Search results for "METHYLATION"

showing 10 items of 607 documents

Impact of Consuming Extra-Virgin Olive Oil or Nuts within a Mediterranean Diet on DNA Methylation in Peripheral White Blood Cells within the PREDIMED…

2017

DNA methylation could be reversible and mouldable by environmental factors, such as dietary exposures. The objective was to analyse whether an intervention with two Mediterranean diets, one rich in extra-virgin olive oil (MedDiet + EVOO) and the other one in nuts (MedDiet + nuts), was influencing the methylation status of peripheral white blood cells (PWBCs) genes. A subset of 36 representative individuals were selected within the PREvención con DIeta MEDiterránea (PREDIMED-Navarra) trial, with three intervention groups in high cardiovascular risk volunteers: MedDiet + EVOO, MedDiet + nuts, and a low-fat control group. Methylation was assessed at baseline and at five-year follow-up. Ingenui…

Male0301 basic medicineTime FactorsMediterranean diet; DNA methylation; nuts; olive oil; blood cellsMediterranean dietADNPhysiologyComorbidity030204 cardiovascular system & hematologyDiet MediterraneanEpigenesis Genetic0302 clinical medicineRisk FactorsLeukocytesNutsCooking (Dried foods)Aged 80 and overchemistry.chemical_classificationDNA methylationNutrition and DieteticsMethylationMiddle AgedOli d'olivaTreatment OutcomeCpG siteCardiovascular DiseasesDNA methylationFemaleDiet HealthyMetilaciólcsh:Nutrition. Foods and food supplyPolyunsaturated fatty acidBlood cellslcsh:TX341-641nutsBiologyMethylationArticle03 medical and health sciencesMediterranean cookingMediterranean dietDiabetes mellitusCuina mediterràniamedicineHumansEpigeneticsOlive OilAgedMetabolismDNAProtective Factorsmedicine.diseaseCuina (Fruita seca)030104 developmental biologychemistrySpainCèl·lules sanguíniesCpG Islandsblood cellsEnergy MetabolismOlive oilFood Science
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Epigenetic outlier profiles in depression: A genome-wide DNA methylation analysis of monozygotic twins

2018

Recent discoveries highlight the importance of stochastic epigenetic changes, as indexed by epigenetic outlier DNA methylation signatures, as a valuable tool to understand aberrant cell function and subsequent human pathology. There is evidence of such changes in different complex disorders as diverse as cancer, obesity and, to a lesser extent, depression. The current study was aimed at identifying outlying DNA methylation signatures of depressive psychopathology. Here, genome-wide DNA methylation levels were measured (by means of Illumina Infinium HumanMethylation450 Beadchip) in peripheral blood of thirty-four monozygotic twins informative for depressive psychopathology (lifetime DSM-IV d…

Male0301 basic medicineTwinslcsh:MedicineBiochemistryGenomeEpigenesis GeneticDatabase and Informatics MethodsMedicine and Health SciencesDepressió psíquicalcsh:ScienceEpigenesisGeneticsDNA methylationMultidisciplinaryDepressionGenomicsMethylationMiddle AgedChromatinNucleic acidsMental depressionCpG sitePhysical SciencesDNA methylationBessonsEpigeneticsFemalegenoma humàDNA modificationChromatin modificationResearch ArticleChromosome biologyStatistical DistributionsAdultCell biologyHealth InformaticsGenomicsBiologyResearch and Analysis MethodsPolymorphism Single Nucleotidemalalties mentalsYoung Adult03 medical and health sciencesMental Health and PsychiatryGeneticsHumansEpigeneticsGeneTreatment GuidelinesHealth Care PolicyBiology and life sciencesMood Disorderslcsh:RDNATwins MonozygoticEpigenèticaProbability TheoryExpressió gènicaHealth Care030104 developmental biologylcsh:QCpG IslandsGene expressionMathematicsDevelopmental Biology
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The SGLT2 inhibitor empagliflozin improves the primary diabetic complications in ZDF rats

2017

Hyperglycemia associated with inflammation and oxidative stress is a major cause of vascular dysfunction and cardiovascular disease in diabetes. Recent data reports that a selective sodium-glucose co-transporter 2 inhibitor (SGLT2i), empagliflozin (Jardiance®), ameliorates glucotoxicity via excretion of excess glucose in urine (glucosuria) and significantly improves cardiovascular mortality in type 2 diabetes mellitus (T2DM). The overarching hypothesis is that hyperglycemia and glucotoxicity are upstream of all other complications seen in diabetes. The aim of this study was to investigate effects of empagliflozin on glucotoxicity, β-cell function, inflammation, oxidative stress and endothel…

Male0301 basic medicineendocrine system diseasesDiabetic CardiomyopathiesFPS-ZM1 RAGE inhibitorClinical BiochemistryAorta ThoracicRAGE receptor for AGEICAM-1 intercellular adhesion molecule-1ECL enhanced chemiluminescence030204 cardiovascular system & hematologyDPP-4 dipeptidyl peptidase-4medicine.disease_causeTNF-α tumor necrosis factor-αBiochemistryeNOS endothelial •NO synthase (type 3)0302 clinical medicineGlucosidesecSOD extracellular superoxide dismutaseInsulin-Secreting CellsCCL-2 see MCP-1HyperlipidemiaHyperinsulinemiaGTN glyceryl trinitrate (nitroglycerin)IFN-γ interferon-γDHE dihydroethidineEndothelial dysfunctionEndothelial dysfunctionIL-6 interleukin-6lcsh:QH301-705.5HO-1 heme oxygenase-1lcsh:R5-920ICAM-1NG normoglycemiaDiabetesNox catalytic subunit of NADPH oxidaseSGLT2 inhibitorβ-cell contentL-012 8-amino-5-chloro-7-phenylpyrido[34-d]pyridazine-14-(2H3H)dione sodium saltChIP chromatin immunoprecipitationC-Reactive ProteinCRP C-reactive proteinAGE advanced glycation end productsHbA1c glycohemoglobinlcsh:Medicine (General)Research PaperZucker diabetic fatty ratsmedicine.medical_specialtyDMSO dimethylsulfoxideMCP-1 monocyte-chemoattractant-protein-1qRT-PCR quantitative reverse transcription polymerase chain reactionZDF Zucker diabetic fatty (rat)Low-grade inflammation03 medical and health sciencesROS reactive oxygen speciesSodium-Glucose Transporter 2Physiology (medical)Internal medicineDiabetes mellitusPKC protein kinase CEmpagliflozinmedicineAnimalsHypoglycemic AgentsBenzhydryl CompoundsCOX2 cyclooxygenase-2SGLT2i SGLT2 inhibitorSodium-Glucose Transporter 2 InhibitorsGlycated HemoglobinACh acetylcholinebusiness.industryOrganic Chemistrynutritional and metabolic diseasesType 2 Diabetes Mellitusmedicine.diseaseH2K9me2 histone3 lysine9 dimethylationRatsRats ZuckerDHFR dihydrofolate reductaseSGLT2 sodium-glucose co-transporter-2Oxidative StresssGC soluable guanylyl cyclaseGlucose030104 developmental biologyEndocrinologylcsh:Biology (General)ALDH-2 mitochondrial aldehyde dehydrogenaseEndothelium VascularAGE/RAGE signalingHG hyperglycemiabusinessOxidative stressRedox Biology
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DNA Methylation Analysis to Unravel Altered Genetic Pathways Underlying Early Onset and Late Onset Neonatal Sepsis. A Pilot Study

2021

Background: Neonatal sepsis is a systemic condition widely affecting preterm infants and characterized by pro-inflammatory and anti-inflammatory responses. However, its pathophysiology is not yet fully understood. Epigenetics regulates the immune system, and its alteration leads to the impaired immune response underlying sepsis. DNA methylation may contribute to sepsis-induced immunosuppression which, if persistent, will cause long-term adverse effects in neonates.Objective: To analyze the methylome of preterm infants in order to determine whether there are DNA methylation marks that may shed light on the pathophysiology of neonatal sepsis.Design: Prospective observational cohort study perf…

Male0301 basic medicinelcsh:Immunologic diseases. AllergyNeonatal intensive care unitgenetic structuresImmunologyPilot ProjectsLate onsetAdaptive ImmunityBioinformaticsCohort StudiesDiagnosis DifferentialSepsissepsis03 medical and health sciences0302 clinical medicineHumansImmunology and AllergyMedicineProspective StudiesEpigeneticsOriginal ResearchGenomeDNA methylationimmunosuppressionNeonatal sepsisbusiness.industryInfant Newbornneonatology and pediatric intensive careMethylationmedicine.diseaseImmunity Innate030104 developmental biologyinflammation030220 oncology & carcinogenesisDNA methylationBiomarker (medicine)FemaleNeonatal Sepsisbusinesslcsh:RC581-607Infant PrematureFrontiers in Immunology
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Frequency and characterization of DNA methylation defects in children born SGA

2012

Various genes located at imprinted loci and regulated by epigenetic mechanisms are involved in the control of growth and differentiation. The broad phenotypic variability of imprinting disorders suggests that individuals with inborn errors of imprinting might remain undetected among patients born small for gestational age (SGA). We evaluated quantitative DNA methylation analysis at differentially methylated regions (DMRs) of 10 imprinted loci (PLAGL1, IGF2R DMR2, GRB10, H19 DMR, IGF2, MEG3, NDN, SNRPN, NESP, NESPAS) by bisulphite pyrosequencing in 98 patients born SGA and 50 controls. For IGF2R DMR2, methylation patterns of additional 47 parent pairs and one mother (95 individuals) of patie…

MaleAdolescentMedizinLocus (genetics)BiologyArticleCohort StudiesGenomic ImprintingGeneticsHumansAbnormalities MultipleEpigeneticsImprinting (psychology)ChildGenetics (clinical)MEG3GeneticsFamily HealthInfant NewbornInfantMethylationSequence Analysis DNASyndromeDNA Methylationfemale genital diseases and pregnancy complicationsPedigreeDifferentially methylated regionsPhenotypeGenetic LociChild PreschoolDNA methylationInfant Small for Gestational AgeFemaleGenomic imprinting
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Transcription intermediary factor 1γ is a tumor suppressor in mouse and human chronic myelomonocytic leukemia.

2011

Transcription intermediary factor 1γ (TIF1γ) was suggested to play a role in erythropoiesis. However, how TIF1γ regulates the development of different blood cell lineages and whether TIF1γ is involved in human hematological malignancies remain to be determined. Here we have shown that TIF1γ was a tumor suppressor in mouse and human chronic myelomonocytic leukemia (CMML). Loss of Tif1g in mouse HSCs favored the expansion of the granulo-monocytic progenitor compartment. Furthermore, Tif1g deletion induced the age-dependent appearance of a cell-autonomous myeloproliferative disorder in mice that recapitulated essential characteristics of human CMML. TIF1γ was almost undetectable in leukemic ce…

MaleAgingAntimetabolites AntineoplasticTumor suppressor geneCellular differentiationMolecular Sequence DataChronic myelomonocytic leukemiaReceptor Macrophage Colony-Stimulating FactorBiologyDecitabinechemistry.chemical_compoundMicemedicineAnimalsHumansGenes Tumor SuppressorPromoter Regions GeneticTranscription factorAgedAged 80 and overMice KnockoutBase SequenceGene Expression Regulation LeukemicCell DifferentiationLeukemia Myelomonocytic ChronicGeneral MedicineDNA MethylationMiddle Agedmedicine.diseaseTRIM33Hematopoietic Stem CellsMolecular biologyDemethylating agentHematopoiesisNeoplasm ProteinsSpecific Pathogen-Free OrganismsHaematopoiesischemistryDNA methylationCancer researchAzacitidineFemaleTranscription FactorsResearch ArticleThe Journal of clinical investigation
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Postnatal loss of Dlk1 imprinting in stem cells and niche astrocytes regulates neurogenesis.

2011

The gene for the atypical NOTCH ligand delta-like homologue 1 (Dlk1) encodes membrane-bound and secreted isoforms that function in several developmental processes in vitro and in vivo. Dlk1, a member of a cluster of imprinted genes, is expressed from the paternally inherited chromosome. Here we show that mice that are deficient in Dlk1 have defects in postnatal neurogenesis in the subventricular zone: a developmental continuum that results in depletion of mature neurons in the olfactory bulb. We show that DLK1 is secreted by niche astrocytes, whereas its membrane-bound isoform is present in neural stem cells (NSCs) and is required for the inductive effect of secreted DLK1 on self-renewal. N…

MaleAgingGenotypeNeurogenesisSubventricular zoneBiologyArticle03 medical and health sciencesGenomic ImprintingMice0302 clinical medicineNeural Stem CellsmedicineAnimalsProtein IsoformsEpigeneticsImprinting (psychology)Stem Cell NicheCells Cultured030304 developmental biologyGenetics0303 health sciencesMultidisciplinaryBase SequenceNeurogenesisCalcium-Binding ProteinsCell MembraneEmbryo MammalianOlfactory BulbNeural stem cellCell biologyMice Inbred C57BLmedicine.anatomical_structureAnimals NewbornAstrocytesDNA methylationNeurogliaIntercellular Signaling Peptides and ProteinsFemaleGenomic imprinting030217 neurology & neurosurgery
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Leisure-Time and Occupational Physical Activity Associates Differently with Epigenetic Aging

2021

Supplemental digital content is available in the text.

MaleAgingLeisure timeliikuntaEpigenesis Genetic0302 clinical medicineTwins DizygoticMedicineOrthopedics and Sports MedicineYoung adult315 Sport and fitness sciencesAge FactorsMETHYLATIONMiddle AgedDNA-metylaatioepigenetiikkaComputingMethodologies_DOCUMENTANDTEXTPROCESSINGFemaleSmoking statusSMOKINGfyysinen aktiivisuusAdultPhysical activityPhysical Therapy Sports Therapy and RehabilitationBIOLOGICAL AGINGYoung Adult03 medical and health sciencesLeisure ActivitiesSex FactorsHumansEpigeneticsExerciseOccupational HealthAgedModels GeneticBasic Sciencesbusiness.industrydNaMTwins Monozygotic030229 sport sciencesDNA MethylationTwin studyfyysinen kuormittavuusikääntyminentyön kuormittavuusbusinessLifestyle habitshuman activitiesQUANTITATIVE GENETICSDemography
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Loss-of-function maternal-effect mutations of PADI6 are associated with familial and sporadic Beckwith-Wiedemann syndrome with multi-locus imprinting…

2020

Abstract Background PADI6 is a component of the subcortical maternal complex, a group of proteins that is abundantly expressed in the oocyte cytoplasm, but is required for the correct development of early embryo. Maternal-effect variants of the subcortical maternal complex proteins are associated with heterogeneous diseases, including female infertility, hydatidiform mole, and imprinting disorders with multi-locus imprinting disturbance. While the involvement of PADI6 in infertility is well demonstrated, its role in imprinting disorders is less well established. Results We have identified by whole-exome sequencing analysis four cases of Beckwith-Wiedemann syndrome with multi-locus imprintin…

MaleBeckwith-Wiedemann SyndromeGenomic imprintingMulti-locus imprinting disturbanceBeckwith–Wiedemann syndromeWhole Exome SequencingProtein-Arginine Deiminase Type 60302 clinical medicinePregnancyImprinting (psychology)ChildGenetics (clinical)Genetics0303 health sciencesDNA methylationPADI6Beckwith-Wiedemann syndrome; DNA methylation; Genomic imprinting; Infertility; Maternal-effect variants; Multi-locus imprinting disturbance; PADI6; Subcortical maternal complex; Adolescent; Adult; Beckwith-Wiedemann Syndrome; Child Preschool; DNA Methylation; Female; Genomic Imprinting; Heterozygote; Humans; Hydatidiform Mole; Infant; Infertility Female; Male; Maternal Inheritance; Mutation; Oocytes; Pedigree; Phenotype; Pregnancy; Protein-Arginine Deiminase Type 6; Siblings; Whole Exome SequencingFemale infertilityMaternal effectHydatidiform MolePedigreePhenotypeChild Preschool030220 oncology & carcinogenesisDNA methylationFemaleMaternal InheritanceInfertility FemaleAdultHeterozygoteAdolescentSubcortical maternal complexBiology03 medical and health sciencesExome SequencingGeneticsmedicineHumansMaternal-effect variantsPreschoolMolecular BiologyLoss function030304 developmental biologyMaternal-effect variantResearchSiblingsInfantmedicine.diseaseHuman geneticsInfertilityMutationOocytesGenomic imprintingDevelopmental BiologyClinical Epigenetics
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New insights into the pathogenesis of Beckwith-Wiedemann and Silver-Russell syndromes: contribution of small copy number variations to 11p15 imprinti…

2011

International audience; The imprinted 11p15 region is organized in two domains, each of them under the control of its own imprinting control region (ICR1 for the IGF2/H19 domain and ICR2 for the KCNQ1OT1/CDKN1C domain). Disruption of 11p15 imprinting results in two fetal growth disorders with opposite phenotypes: the Beckwith-Wiedemann (BWS) and the Silver-Russell (SRS) syndromes. Various 11p15 genetic and epigenetic defects have been demonstrated in BWS and SRS. Among them, isolated DNA methylation defects account for approximately 60% of patients. To investigate whether cryptic copy number variations (CNVs) involving only part of one of the two imprinted domains account for 11p15 isolated…

MaleBeckwith–Wiedemann syndrome[SDV.GEN] Life Sciences [q-bio]/GeneticsMESH: Base SequenceMESH: DNA MethylationCopy-number variationImprinting (psychology)[SDV.BDD]Life Sciences [q-bio]/Development BiologyGenetics (clinical)GeneticsComparative Genomic Hybridization0303 health sciencesKCNQ1OT1MESH: Polymorphism Single Nucleotide030305 genetics & hereditycopy number variation11p15 regionPedigreegenomic imprintingMESH: Silver-Russell SyndromeDNA methylationBeckwith-Wiedemann syndromeFemaleMESH: DNA Copy Number VariationsMESH: Beckwith-Wiedemann SyndromeAdultDNA Copy Number VariationsMESH: PedigreeBiologyPolymorphism Single Nucleotide03 medical and health sciences[SDV.BDD] Life Sciences [q-bio]/Development BiologyGeneticsmedicineHumansEpigenetics030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsMESH: HumansBase SequenceChromosomes Human Pair 11MESH: AdultDNA Methylationmedicine.diseaseMESH: MaleMESH: Genomic ImprintingMESH: Comparative Genomic HybridizationUniparental IsodisomySilver-Russell syndromeMESH: Chromosomes Human Pair 11Genomic imprintingMESH: Femalefetal growthfetal growth.
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