Search results for "imprint"

showing 10 items of 194 documents

The imprint of subduction fluids on subducted MORB-derived melts (Sierra del Convento Mélange, Cuba)

2011

International audience; Major and trace element signatures and Sr-Nd-Pb isotope data for muscovite (Ms)-bearing amphibolite blocks and associated muscovite-bearing trondhjemite and quartz-muscovite rocks from the Sierra del Convento melange (eastern Cuba) indicate that Proto-Caribbean oceanic crust underwent wet partial melting processes during Mesozoic subduction and after accretion to the upper plate. Trace element normalized patterns of Ms-bearing amphibolites are enriched in light rare earth elements (LREE) and large-ion lithophile elements (LILE) and evidence variable trace element transfer from the Proto-Caribbean subducting slab to the mantle wedge. Ms-bearing trondhjemites show LREE…

010504 meteorology & atmospheric sciencesMantle wedge[SDE.MCG]Environmental Sciences/Global ChangesFluid compositionTrondhjemiteGeochemistrySedimentary imprint010502 geochemistry & geophysics01 natural sciences[SDU.STU.GC]Sciences of the Universe [physics]/Earth Sciences/GeochemistryGeochemistry and PetrologyOceanic crust0105 earth and related environmental sciencesBasaltTrace elementsSubductionbiologyPartial meltingTrace elementGeologySr-Nd-Pb isotopesbiology.organism_classification13. Climate actionAdakiteLileGeologySlab meltsLithos
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Chemical host detection and differential attraction in a parasitic pea crab infecting two echinoids

2011

Mechanisms of host detection and host choice are important for mobile parasites or symbionts that frequently move among host individuals. The parasitic pea crab Dissodactylus primitivus is an ectoparasite exploiting asymmetrically two spatangoid echinoid hosts, Meoma ventricosa and Plagiobrissus grandis. The entire life cycle takes place on M. ventricosa, while only adults colonize P. grandis, the host where female's fecundity is the greatest. Dissodactylus primitivus frequently exhibits host-switching, a behaviour that raises the question of host detection. To test if adult crabs are able to detect potential hosts and are attracted to the host where their fitness is greater, crab olfactory…

0106 biological sciences[ SDV.MP.PAR ] Life Sciences [q-bio]/Microbiology and Parasitology/Parasitologyanimal structuresChemical detectionZoologyAquatic ScienceGeneralist and specialist species010603 evolutionary biology01 natural sciencesMeoma ventricosaPea crab[ SDV.EE.IEO ] Life Sciences [q-bio]/Ecology environment/Symbiosis[SDV.MP.PAR]Life Sciences [q-bio]/Microbiology and Parasitology/ParasitologyEcology Evolution Behavior and SystematicsDissodactylus primitivus[ SDE.BE ] Environmental Sciences/Biodiversity and EcologyPea crabbiologyDecapodaEcology010604 marine biology & hydrobiologyfood and beveragesImprintingbiology.organism_classificationFecundityAttractionCrustaceanParasiteHabitatHost-switchingEchinoidea [Sea urchins]Echinoid[SDE.BE]Environmental Sciences/Biodiversity and Ecology[SDV.EE.IEO]Life Sciences [q-bio]/Ecology environment/Symbiosis
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The close link between the fetal programming imprinting and neurodegeneration in adulthood: The key role of “hemogenic endothelium” programming

2021

The research on neurodegenerative diseases (NeuroDegD) has been traditionally focused on later life stages. There is now an increasing evidence, that they may be programmed during early development. Here, we propose that NeuroDegD are the result of the complex process of imprinting on fetal hemogenic endothelium, from which the microglial cells make to origin. The central role of placenta and epigenetic mechanisms (methylation of DNA, histone modifications and regulation by non-coding RNAs) in mediating the short and long-term effects has been also described. Precisely, it reports their role in impacting plasticity and memory of microglial cells. In addition, we also underline the necessity…

0301 basic medicineAgingHemangioblastsCell PlasticityRisk AssessmentEpigenesis GeneticFetal DevelopmentMolecular Imprinting03 medical and health sciences0302 clinical medicineEpigenetic factors as biomarkers Sex dimorphism Fetal developmental programming Hemogenic endothelium Microglia plasticity and memory Neurodegenerative diseasesmedicineHumansSettore MED/05 - Patologia ClinicaEpigeneticsFetal programmingImprinting (organizational theory)Hemogenic endotheliumSex CharacteristicsBiological Variation Individualbiologybusiness.industryNeurodegenerationGene Expression Regulation DevelopmentalNeurodegenerative Diseasesmedicine.diseaseLife stage030104 developmental biologyHistonePrenatal stressbiology.proteinMicrogliabusinessNeuroscienceBiomarkers030217 neurology & neurosurgeryDevelopmental BiologyMechanisms of Ageing and Development
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Genomic Imprinting and the Regulation of Postnatal Neurogenesis

2017

Most genes required for mammalian development are expressed from both maternally and paternally inherited chromosomal homologues. However, there are a small number of genes known as “imprinted genes” that only express a single allele from one parent, which is repressed on the gene from the other parent. Imprinted genes are dependent on epigenetic mechanisms such as DNA methylation and post-translational modifications of the DNA-associated histone proteins to establish and maintain their parental identity. In the brain, multiple transcripts have been identified which show parental origin-specific expression biases. However, the mechanistic relationship with canonical imprinting is unknown. R…

0301 basic medicineGeneticsReviewBiologyGene dosage03 medical and health sciences030104 developmental biology0302 clinical medicineHistoneDNA methylationbiology.proteinGeneral Earth and Planetary SciencesEpigeneticsImprinting (psychology)AlleleGenomic imprintingGene030217 neurology & neurosurgeryGeneral Environmental ScienceBrain Plasticity
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Novel deletion in 11p15.5 imprinting center region 1 in a patient with Beckwith-Wiedemann syndrome provides insight into distal enhancer regulation a…

2016

Background Beckwith–Wiedemann syndrome (BWS) is an early-onset overgrowth disorder with a high risk for embryonal tumors. It is mainly caused by dysregulation of imprinted genes on chromosome 11p15.5; however, the driving forces in the development of tumors are not fully understood. Procedure We report on a female patient presenting with macrosomia, macroglossia, organomegaly and extensive bilateral nephroblastomatosis. Adjuvant chemotherapy was initiated; however, the patient developed hepatoblastoma and Wilms tumor at 5 and 12 months of age, respectively. Subsequent radiofrequency ablation of the liver tumor and partial nephrectomy followed by consolidation therapy achieved complete remis…

0301 basic medicineHepatoblastomaPathologymedicine.medical_specialtyBeckwith-Wiedemann SyndromeBeckwith–Wiedemann syndrome030105 genetics & hereditymedicine.disease_cause03 medical and health sciencesGenomic ImprintingInsulin-Like Growth Factor IIMacroglossiaMedicineHumansImprinting (psychology)NephroblastomatosisSequence Deletionbusiness.industryChromosomes Human Pair 11Infant NewbornWilms' tumorHematologyDNA Methylationmedicine.diseasePrognosis030104 developmental biologyCell Transformation NeoplasticPhenotypeOncologyPediatrics Perinatology and Child HealthCancer researchFemalemedicine.symptombusinessGenomic imprintingCarcinogenesisPediatric bloodcancer
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The DNA methylation profile of human spermatogonia at single-cell- and single-allele-resolution refutes its role in spermatogonial stem cell function…

2019

Human spermatogonial stem cells (hSSCs) have potential in fertility preservation of prepubertal boys or in treatment of male adults suffering from meiotic arrest. Prior to therapeutic application, in vitro propagation of rare hSSCs is mandatory. As the published data points to epigenetic alterations in long-term cell culture of spermatogonia (SPG), an initial characterisation of their DNA methylation state is important. Testicular biopsies from five adult normogonadotropic patients were converted into aggregate-free cell suspensions. FGFR3-positive (FGFR3+) SPG, resembling a very early stem cell state, were labelled with magnetic beads and isolated in addition to unlabelled SPG (FGFR3-). DN…

0301 basic medicineHomeobox protein NANOGMaleEmbryologyBiologyEpigenesis Genetic03 medical and health sciences0302 clinical medicineGeneticsmedicineHumansReceptor Fibroblast Growth Factor Type 3EpigeneticsSpermatogenesisMolecular BiologyAllelesMEG3030219 obstetrics & reproductive medicineKCNQ1OT1Stem CellsObstetrics and GynecologyCell DifferentiationCell BiologyMethylationDNA MethylationMolecular biologySpermatozoaSpermatogonia030104 developmental biologymedicine.anatomical_structureReproductive MedicineDNA methylationGenomic imprintingGerm cellDevelopmental BiologyMolecular human reproduction
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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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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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Maternal Inheritance of a Recessive RBP4 Defect in Canine Congenital Eye Disease

2018

SUMMARY Maternally skewed transmission of traits has been associated with genomic imprinting and oocyte-derived mRNA. We report canine congenital eye malformations, caused by an amino acid deletion (K12del) near the N terminus of retinol-binding protein (RBP4). The disease is only expressed when both dam and offspring are deletion homozygotes. RBP carries vitamin A (retinol) from hepatic stores to peripheral tissues, including the placenta and developing eye, where it is required to synthesize retinoic acid. Gestational vitamin A deficiency is a known risk factor for ocular birth defects. The K12del mutation disrupts RBP folding in vivo, decreasing its secretion from hepatocytes to serum. T…

0301 basic medicineMaleNon-Mendelian inheritanceProtein Foldingcongenital eye defectEye Diseasesgenetic structuresNATIVE DISULFIDE BONDSMedical PhysiologyRetinoic acidReproductive health and childbirth413 Veterinary scienceMicrophthalmiavitamin Achemistry.chemical_compoundPlasmaA-vitamiini2.1 Biological and endogenous factorsMicrophthalmosPrealbuminCRYSTAL-STRUCTUREAetiologyBase Pairinglcsh:QH301-705.5Sequence DeletionPediatricwhole genome sequencingVITAMIN-A-DEFICIENCYANOPHTHALMIAPenetrancePedigreemedicine.anatomical_structurePhenotypeFemalemedicine.medical_specialtyGenotypeENDOPLASMIC-RETICULUMGenes RecessiveMETABOLISMBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesDogscanine geneticsInternal medicinePlacentaRETINOL-BINDING-PROTEINGeneticsmedicineAnimalsHumansRecessiveMALFORMATIONSBIOCHEMICAL BASISAmino Acid SequenceAlleleEye Disease and Disorders of VisionNutritiongenome-wide association study030102 biochemistry & molecular biologywestern blottingMUTATIONSta1184RBP4maternal inheritancemedicine.diseaseRetinol-Binding ProteinsRetinol binding proteinnuclear magnetic resonance030104 developmental biologyEndocrinologychemistryGeneslcsh:Biology (General)microphthalmiaGenetic LociHela Cells1182 Biochemistry cell and molecular biologyCongenital Structural Anomalies3111 BiomedicineBiochemistry and Cell BiologyDigestive DiseasesGenomic imprintingRetinol-Binding Proteins PlasmaHeLa Cells
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