Search results for "-n"

showing 10 items of 5782 documents

CYP27A1, CYP24A1, and RXR-α Polymorphisms, Vitamin D, and Multiple Sclerosis: a Pilot Study.

2018

Multiple sclerosis (MS) is a neurodegenerative autoimmune disease resulting from a complex interaction of genetic and environmental factors. Hypovitaminosis D seems to contribute to MS susceptibility as both an environmental and a genetic risk factor. The aim of our study was to investigate the association of SNPs in CYP27A1, CYP24A1, and RXR- α genes, vitamin D status, and MS risk. We performed a nested case-control study on patients with multiple sclerosis and healthy controls. Serum 25(OH)D3 levels and genotyping of CYP27A1, CYP24A1, and RXR-α -SNPs were investigated both in MS patients and in healthy controls. Serum 25(OH)D3 levels were measured by a high-performance liquid chromatograp…

0301 basic medicineAdultMalemedicine.medical_specialtyMultiple SclerosisRXRSingle-nucleotide polymorphismPilot ProjectsPolymorphism Single Nucleotide03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineInternal medicineGenotypemedicineVitamin D and neurologyHumansVitamin DAlleleVitamin D3 24-HydroxylaseGenotypingAutoimmune disease25-Hydroxyvitamin D 2Retinoid X Receptor alphabusiness.industryMultiple sclerosisGeneral MedicineMiddle Agedmedicine.diseaseMinor allele frequencyCYP24A1030104 developmental biologyEndocrinologyCase-Control StudiesCYP27A1Cholestanetriol 26-MonooxygenaseFemalebusiness030217 neurology & neurosurgeryJournal of molecular neuroscience : MN
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Characterization of NO-Induced Nitrosative Status in Human Placenta from Pregnant Women with Gestational Diabetes Mellitus

2017

Dysregulation of NO production is implicated in pregnancy-related diseases, including gestational diabetes mellitus (GDM). The role of NO and its placental targets in GDM pregnancies has yet to be determined. S-Nitrosylation is the NO-derived posttranslational protein modification that can modulate biological functions by forming NO-derived complexes with longer half-life, termed S-nitrosothiol (SNO). Our aim was to examine the presence of endogenous S-nitrosylated proteins in cysteine residues in relation to antioxidant defense, apoptosis, and cellular signal transduction in placental tissue from control (n=8) and GDM (n=8) pregnancies. S-Nitrosylation was measured using the biotin-switch …

0301 basic medicineAgingendocrine system diseasesPlacentaNitric Oxide Synthase Type IIExpressionApoptosisBiochemistryBody Mass Index0302 clinical medicineNitric-oxidePregnancyMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3biologyCaspase 3lcsh:CytologyNitrosylationP38General MedicineCatalaseCaspase 9TrophoblastsGestational diabetesmedicine.anatomical_structureCatalase030220 oncology & carcinogenesisFemaleResearch ArticleAdultmedicine.medical_specialtyArticle SubjectNitrosationNitric OxidePathophysiology03 medical and health sciencesErk1/2Internal medicinePlacentamedicineHumanslcsh:QH573-671Protein kinase BPregnancyFetusNitratesS-NitrosothiolsCesarean SectionCell BiologyPeroxiredoxinsmedicine.diseaseProtein s-nitrosylationDiabetes Gestational030104 developmental biologyEndocrinologyOxidative stressCase-Control Studiesbiology.proteinPeroxiredoxinProto-Oncogene Proteins c-aktOxidative Medicine and Cellular Longevity
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A novel microglial subset plays a key role in myelinogenesis in developing brain.

2017

Microglia are resident macrophages of the central nervous system that contribute to homeostasis and neuroinflammation. Although known to play an important role in brain development, their exact function has not been fully described. Here, we show that in contrast to healthy adult and inflammation-activated cells, neonatal microglia show a unique myelinogenic and neurogenic phenotype. A CD11c(+) microglial subset that predominates in primary myelinating areas of the developing brain expresses genes for neuronal and glial survival, migration, and differentiation. These cells are the major source of insulin-like growth factor 1, and its selective depletion from CD11c(+) microglia leads to impa…

0301 basic medicineAgingmedicine.medical_treatmentNews & ViewsInsulin-Like Growth Factor IMyelin SheathCell AggregationNeural PlateMicrogliaACTIVATED MICROGLIAGeneral NeuroscienceExperimental autoimmune encephalomyelitisNeurogenesisIGF1BrainGene Expression Regulation DevelopmentalADULT BRAINUp-RegulationALZHEIMERS-DISEASEmedicine.anatomical_structureEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITISMyelinogenesisGROWTHFemaleMicrogliaCNSEncephalomyelitis Autoimmune ExperimentalNeurogenesisCentral nervous systemCD11cBiologyGeneral Biochemistry Genetics and Molecular BiologyDEPENDENT MANNER03 medical and health sciencesmedicinePOSTNATAL-DEVELOPMENTAnimalsMolecular BiologyNeuroinflammationGeneral Immunology and MicrobiologyCD11cGrowth factorGene Expression ProfilingCENTRAL-NERVOUS-SYSTEMmedicine.diseaseGALECTIN-1CD11c AntigenMice Inbred C57BL030104 developmental biologynervous systemAnimals NewbornImmunologymyelinogenesisNeuroscienceBiomarkersThe EMBO journal
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CD36 gene polymorphism is associated with Alzheimer's disease.

2017

IF 3.112; International audience; CD36 gene encodes a membrane glycoprotein (type B scavenger receptor) present on the surface of many types of cells and having multiple cellular functions ranging from angiogenesis to gustatory perception of fatty acids. Using a case control genetic association approach we have analyzed selected single nucleotide polymorphisms (SNP's) in a total of 859 patients with Alzheimer's disease (AD) and controls and have identified the allele A in rs3211892 polymorphism of CD36 gene as significantly increasing the risk of AD. Additionally we have investigated, in the same sample of control subjects and patients, SNP's in ApoE gene and confirmed that the previously i…

0301 basic medicineApolipoprotein EMESH : Oxidative StressCD36 AntigensMaleMESH : Polymorphism GeneticCD36MESH : AgedMESH : Alzheimer DiseaseMESH : GenotypeBiochemistryGeneMESH: Genotype0302 clinical medicineMESH: CholesterolMESH : FemaleMESH : CholesterolGeneticsMESH: AgedMESH: Oxidative StressbiologyMESH: Polymorphism Single NucleotideMESH : Polymorphism Single NucleotideMESH: Genetic Predisposition to DiseaseGeneral Medicine3. Good healthMESH : Antigens CD36CholesterolInterleukin 18FemaleApoEGenotypeMESH : MaleSingle-nucleotide polymorphismPolymorphism Single NucleotideMMSEAssociation03 medical and health sciencesAlzheimer DiseaseMESH: Polymorphism GeneticSNPHumansGenetic Predisposition to Disease[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyAllelePolymorphism[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyGenetic associationAgedPolymorphism GeneticMESH: HumansMESH: Antigens CD36MESH : HumansMESH: MaleOxidative Stress030104 developmental biologybiology.proteinMESH : Genetic Predisposition to DiseaseGene polymorphismCD36MESH: Female030217 neurology & neurosurgeryMESH: Alzheimer Disease
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Altered gastrointestinal motility in an animal model of Lesch-Nyhan disease.

2018

Mutations in the HGPRT1 gene, which encodes hypoxanthine-guanine phosphoribosyltransferase (HGprt), housekeeping enzyme responsible for recycling purines, lead to Lesch-Nyhan disease (LND). Clinical expression of LND indicates that HGprt deficiency has adverse effects on gastrointestinal motility. Therefore, we aimed to evaluate intestinal motility in HGprt knockout mice (HGprt(−)). Spontaneous and neurally evoked mechanical activity was recorded in vitro as changes in isometric tension in circular muscle strips of distal colon. HGprt(−) tissues showed a lower in amplitude spontaneous activity and atropine-sensitivity neural contraction compared to control mice. The responses to carbachol a…

0301 basic medicineAtropineMaleHypoxanthine PhosphoribosyltransferaseLesch-Nyhan SyndromeDopaminemedicine.disease_causeSettore BIO/09 - FisiologiaLesch-NyhanMice0302 clinical medicineEnzyme InhibitorsEvoked PotentialsMyenteric plexusHGprt deficient miceNeurotransmitter AgentsBrainNG-Nitroarginine Methyl EsterKnockout mouseCytokinesAcetylcholinemedicine.drugmedicine.medical_specialtyCarbacholTyrosine 3-MonooxygenaseColonMotilityMice TransgenicIn Vitro TechniquesEndocrine and Autonomic SystemArticleContractility03 medical and health sciencesCellular and Molecular NeuroscienceDopamineInternal medicinemedicineAnimalsCytokineEndocrine and Autonomic Systemsbusiness.industryMuscle SmoothBenzazepinesMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyGene Expression RegulationHGprt enzymeFaceOxidative streCarbacholNeurology (clinical)Lipid PeroxidationbusinessGastrointestinal MotilityReactive Oxygen Species030217 neurology & neurosurgeryOxidative stressAutonomic neuroscience : basicclinical
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The genetic prehistory of the Baltic Sea region

2018

Correction: Nature communications 9 (2018), art. no. 1494 doi:10.1038/s41467-018-03872-y While the series of events that shaped the transition between foraging societies and food producers are well described for Central and Southern Europe, genetic evidence from Northern Europe surrounding the Baltic Sea is still sparse. Here, we report genome-wide DNA data from 38 ancient North Europeans ranging from similar to 9500 to 2200 years before present. Our analysis provides genetic evidence that hunter-gatherers settled Scandinavia via two routes. We reveal that the first Scandinavian farmers derive their ancestry from Anatolia 1000 years earlier than previously demonstrated. The range of Mesolit…

0301 basic medicineBaltic StatesSteppeRange (biology)Population DynamicsDIVERSITYGeneral Physics and Astronomy615 History and ArchaeologyStone Age0302 clinical medicinelcsh:ScienceHistory AncientAncient DNA ; Baltic Sea region ; Stone AgeTransients and MigrantsGENOMES SUGGESTMultidisciplinarygeography.geographical_feature_categoryFossilsCHROMOSOME HAPLOGROUP-NQ1184 Genetics developmental biology physiologyAgriculturehumanitiesADMIXTUREpopulation characteristicsgeographic locationsGene FlowEUROPESciencePastoralismScandinavian and Nordic CountriesEURASIASEQUENCEGeneral Biochemistry Genetics and Molecular BiologyWhite PeoplePrehistory03 medical and health sciencesANCIENT DNAHumans14. Life underwaterAuthor CorrectionMesolithicgeographyGenome HumanGeneral ChemistryBefore PresentArchaeologyHUNTER-GATHERERS030104 developmental biologyAncient DNAlcsh:QEARLY FARMERS030217 neurology & neurosurgeryNature Communications
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Exploration of Fas S-Nitrosylation by the Biotin Switch Assay

2017

International audience; S-nitrosylation is the covalent attachment of nitric oxide radical to the thiol side chain of cysteine. The death receptor Fas/CD95 can be S-nitrosylated in cancer cell lines by NO donors or iNOS activation. This posttranslational modification (PTM) induces Fas aggregation into lipid rafts and enhances FasL-mediated signaling and apoptosis. In this report, we describe the detection of Fas S-nitrosylation by the most commonly used method, the biotin switch assay (BSA) technique, that allows the detection of this very labile covalent modification in cells or tissues. Briefly, this technique relies on the ability of ascorbate to reduce the covalent bond between the NO r…

0301 basic medicineBiotin switch assaybiologyChemistryNitrosylationNeutrAvidinNitric oxideS-NitrosylationFas receptorGlyceryl trinitrate3. Good health03 medical and health sciences030104 developmental biology0302 clinical medicineBiochemistryApoptosisCovalent bondFas S030220 oncology & carcinogenesisBiotinylationbiology.protein[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyLipid raft[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCysteine
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The role of CD40 and CD40L in bone mineral density and in osteoporosis risk: A genetic and functional study.

2015

Compelling data are revealing that the CD40/CD40L system is involved in bone metabolism. Furthermore, we have previously demonstrated that polymorphisms in both genes are associated with bone phenotypes. The aim of this study is to further characterize this association and to identify the causal functional mechanism. We conducted an association study of BMD with 15 SNPs in CD40/CD40L genes in a population of 779 women. In addition, we assessed the functionality of this association through the study of the allele-dependent expression of CD40 and CD40L in peripheral blood leukocytes (PBLs) and in human osteoblasts (OBs) obtained from bone explants by qPCR and by sequencing. When an allelic im…

0301 basic medicineBone densityTranscription GeneticPhysiologyEndocrinology Diabetes and MetabolismInheritance PatternsCohort Studies0302 clinical medicineBone DensityGenes ReporterRisk FactorsPromoter Regions GeneticGeneticseducation.field_of_studyhemic and immune systemsMethylationMiddle AgedPhenotypeDNA methylationFemalemusculoskeletal diseasesmedicine.medical_specialtyHistologyPopulationCD40 Ligand030209 endocrinology & metabolismSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideBone and Bones03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseAlleleCD40 AntigenseducationAllelesGenetic Association StudiesGenetic associationModels GeneticOsteoprotegerinPromoterDNA Methylation030104 developmental biologyEndocrinologySpainOsteoporosisCpG IslandsBone
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Haploinsufficiency of the Primary Familial Brain Calcification Gene SLC20A2 Mediated by Disruption of a Regulatory Element

2020

OBJECTIVE Primary familial brain calcification (PFBC) is a rare cerebral microvascular calcifying disorder with diverse neuropsychiatric expression. Five genes were reported as PFBC causative when carrying pathogenic variants. Haploinsufficiency of SLC20A2, which encodes an inorganic phosphate importer, is a major cause of autosomal-dominant PFBC. However, PFBC remains genetically unexplained in a proportion of patients, suggesting the existence of additional genes or cryptic mutations. We analyzed exome sequencing data of 71 unrelated, genetically unexplained PFBC patients with the aim to detect copy number variations that may disrupt the expression of core PFBC-causing genes. METHODS Afte…

0301 basic medicineBrain DiseasesDNA Copy Number VariationsSodium-Phosphate Cotransporter Proteins Type IIIHEK 293 cellsBrainHaploinsufficiencyBiologyMolecular biologyReverse transcriptase03 medical and health sciencesHEK293 Cells030104 developmental biology0302 clinical medicineNeurologyMutationHumansNeurology (clinical)Copy-number variationAlleleHaploinsufficiencyEnhancerGene030217 neurology & neurosurgeryExome sequencingMovement Disorders
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The iNOS Activity During an Immune Response Controls the CNS Pathology in Experimental Autoimmune Encephalomyelitis

2019

Inducible nitric oxide synthase (iNOS) plays a critical role in the regulation of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). Previous studies have shown that iNOS plays pathogenic as well as regulatory roles in MS and EAE. However, how does iNOS alters the pathophysiology of the central nervous system (CNS) in neuronal autoimmunity is not clearly understood. In the present work, we show that treatment of mice with L-NAME, an iNOS inhibitor, during the antigen-priming phase primarily alters brain pathology, while in the subsequent effector phase of the immune response, the spinal cord is involved. Inhibition of iNOS during the priming phase of the immune res…

0301 basic medicineCD4-Positive T-LymphocytesPathologyexperimental autoimmune encephalomyelitisNitric Oxide Synthase Type IIApoptosismedicine.disease_causeAutoimmunityMice0302 clinical medicineImmunology and AllergyEnzyme InhibitorsOriginal ResearchMice KnockoutbiologyExperimental autoimmune encephalomyelitisautoimmunityCell DifferentiationNitric oxide synthaseOligodendrogliamedicine.anatomical_structureNG-Nitroarginine Methyl EsterIntegrin alpha Mlcsh:Immunologic diseases. Allergymedicine.medical_specialtyEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisLymphoid TissueCentral nervous systemImmunology03 medical and health sciencesInterferon-gammaImmune systemmedicineAnimalsHumansNOS2−/− neuroinflammationNeuroinflammationbusiness.industryMultiple sclerosisinducible nitric oxide synthaseDendritic Cellsmedicine.diseasecentral nervous systemMice Inbred C57BL030104 developmental biologybiology.proteinbusinesslcsh:RC581-607030215 immunologyGranulocytesFrontiers in Immunology
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