Search results for "PRI"

showing 10 items of 17196 documents

Relationship Between Body Mass Index, ApoE4 Status, and PET-Based Amyloid and Neurodegeneration Markers in Amyloid-Positive Subjects with Normal Cogn…

2018

Body weight loss in late-life is known to occur at a very early stage of Alzheimer's disease (AD). Apolipoprotein E4 (ApoE4) represents a major genetic risk factor for AD and is linked to an increased cortical amyloid-β (Aβ) accumulation. Since the relationship between body weight, ApoE4, and AD pathology is poorly investigated, we aimed to evaluate whether ApoE4 allelic status modifies the association of body mass index (BMI) with markers of AD pathology. A total of 368 Aβ-positive cognitively healthy or mild cognitive impaired subjects had undergone [18F]-AV45-PET, [18F]-FDG-PET, and T1w-MRI examinations. Composite cortical [18F]-AV45 uptake and [18F]-FDG uptake in posterior cingulate cor…

0301 basic medicineMaleApolipoprotein E4Body Mass Index0302 clinical medicineCognitionWeight lossCognitive declineAniline CompoundsGeneral NeuroscienceNeurodegenerationBrainCognitionNeurodegenerative DiseasesGeneral MedicinePsychiatry and Mental healthClinical PsychologyEthylene GlycolsFemalemedicine.symptommedicine.medical_specialtyAmyloidHeterozygote03 medical and health sciencesFluorodeoxyglucose F18Internal medicinemental disordersWeight LossmedicineHumansCognitive DysfunctionEffects of sleep deprivation on cognitive performanceAdaptor Proteins Signal TransducingAgedbusiness.industryZebrafish Proteinsmedicine.diseaseCortex (botany)Repressor Proteins030104 developmental biologyEndocrinologyGlucosePosterior cingulatePositron-Emission TomographyGeriatrics and GerontologyRadiopharmaceuticalsbusinessNeuroscienceBody mass index030217 neurology & neurosurgeryFollow-Up StudiesJournal of Alzheimer's disease : JAD
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Somatic copy number alterations are associated with EGFR amplification and shortened survival in patients with primary glioblastoma.

2019

Glioblastoma (GBM) is the most common malignant primary tumor of the central nervous system. With no effective therapy, the prognosis for patients is terrible poor. It is highly heterogeneous and EGFR amplification is its most frequent molecular alteration. In this light, we aimed to examine the genetic heterogeneity of GBM and to correlate it with the clinical characteristics of the patients. For that purpose, we analyzed the status of EGFR and the somatic copy number alterations (CNAs) of a set of tumor suppressor genes and oncogenes. Thus, we found GBMs with high level of EGFR amplification, low level and with no EGFR amplification. Highly amplified tumors showed histological features of…

0301 basic medicineMaleCancer ResearchBiopsyL-amp GB EGFR-low amplified glioblastomamedicine.disease_causewt wildtypeMYBPC3 myosin-binding protein C0302 clinical medicineHIC1 hypermethylated in cancer 1Gene duplicationIn Situ Hybridization FluorescenceIDH2 isocitrate dehydrogenase 2MutationRB-pat RB signaling pathwayEGFRvIII epidermal growth factor receptor variant number IIIPAH phenylalanine hydroxylaseGBM glioblastoma IDH-wildtype (glioblastoma multiforme primary glioblastoma).ANOVA ANalysis Of VArianceN-amp GB EGFR-no amplified glioblastomaMiddle AgedCDKN2A cyclin-dependent kinase inhibitor 2Alcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisPrimary tumorImmunohistochemistryH-amp GB EGFR-high amplified glioblastomaErbB ReceptorsTKR-pat tyrosine-kinase receptors signaling pathway030220 oncology & carcinogenesisDisease ProgressionCDK6 cyclin-dependent kinase 6CDH1 Cadherin 1FemaleCREM cAMP response element modulatorIHC immunohistochemistryAdultOriginal articleDNA Copy Number VariationsCDKN1B cyclin-dependent kinase inhibitor 1BBiologyRARB retinoic acid receptor betaCNS central nervous systemlcsh:RC254-282IDH1 isocitrate dehydrogenase 1BCL2 B-cell cll/ lymphoma 2CNAs copy number algerationsWHO World Health Organization03 medical and health sciencesYoung Adultp53-pat p53 signaling pathwaymedicineBiomarkers TumorTMA tissue microarrayPTENHumansProtein kinase BPI3K/AKT/mTOR pathwaySurvival analysisAgedGenetic heterogeneityGene AmplificationGFAP glial fibrillary acidic proteinMLPA multiplex ligation-dependent probe amplificationmedicine.diseaseFISH fluorescence in situ hibridizationSurvival AnalysisCDKN2B cyclin-dependent kinase inhibitor 2BPTEN phosphatase and tensin homologEGFR epidermal growth factor receptorCNV-load load of copy number variations030104 developmental biologyMutationPARK2 parkinCancer researchbiology.proteinTCGA The Cancer Genome AtlasLARGE1 acetylglucosaminyltransferase-like protein 1GlioblastomaCHD7 Chromodomain Helicase DNA Binding Protein 7DAPI 4′6-diamidino-2-phenylindoleNeoplasia (New York, N.Y.)
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Phenotypic spectrum and extent of DNA methylation defects associated with multilocus imprinting disturbances.

2016

Aim: To characterize the genotypic and phenotypic extent of multilocus imprinting disturbances (MLID). Materials & methods: We analyzed 37 patients with imprinting disorders (explorative cohort) for DNA methylation changes using the Infinium HumanMethylation450 BeadChip. For validation, three independent cohorts with imprinting disorders or cardinal features thereof were analyzed (84 patients with imprinting disorders, 52 with growth disorder, 81 with developmental delay). Results: In the explorative cohort 21 individuals showed array-based MLID with each one displaying an Angelman or Temple syndrome phenotype, respectively. Epimutations in ZDBF2 and FAM50B were associated with severe …

0301 basic medicineMaleCancer ResearchDevelopmental DisabilitiesMedizinBiology03 medical and health sciencesGenomic ImprintingGenotypeGeneticsHumansImprinting (psychology)Genetic Association StudiesGeneticsProteinsMethylationSequence Analysis DNATemple SyndromeDNA MethylationPhenotypeDNA-Binding Proteins030104 developmental biologyPhenotypeCase-Control StudiesCohortDNA methylationFemaleEpigenomics
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Maternal eNOS deficiency determines a fatty liver phenotype of the offspring in a sex dependent manner

2016

ABSTRACT Maternal environmental factors can impact on the phenotype of the offspring via the induction of epigenetic adaptive mechanisms. The advanced fetal programming hypothesis proposes that maternal genetic variants may influence the offspring's phenotype indirectly via epigenetic modification, despite the absence of a primary genetic defect. To test this hypothesis, heterozygous female eNOS knockout mice and wild type mice were bred with male wild type mice. We then assessed the impact of maternal eNOS deficiency on the liver phenotype of wild type offspring. Birth weight of male wild type offspring born to female heterozygous eNOS knockout mice was reduced compared to offspring of wil…

0301 basic medicineMaleCancer Researchmedicine.medical_specialtyHeterozygoteNitric Oxide Synthase Type IIIOffspringBiology03 medical and health sciencesGenomic ImprintingMiceSex FactorsEnosInternal medicineFetal programmingmedicineAnimalsEpigeneticsMolecular BiologyGeneFatty liverWild typeHeterozygote advantageDNA Methylationmedicine.diseasebiology.organism_classificationFatty LiverMice Inbred C57BL030104 developmental biologyEndocrinologyPhenotypeKnockout mouseeNOSCarbohydrate MetabolismFemaleEpigeneticsInstitut für ErnährungswissenschaftmetabolismResearch Paper
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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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Network effects and pathways in Deep brain stimulation in Parkinson's disease.

2016

Deep brain stimulation of subthalamic nucleus (STN-DBS) became a standard therapeutic option in Parkinson's disease (PD), even though the underlying modulated network of STN-DBS is still poorly described. Probabilistic tractography and connectivity analysis as derived from diffusion tensor imaging (DTI) were performed together with modelling of implanted electrode positions and linked postoperative clinical outcome. Fifteen patients with idiopathic PD without dementia were selected for DBS treatment. After pre-processing, probabilistic tractography was run from cortical and subcortical seeds of the hypothesized network to targets represented by the positions of the active DBS contacts. The …

0301 basic medicineMaleDeep brain stimulationParkinson's diseaseNerve netmedicine.medical_treatmentDeep Brain Stimulationbehavioral disciplines and activities03 medical and health sciences0302 clinical medicineSubthalamic NucleusmedicineHumansAgedSupplementary motor areaMotor CortexBrainParkinson DiseaseMiddle AgedSMA*medicine.diseasenervous system diseasesElectrodes ImplantedSubthalamic nucleussurgical procedures operative030104 developmental biologymedicine.anatomical_structureDiffusion Tensor ImagingTreatment Outcomenervous systemFemalePrimary motor cortexNerve NetPsychologytherapeuticsNeuroscience030217 neurology & neurosurgeryDiffusion MRIAnnual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual International Conference
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Sweet taste of prosocial status signaling: When eating organic foods makes you happy and hopeful.

2018

As the current research suggests that there are links between prosocial acts and status signaling (including sustainable consumer choices), we empirically study (with three experiments) whether food consumers go green to be seen. First, we examine how activating a motive for status influences prosocial organic food preferences. Then, we examine how the social visibility of the choice (private vs. public) affects these preferences. We found that when consumers' desire for status was elicited, they preferred organic food products significantly over their nonorganic counterparts; making the choice situation visible created the same effect. Finally, we go beyond consumers' evaluative and behavi…

0301 basic medicineMaleEmotionsHappinessLUXURY BRANDSChoice BehaviorStatusCONSPICUOUS CONSERVATIONEatingSurveys and QuestionnairesCOMPETITIVE ALTRUISMta512General Psychologymedia_common2. Zero hungerCONSUMER-BEHAVIORNutrition and DieteticsTaste (sociology)05 social scienceskuluttajakäyttäytyminenCHOICEProsocial signalingluomuruokaElevation (emotion)Prosocial behaviorTasteFemaleFood OrganicNonconscious behaviorDiet HealthyPsychologySocial psychologyConspicuous conservationAdultmedicine.medical_specialty515 Psychologymedia_common.quotation_subjectGREENprososiaalisuussosiaalinen asema03 medical and health sciencesFood PreferencesYoung AdulttunteetOrganic foodInternal medicine0502 economics and businessmedicineSOCIAL FACILITATIONHumansConsumer behaviourConsumption (economics)Social facilitationMotivation030109 nutrition & dieteticsCONSUMPTIONMotivational primingConsumer BehaviorCompetitive altruismSenso-emotional experienceEndocrinology416 Food Scienceta5141050211 marketingPURCHASE INTENTIONFollow-Up StudiesAppetite
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Blimp1 Prevents Methylation of Foxp3 and Loss of Regulatory T Cell Identity at Sites of Inflammation

2018

Summary Foxp3+ regulatory T (Treg) cells restrict immune pathology in inflamed tissues; however, an inflammatory environment presents a threat to Treg cell identity and function. Here, we establish a transcriptional signature of central nervous system (CNS) Treg cells that accumulate during experimental autoimmune encephalitis (EAE) and identify a pathway that maintains Treg cell function and identity during severe inflammation. This pathway is dependent on the transcriptional regulator Blimp1, which prevents downregulation of Foxp3 expression and “toxic” gain-of-function of Treg cells in the inflamed CNS. Blimp1 negatively regulates IL-6- and STAT3-dependent Dnmt3a expression and function …

0301 basic medicineMaleEncephalomyelitis Autoimmune ExperimentalBlimp1CNS2Regulatory T cellInflammationchemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryGeneral Biochemistry Genetics and Molecular BiologyArticleepigenetic regulationDNA Methyltransferase 3AEpigenesis Genetic03 medical and health sciencesGenomic ImprintingMice0302 clinical medicineImmune systemDownregulation and upregulationmedicineAnimalsEpigeneticsDNA (Cytosine-5-)-Methyltransferaseslcsh:QH301-705.5Regulation of gene expressionInterleukin-6FOXP3Forkhead Transcription FactorsDNA methyltransferaseshemic and immune systemsDNA Methylation3. Good healthCell biologyddc:Mice Inbred C57BL030104 developmental biologymedicine.anatomical_structureregulatory T cellslcsh:Biology (General)inflammationFoxp3DNA methylationFemalePositive Regulatory Domain I-Binding Factor 1medicine.symptomCNS030217 neurology & neurosurgeryCell Reports
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Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses

2016

Article

0301 basic medicineMaleEpidemiologyPhysiologychemistry.chemical_compoundinsufficient sleep0302 clinical medicineHigh-density lipoproteinFinlandSleep restrictionGENERAL-POPULATIONINSULIN-RESISTANCEeducation.field_of_studyMultidisciplinarytulehdusCARDIOVASCULAR RISKGLUCOSE-METABOLISMta3142Chronic inflammationMiddle AgedSleep in non-human animals3. Good healthSleep deprivationCholesterolMetabolomeFemalemedicine.symptomAdultmedicine.medical_specialtyACUTE-PHASE RESPONSELIVER-X-RECEPTORSPopulationBiologyta3111Articlesleep restriction03 medical and health sciencesInsulin resistanceMetabolic DiseasesInternal medicinemedicineMetabolomeHumansCORONARY-HEART-DISEASEeducationLiver X receptorDyslipidaemiasAgedCASSETTE TRANSPORTER G1Gene Expression Profilingta1182ta3121medicine.diseaseSleep deprivation030104 developmental biologyEndocrinologychemistryinflammationcholesterol metabolismSleep Deprivation3111 BiomedicineGene expressionHIGH-DENSITY-LIPOPROTEIN030217 neurology & neurosurgeryBlood Chemical AnalysisScientific Reports
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Benign nocturnal alternating hemiplegia of childhood

2018

Objective: To describe the clinical spectrum of benign nocturnal alternating hemiplegia of childhood (BNAHC) including long-term follow-up data of previously published cases and to propose an underlying genetic cause of this disorder. Methods: We studied the medical data of two novel patients, reviewed the literature on BNAHC, and gathered information of the most recent follow-up of published cases regarding the course of episodes, further development, attempted drugs, ancillary investigations, and sequelae. Results: All patients, i.e. two novel cases and twelve patients identified in the literature (13 boys, 1 girl, age at onset four months to three years), experienced episodes of hemipleg…

0301 basic medicineMaleExome sequencingPediatricsmedicine.medical_specialtyHeterozygoteHemiplegiaNerve Tissue ProteinsPATIENTSensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]03 medical and health sciences0302 clinical medicinePRRT2 MUTATIONSmedicineHumansIctalPAROXYSMAL KINESIGENIC DYSKINESIAFamily historyPRRT2 geneExome sequencingCryingbusiness.industryAlternating hemiplegia of childhoodInfantMembrane ProteinsGeneral MedicineParoxysmal dyskinesiamedicine.diseaseDisorders of movement Donders Center for Medical Neuroscience [Radboudumc 3]GENESleep deprivation030104 developmental biologyPhenotypeTreatment OutcomeSYNAPTIC-TRANSMISSIONMigraineMIGRAINEChild PreschoolPediatrics Perinatology and Child HealthDisease ProgressionNeurology (clinical)medicine.symptombusinessINFANTILE CONVULSIONS030217 neurology & neurosurgeryGene DeletionBenign nocturnal alternating hemiplegia of childhoodEuropean Journal of Paediatric Neurology
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