Search results for "Tos"

showing 10 items of 12217 documents

Characterization of the Clinical and Immunologic Phenotype and Management of 157 Individuals with 56 Distinct Heterozygous NFKB1 Mutations

2020

Contains fulltext : 229571.pdf (Publisher’s version ) (Closed access) BACKGROUND: An increasing number of NFKB1 variants are being identified in patients with heterogeneous immunologic phenotypes. OBJECTIVE: To characterize the clinical and cellular phenotype as well as the management of patients with heterozygous NFKB1 mutations. METHODS: In a worldwide collaborative effort, we evaluated 231 individuals harboring 105 distinct heterozygous NFKB1 variants. To provide evidence for pathogenicity, each variant was assessed in silico; in addition, 32 variants were assessed by functional in vitro testing of nuclear factor of kappa light polypeptide gene enhancer in B cells (NF-κB) signaling. RESU…

0301 basic medicineMaleNF-KAPPA-BMedizinlnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]Fluorescent Antibody TechniqueAutoimmunityDiseaseNUCLEAR-FACTORKaplan-Meier Estimatemedicine.disease_causeHypogammaglobulinemia0302 clinical medicineNFKB1 variants and mutations; autosomal dominant inheritance; common variable immunodeficiency; reduced penetrance; variable expressivityHDE PEDImmunology and Allergyvariants and mutationsNF-κB1-related phenotypeImmunodeficiencyIMMUNODEFICIENCY*NF-?B1-related phenotypeNFKB1 variants and mutations1184 Genetics developmental biology physiologycommon variable immunodeficiencyDisease ManagementMiddle AgedNF-kappa B1-related phenotypereduced penetrancePrognosisPenetranceImmunohistochemistryMagnetic Resonance Imaging3. Good healthPhenotypeNFKB1 variant*NFKB1 variant*common variable immunodeficiencyFemaleHaploinsufficiency*reduced penetranceNFKB1 mutationAdultHeterozygote*NFKB1 mutationImmunologyHAPLOINSUFFICIENCYArticle03 medical and health sciencesvariable expressivityautosomal dominantmedicineHumansGenetic Predisposition to DiseaseGenetic Association StudiesAgedbusiness.industryCommon variable immunodeficiencyNF-kappa B p50 SubunitNF-KAPPA-B1Immune dysregulationmedicine.diseaseautosomal dominant inheritance030104 developmental biologyBiological Variation PopulationImmunologyCELLSMutation*autosomal dominantPrimary immunodeficiency3111 BiomedicinebusinessTomography X-Ray ComputedBiomarkers030215 immunology
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Marathon Race Affects Neutrophil Surface Molecules: Role of Inflammatory Mediators

2016

The fatigue induced by marathon races was observed in terms of inflammatory and immunological outcomes. Neutrophil survival and activation are essential for inflammation resolution and contributes directly to the pathogenesis of many infectious and inflammatory conditions. The aim of this study was to investigate the effect of marathon races on surface molecules related to neutrophil adhesion and extrinsic apoptosis pathway and its association with inflammatory markers. We evaluated 23 trained male runners at the Sao Paulo International Marathon 2013. The following components were measured: hematological and inflammatory mediators, muscle damage markers, and neutrophil function. The maratho…

0301 basic medicineMaleNeutrophilsPhysiologylcsh:MedicineApoptosisDNA fragmentationPathology and Laboratory MedicineBiochemistryNeutrophil ActivationRunningPathogenesischemistry.chemical_compoundWhite Blood CellsLeukocyte Count0302 clinical medicineAnimal CellsImmune PhysiologyMedicine and Health Scienceslcsh:ScienceImmune ResponseInnate Immune SystemMultidisciplinarybiologyCell DeathInterleukinHematologyFas receptorBody FluidsNucleic acidsBloodHematocritCell ProcessesAntigens SurfaceCytokinesTumor necrosis factor alphamedicine.symptomCellular TypesAnatomyInflammation MediatorsResearch ArticleAdultCell SurvivalImmune CellseducationImmunologyInflammation03 medical and health sciencesSigns and SymptomsDiagnostic MedicineLactate dehydrogenasemedicineGeneticsHumansLeukocyte RollingHemoglobinInflammationBlood Cellsbusiness.industrylcsh:RBiology and Life SciencesProteins030229 sport sciencesCell BiologyDNAMolecular DevelopmentBlood Counts030104 developmental biologychemistryApoptosisImmune SystemImmunologybiology.proteinCreatine kinaselcsh:Qbusinesshuman activitiesDevelopmental BiologyPLoS ONE
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A Mediterranean Diet Rich in Extra-Virgin Olive Oil Is Associated with a Reduced Prevalence of Nonalcoholic Fatty Liver Disease in Older Individuals …

2019

Los autores de este trabajo forman parte de PREDIMED study investigators. Son los siguientes: Principales: Xavier Pintó, Marta Fanlo-Maresma, Emili Corbella, Xavier Corbella, M Teresa Mitjavila, Juan J Moreno, Rosa Casas, Ramon Estruch, Dolores Corella, Mònica Bulló, Miguel Ruiz-Canela, Olga Castañer, J Alfredo Martinez, Emilio Ros, PREDIMED Study Investigators. PREDIMED Study investigators: Estruch R, Martínez-González MA, Corella D, Fitó M, Ros E, Salas-Salvadó J, Arós F, Aldamiz-Echevarría M, Alonso-Gómez AM, Berjón J, Forga L, Gállego J, García-Layana A, Larrauri A, Portu-Zapirain J, Timiraos J, Ros E, Covas MI, Martínez-González MA, Salas-Salvadó J, Pérez-Heras A, Serra-Mir M, Pi-Sunye…

0301 basic medicineMalePREDIMEDMedicine (miscellaneous)030209 endocrinology & metabolismHepatic steatosisnutsDiet Mediterranean03 medical and health sciences0302 clinical medicineNon-alcoholic Fatty Liver DiseaseRisk FactorsMediterranean dietPrevalenceHumansDiet Fat-RestrictedDietary fatAged030109 nutrition & dieteticsNutrition and DieteticsPhilosophyMiddle AgedPredimedMagnetic Resonance ImagingPrimary PreventionEditorialLiverCardiovascular DiseasesSpainFemaleHumanitiesOlive oilOlive oilDietary fat
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Combined effects of the PNPLA3 rs738409, TM6SF2 rs58542926, and MBOAT7 rs641738 variants on NAFLD severity: a multicenter biopsy-based study.

2016

The PNPLA3 p.I148M, TM6SF2 p.E167K, and MBOAT7 rs641738 variants represent genetic risk factors for nonalcoholic fatty liver disease (NAFLD). Here we investigate if these polymorphisms modulate both steatosis and fibrosis in patients with NAFLD. We recruited 515 patients with NAFLD (age 16–88 years, 280 female patients). Liver biopsies were performed in 320 patients. PCR-based assays were used to genotype the PNPLA3, TM6SF2, and MBOAT7 variants. Carriers of the PNPLA3 and TM6SF2 risk alleles showed increased serum aspartate aminotransferase and alanine transaminase activities (P 0.05). The MBOAT7 variant was solely associated with increased fibrosis (P = 0.046). In the multivariate model, v…

0301 basic medicineMalePathologyBiopsyBiochemistryGastroenterologySeverity of Illness Index0302 clinical medicineEndocrinologyFibrosisNon-alcoholic Fatty Liver DiseaseGenotypeNonalcoholic fatty liver diseaseAged 80 and overeducation.field_of_studybiologyFatty liverMiddle AgedLiver030211 gastroenterology & hepatologyFemaleAdultmedicine.medical_specialtyAdolescentGenotypePolymorphism Single Nucleotide03 medical and health sciencesYoung AdultInternal medicinemedicineHumansAdiponutrinGenetic Predisposition to DiseaseeducationAllelesGenetic Association StudiesAgedbusiness.industryMembrane ProteinsCell BiologyLipasemedicine.diseaseFibrosisFatty Liver030104 developmental biologyAlanine transaminasebiology.proteinSteatosisbusinessPatient-Oriented and Epidemiological ResearchAcyltransferasesTM6SF2Journal of lipid research
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Dietary salt promotes ischemic brain injury and is associated with parenchymal migrasome formation

2018

Sodium chloride promotes vascular fibrosis, arterial hypertension, pro-inflammatory immune cell polarization and endothelial dysfunction, all of which might influence outcomes following stroke. But despite enormous translational relevance, the functional importance of sodium chloride in the pathophysiology of acute ischemic stroke is still unclear. In the current study, we show that high-salt diet leads to significantly worse functional outcomes, increased infarct volumes, and a loss of astrocytes and cortical neurons in acute ischemic stroke. While analyzing the underlying pathologic processes, we identified the migrasome as a novel, sodium chloride-driven pathomechanism in acute ischemic …

0301 basic medicineMalePathologyMacroglial CellsSodium ChlorideVascular MedicineBrain IschemiaMice0302 clinical medicineCytosolAnimal CellsMedicine and Health SciencesMedicineEndothelial dysfunctionStrokeNeuronsCerebral CortexCerebral IschemiaMultidisciplinaryQRPathophysiologyStrokeChemistryNeurologyPhysical SciencesImmunohistochemistryMedicineCellular Structures and OrganellesCellular TypesIntracellularResearch Articlemedicine.medical_specialtyScienceCerebrovascular DiseasesGlial Cells03 medical and health sciencesImmune systemIn vivoParenchymaAnimalscardiovascular diseasesVesiclesSodium Chloride DietaryMicroglial CellsNutritionIschemic StrokeOrganellesbusiness.industryChemical CompoundsBiology and Life SciencesCell Biologymedicine.diseaseDiet030104 developmental biologyCellular NeuroscienceAstrocytesBrain InjuriesSaltsbusiness030217 neurology & neurosurgeryNeurosciencePLoS ONE
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INTU -related oral-facial-digital syndrome type VI: a confirmatory report

2018

Oral-facial-digital (OFD) syndromes are a subgroup of ciliopathies distinguished by the co-occurrence of hamartomas and/or multiple frenula of the oral region and digital anomalies. Several clinical forms of OFD syndromes are distinguished by their associated anomalies and/or inheritance patterns, and at least 20 genetic types of OFD syndromes have been delineated. We describe here a child with preaxial and postaxial polydactyly, lingual hamartoma, a congenital heart defect, delayed development and cerebellar peduncles displaying the molar tooth sign. Whole-exome sequencing and SNP array identified compound heterozygous variants in the INTU gene, which encodes a protein involved in the posi…

0301 basic medicineMalePathologymedicine.medical_specialtyCiliary basal bodyCompound heterozygosityCiliopathies03 medical and health sciencesIntraflagellar transportCPLANEGeneticsmedicineInheritance PatternsHamartomaHumansINTU[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsGenetics (clinical)business.industryInfant NewbornInfantMembrane ProteinsOrofaciodigital Syndromesmedicine.diseasePhenotypeMagnetic Resonance ImagingCytoskeletal Proteins030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsNGSoral-facial-digital syndromebusinessSNP array
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CAMKIIγ suppresses an efferocytosis pathway in macrophages and promotes atherosclerotic plaque necrosis

2017

Atherosclerosis is the underlying etiology of cardiovascular disease, the leading cause of death worldwide. Atherosclerosis is a heterogeneous disease in which only a small fraction of lesions lead to heart attack, stroke, or sudden cardiac death. A distinct type of plaque containing large necrotic cores with thin fibrous caps often precipitates these acute events. Here, we show that Ca2+/calmodulin-dependent protein kinase gamma (CaMKII gamma) in macrophages plays a major role in the development of necrotic, thin-capped plaques. Macrophages in necrotic and symptomatic atherosclerotic plaques in humans as well as advanced atherosclerotic lesions in mice demonstrated activation of CaMKII. We…

0301 basic medicineMalePathologymedicine.medical_specialtyPhagocytosisGene ExpressionInflammationApoptosisMice TransgenicBiologyPHAGOCYTOSISLIPID MEDIATORS03 medical and health sciencesNecrosisENDOPLASMIC-RETICULUM STRESSINFLAMMATIONCa2+/calmodulin-dependent protein kinaseC/EBP HOMOLOGOUS PROTEINmedicineMacrophageAnimalsHumansKINASE-IILiver X receptorEfferocytosisCells CulturedLiver X ReceptorsAPOE-DEFICIENT MICEc-Mer Tyrosine KinaseATF6MacrophagesAPOPTOTIC CELL ACCUMULATIONGeneral MedicineMERTKAtherosclerosisPlaque AtheroscleroticActivating Transcription Factor 6Enzyme ActivationMice Inbred C57BL030104 developmental biologyRESOLUTIONmedicine.symptomCalcium-Calmodulin-Dependent Protein Kinase Type 2LIVER-X-RECEPTORResearch ArticleSignal TransductionJournal of Clinical Investigation
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Autosomal recessive variations of TBX6 , from congenital scoliosis to spondylocostal dysostosis

2017

International audience; Proximal 16p11.2 microdeletions are recurrent microdeletions with an overall prevalence of 0.03%. In patients with segmentation defects of the vertebra (SDV), a burden of this microdeletion was observed with TBX6 as a candidate gene for SDV. In a published cohort of patients with congenital scoliosis (CS), TBX6 haploinsufficiency was compound heterozygous with a common haplotype. Besides, a single three-generation family with spondylocostal dysostosis (SCD) was reported with a heterozygous stop-loss of TBX6. These observations questioned both on the inheritance mode and on the variable expressivity associated with TBX6-associated SDV. Based on a national recruitment …

0301 basic medicineMalePediatricsmedicine.medical_specialtyCandidate geneGenotypeScoliosis030105 genetics & heredityCompound heterozygosity03 medical and health sciences[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyGeneticsmedicineInheritance ModeMissense mutationHumansAbnormalities MultipleGenetic Predisposition to DiseaseChildGenetics (clinical)GeneticsHernia Diaphragmaticbusiness.industryHaplotypeInfantmedicine.diseaseSpondylocostal dysostosisSpine3. Good healthPedigree030104 developmental biologyHaplotypesScoliosisChild PreschoolMutationFemalebusinessHaploinsufficiencyT-Box Domain Proteins[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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NKCC1-Mediated GABAergic Signaling Promotes Postnatal Cell Death in Neocortical Cajal-Retzius Cells.

2016

During early development, a substantial proportion of central neurons undergoes programmed cell death. This activity-dependent process is essential for the proper structural and functional development of the brain. To uncover cell type-specific differences in the regulation of neuronal survival versus apoptosis, we studied activity-regulated cell death in Cajal-Retzius neurons (CRNs) and the overall neuronal population in the developing mouse cerebral cortex. CRNs in the upper neocortical layer represent an early-born neuronal population, which is important for cortical development and largely disappears by apoptosis during neonatal stages. In contrast to the overall neuronal population, ac…

0301 basic medicineMaleProgrammed cell deathCognitive NeuroscienceApoptosisNeocortexReceptors Cell SurfaceBiologygamma-Aminobutyric acid03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicinemedicineAnimalsLectins C-TypeGABAergic NeuronsCells Culturedgamma-Aminobutyric AcidMice KnockoutNeocortexGABAA receptorDepolarizationInterstitial Cells of CajalReceptors GABA-AMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurenervous systemAnimals NewbornCerebral cortexApoptosisFemaleSignal transductionNeuroscience030217 neurology & neurosurgerymedicine.drugSignal TransductionCerebral cortex (New York, N.Y. : 1991)
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Androgen-inducible gene 1 increases the ER Ca(2+) content and cell death susceptibility against oxidative stress.

2016

Androgen-induced gene 1 (AIG1) is a transmembrane protein implicated with survival (its expression level was shown to correlate with the survival of patients suffering from hepatocellular carcinoma) and Ca(2+) signaling (over-expression of AIG1 increased transcription mediated by the Ca(2+)-dependent nuclear factor of activated T cells). We aimed to shed light on this less-studied protein and investigated its tissue expression, genomic organization, intracellular localization and membrane topology as well as its effects on cell death susceptibility and the Ca(2+) content of the endoplasmic reticulum. Immunoblotting of mouse tissues demonstrated highest expression of AIG1 in the liver, lung …

0301 basic medicineMaleProgrammed cell deathGene ExpressionBiologyEndoplasmic Reticulum03 medical and health sciencesMiceProtein DomainsGene expressionGeneticsAnimalsSex CharacteristicsCell DeathEndoplasmic reticulumMembrane ProteinsGeneral MedicineEmbryo MammalianMolecular biologyTransmembrane proteinCell biologyMice Inbred C57BLTransmembrane domainCytosolAlternative SplicingOxidative Stress030104 developmental biologyMembrane proteinOrgan SpecificityMembrane topologyCalciumFemaleGene
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