrecipitation TechniquesErbB ReceptorsChemistryOncologySpectrophotometry030220 oncology & carcinogenesisPhysical SciencesErlotinibDimerizationProtein BindingResearch Articlemedicine.drugChemical physicsMice NudeMolecular Probe TechniquesAdenocarcinoma of LungAdenocarcinomaBiologyResearch and Analysis Methods03 medical and health sciencesGefitinibGrowth factor receptorCell Line TumormedicineAnimalsHumansImmunoprecipitationMolecular Biology TechniquesLung cancerProtein Kinase InhibitorsMolecular BiologyCell ProliferationCell growthlcsh:RReproducibility of ResultsBiology and Life SciencesDimers (Chemical physics)medicine.diseaseMolecular biologyIsogenic human disease modelsProbe Hybridizationrespiratory tract diseasesHEK293 Cells030104 developmental biologyChemical PropertiesSpecimen Preparation and TreatmentFocal Adhesion Protein-Tyrosine KinasesMutationEnzymologylcsh:QProtein MultimerizationProto-Oncogene Proteins c-aktCytogenetic TechniquesPLOS ONE
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NEGR1 and FGFR2 cooperatively regulate cortical development and core behaviours related to autism disorders in mice.

2018

See Contreras and Hippenmeyer (doi:10.1093/brain/awy218) for a scientific commentary on this article. Autism spectrum disorders (ASDs) are complex conditions with diverse aetiologies. Szczurkowska et al. demonstrate that two ASD-related molecules – FGFR2 and Negr1 – physically interact to act on the same downstream pathway, and regulate cortical development and ASD-relevant behaviours in mice. Identifying common mechanisms in ASDs may reveal targets for pharmacological intervention.

0301 basic medicineMAPK/ERK pathwaygenetic structuresAutism Spectrum DisorderFGFR2 signalingFibroblast growth factorReceptor tyrosine kinaseMiceautism; development; cell adhesion; in utero electroporation; FGFR2 signaling0302 clinical medicineCell MovementCerebral CortexMice KnockoutbiologyBehavior AnimalKinaseCell adhesion moleculeCell biologyProtein TransportSignal Transductionmusculoskeletal diseasesMAP Kinase Signaling SystemCell Adhesion Molecules NeuronalDendritic SpinesNeurogenesisautismDown-Regulationbehavioral disciplines and activities03 medical and health sciencesmental disordersmedicineAnimalsHumansAutistic DisorderReceptor Fibroblast Growth Factor Type 2developmentProtein kinase BFibroblast growth factor receptor 2Cell Membranecell adhesionOriginal Articlesin utero electroporationmedicine.diseaseMice Inbred C57BLDisease Models Animal030104 developmental biologyHEK293 Cellsbiology.proteinAutismNeurology (clinical)030217 neurology & neurosurgeryBrain : a journal of neurology
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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
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