Search results for "cellular"

showing 10 items of 6449 documents

Gut Microbiota Restricts NETosis in Acute Mesenteric Ischemia-Reperfusion Injury.

2020

Objective: Recruitment of neutrophils and formation of neutrophil extracellular traps (NETs) contribute to lethality in acute mesenteric infarction. To study the impact of the gut microbiota in acute mesenteric infarction, we used gnotobiotic mouse models to investigate whether gut commensals prime the reactivity of neutrophils towards formation of neutrophil extracellular traps (NETosis). Approach and Results: We applied a mesenteric ischemia-reperfusion (I/R) injury model to germ-free (GF) and colonized C57BL/6J mice. By intravital imaging, we quantified leukocyte adherence and NET formation in I/R-injured mesenteric venules. Colonization with gut microbiota or monocolonization with Esch…

0301 basic medicineMaleExtracellular TrapsMesenteric infarctionLipopolysaccharideNeutrophilsGut floraExtracellular Traps03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAcute mesenteric ischemiaVenulesmedicineCell AdhesionEscherichia coliLeukocytesAnimalsGerm-Free LifeLeukocyte RollingMesenteryCells CulturedMice Knockoutbiologybusiness.industryNeutrophil extracellular trapsbiology.organism_classificationmedicine.diseaseGastrointestinal MicrobiomeMice Inbred C57BLToll-Like Receptor 4Disease Models Animal030104 developmental biologychemistryNeutrophil Infiltration030220 oncology & carcinogenesisMesenteric IschemiaReperfusion InjuryImmunologyHost-Pathogen InteractionsFemaleCardiology and Cardiovascular MedicinebusinessReperfusion injuryBacillus subtilisSignal TransductionArteriosclerosis, thrombosis, and vascular biology
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Expression quantitative trait loci for PAX8 contributes to the prognosis of hepatocellular carcinoma

2017

Paired-box family member PAX8 encodes a transcription factor that has a role in cell differentiation and cell growth and may participate in the prognosis of hepatocellular carcinoma (HCC). By bioinformatics analysis, we identified several single nucleotide polymorphisms (SNPs) within a newly identified long non-coding RNA (lncRNA) AC016683.6 as expression quantitative trait loci (eQTLs) for PAX8. Hence, we hypothesized that PAX8eQTLs in lncRNA AC016683.6 may influence the HCC prognosis. We then performed a case-only study to assess the association between the two SNPs as well as the prognosis of HCC in 331 HBV-positive HCC patients without surgical treatment. Cox proportional hazard models …

0301 basic medicineMaleHeredityPaired BoxCancer Treatmentlcsh:MedicineBiochemistry0302 clinical medicineMathematical and Statistical TechniquesMedicine and Health Scienceslcsh:ScienceMultidisciplinaryPharmaceuticsLiver DiseasesLiver NeoplasmsMiddle AgedPrognosisNucleic acidsSurvival RateGenetic MappingOncology030220 oncology & carcinogenesisHepatocellular carcinomaPhysical SciencesRegression AnalysisFemaleLiver cancerStatistics (Mathematics)Research ArticleCarcinoma HepatocellularGenotypeQuantitative Trait LociSingle-nucleotide polymorphismVariant GenotypesGastroenterology and HepatologyResearch and Analysis MethodsCarcinomasPolymorphism Single Nucleotide03 medical and health sciencesPAX8 Transcription FactorProtein DomainsDrug TherapyDiagnostic MedicineGastrointestinal TumorsCarcinomamedicineGeneticsChemotherapyHumansGenetic Predisposition to DiseaseAlleleStatistical MethodsNon-coding RNASurvival rateSurvival analysisAllelesbusiness.industrylcsh:RCancers and NeoplasmsBiology and Life SciencesProteinsHepatocellular Carcinomamedicine.disease030104 developmental biologyExpression quantitative trait lociCancer researchLong non-coding RNAsRNAlcsh:QbusinessMathematicsPLoS ONE
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Generation of a disease-specific iPS cell line derived from a patient with Charcot-Marie-Tooth type 2K lacking functional GDAP1 gene

2016

Human CMT2-FiPS4F1 cell line was generated from fibroblasts of a patient with Charcot-Marie-Tooth disease harbouring the following mutations in the GDAP1 gene in heterozygosis: p.Q163X/p.T288NfsX3. This patient did not present mutations in the PM22, MPZ or GJB genes. Human reprogramming factors OCT3/4, KLF4, SOX2 and C-MYC were delivered using a non-integrative methodology that involves the use of Sendai virus.

0301 basic medicineMaleHeterozygoteCellular differentiationCèl·lulesDNA Mutational AnalysisGenetic VectorsInduced Pluripotent Stem CellsKaryotypeNerve Tissue ProteinsBiologyPolymorphism Single NucleotideSendai virusCell Line03 medical and health sciencesKruppel-Like Factor 4stomatognathic systemCharcot-Marie-Tooth DiseaseHumansInduced pluripotent stem cellGeneTranscription factorMedicine(all)GeneticsBase SequenceHeterozygote advantageCell DifferentiationCell BiologyGeneral MedicineFibroblastsbiology.organism_classificationCellular ReprogrammingSendai virus030104 developmental biologyMicroscopy FluorescenceKLF4embryonic structuresSistema nerviós MalaltiesReprogrammingDevelopmental BiologyTranscription Factors
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The Effect of a Novel c.820C>T (Arg274Trp) Mutation in the Mitofusin 2 Gene on Fibroblast Metabolism and Clinical Manifestation in a Patient

2017

Charcot-Marie-Tooth disease type 2A (CMT2A) is an autosomal dominant axonal peripheral neuropathy caused by mutations in the mitofusin 2 gene (MFN2). Mitofusin 2 is a GTPase protein present in the outer mitochondrial membrane and responsible for regulation of mitochondrial network architecture via the fusion of mitochondria. As that fusion process is known to be strongly dependent on the GTPase activity of mitofusin 2, it is postulated that the MFN2 mutation within the GTPase domain may lead to impaired GTPase activity, and in turn to mitochondrial dysfunction. The work described here has therefore sought to verify the effects of MFN2 mutation within its GTPase domain on mitochondrial and e…

0301 basic medicineMaleHydrolasesMutantMFN2lcsh:MedicineGTPaseMitochondrionmedicine.disease_causeEndoplasmic ReticulumBiochemistryGTP Phosphohydrolases0302 clinical medicineMental RetardationAnimal CellsCharcot-Marie-Tooth DiseaseMedicine and Health SciencesMissense mutationlcsh:ScienceEnergy-Producing OrganellesCells CulturedConnective Tissue CellsGeneticsMutationMultidisciplinarySecretory PathwayOrganic CompoundsMonosaccharidesTryptophanMitochondrial DNACell biologyMitochondriaEnzymesNucleic acidsChemistryNeurologyConnective TissueCell ProcessesPhysical SciencesCellular Structures and OrganellesCellular TypesAnatomyResearch ArticleForms of DNACarbohydratesMutation MissenseBiologyBioenergeticsArgininePolymorphism Single NucleotideMitochondrial Proteins03 medical and health sciencesMitofusin-2Young AdultmedicineGeneticsHumansEndoplasmic reticulumlcsh:ROrganic ChemistryChemical CompoundsBiology and Life SciencesProteinsCell BiologyDNAFibroblastsGuanosine Triphosphatase030104 developmental biologyBiological TissueGlucoseAmino Acid SubstitutionCase-Control StudiesMutationEnzymologylcsh:Q030217 neurology & neurosurgeryPLoS ONE
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Maternal inflammation has a profound effect on cortical interneuron development in a stage and subtype-specific manner

2018

AbstractSevere infections during pregnancy are one of the major risk factors for cognitive impairment in the offspring. It has been suggested that maternal inflammation leads to dysfunction of cortical GABAergic interneurons that in turn underlies cognitive impairment of the affected offspring. However, the evidence comes largely from studies of adult or mature brains and how the impairment of inhibitory circuits arises upon maternal inflammation is unknown. Here we show that maternal inflammation affects multiple steps of cortical GABAergic interneuron development, i.e., proliferation of precursor cells, migration and positioning of neuroblasts, as well as neuronal maturation. Importantly,…

0301 basic medicineMaleInterneuronOffspringNeurogenesisMothersInflammationBiologyInhibitory postsynaptic potentialArticle03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicineNeuroblastCell MovementInterneuronsPregnancyPrecursor cellmedicineAnimalsCognitive DysfunctionGABAergic NeuronsMolecular BiologyCell ProliferationCerebral CortexInflammationPregnancyCell growthNeurogenesisCognitionmedicine.diseaseMice Inbred C57BLPsychiatry and Mental health030104 developmental biologymedicine.anatomical_structurenervous systemPrenatal Exposure Delayed EffectsGABAergicFemalemedicine.symptomPsychiatric disordersNeuroscience030217 neurology & neurosurgeryNeuroscience
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Increased PD-1 Expression and Altered T Cell Repertoire Diversity Predict Mortality in Patients with Septic Shock: A Preliminary Study

2017

Sepsis causes impairment of innate and adaptive immunity by multiple mechanisms, including depletion of immune effector cells and T cell exhaustion. Although lymphocyte dysfunction is associated with increased mortality and potential reactivation of latent viral infection in patients with septic shock, the relation between viral reactivation and lymphocyte dysfunction is obscure. The objectives of this study were 1) to determine the relation of lymphocyte dysfunction to viral reactivation and mortality, and 2) to evaluate recovery of lymphocyte function during septic shock, including T cell receptor (TCR) diversity and the expression of programmed death 1 (PD-1). In 18 patients with septic …

0301 basic medicineMaleLymphocyteReceptor expressionProgrammed Cell Death 1 Receptorlcsh:MedicineCytomegalovirusGene ExpressionArtificial Gene Amplification and ExtensionPathology and Laboratory MedicineImmune ReceptorsBiochemistryPolymerase Chain ReactionMonocytesWhite Blood Cells0302 clinical medicineSpectrum Analysis TechniquesAnimal CellsT-Lymphocyte SubsetsMedicine and Health SciencesLymphocyteslcsh:ScienceAged 80 and overMultidisciplinaryImmune System ProteinsT CellsMiddle AgedAcquired immune systemFlow CytometryPrognosisShock Septicmedicine.anatomical_structurePhenotypeSpectrophotometryShock (circulatory)Cytomegalovirus InfectionsFemaleCytophotometrymedicine.symptomCellular TypesResearch ArticleSignal TransductionT cellImmune CellsImmunologyReceptors Antigen T-CellBiologyResearch and Analysis MethodsMicrobiologyImmunophenotypingSepsis03 medical and health sciencesImmune systemSigns and SymptomsDiagnostic MedicineSepsisVirologymedicineHumansMolecular Biology TechniquesMolecular BiologyAgedBlood CellsSeptic shocklcsh:RBiology and Life SciencesProteins030208 emergency & critical care medicineCell BiologyHLA-DR Antigensmedicine.diseaseViral ReplicationT Cell Receptors030104 developmental biologyCase-Control StudiesImmunologylcsh:QBiomarkersPLoS ONE
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Social stress during adolescence activates long-term microglia inflammation insult in reward processing nuclei

2018

The experience of social stress during adolescence is associated with higher vulnerability to drug use. Increases in the acquisition of cocaine self-administration, in the escalation of cocaine-seeking behavior, and in the conditioned rewarding effects of cocaine have been observed in rodents exposed to repeated social defeat (RSD). In addition, prolonged or severe stress induces a proinflammatory state with microglial activation and increased cytokine production. The aim of the present work was to describe the long-term effects induced by RSD during adolescence on the neuroinflammatory response and synaptic structure by evaluating different glial and neuronal markers. In addition to an inc…

0301 basic medicineMaleMacroglial CellsHippocampuslcsh:MedicineSocial SciencesCell CountPathology and Laboratory MedicineHippocampusSocial defeatMice0302 clinical medicineCocaineAnimal CellsConditioning PsychologicalMedicine and Health SciencesPsychologylcsh:ScienceImmune ResponseNeuronsMultidisciplinaryMicrogliaAnimal BehaviorBrainChemistrymedicine.anatomical_structureBehavioral PharmacologyAnimal SocialityPhysical SciencesMicrogliamedicine.symptomCellular TypesAnatomyResearch ArticleInfralimbic cortexImmunologyPsychological StressInflammationGlial CellsNucleus accumbensProinflammatory cytokine03 medical and health sciencesAlkaloidsSigns and SymptomsRewardDiagnostic MedicineRecreational Drug UseMental Health and PsychiatrymedicineAnimalsMicroglial CellsSocial stressPharmacologyInflammationBehaviorbusiness.industrylcsh:RChemical CompoundsBiology and Life SciencesCell Biology030104 developmental biologyAstrocytesCellular Neurosciencelcsh:QbusinessNeuroscienceZoology030217 neurology & neurosurgeryStress PsychologicalNeuroscience
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Odiparcil, a potential glycosaminoglycans clearance therapy in mucopolysaccharidosis VI—Evidence from in vitro and in vivo models

2020

International audience; Mucopolysaccharidoses are a class of lysosomal storage diseases, characterized by enzymatic deficiency in the degradation of specific glycosaminoglycans (GAG). Pathological accumulation of excess GAG leads to multiple clinical symptoms with systemic character, most severely affecting bones, muscles and connective tissues. Current therapies include periodic intravenous infusion of supplementary recombinant enzyme (Enzyme Replacement Therapy-ERT) or bone marrow transplantation. However, ERT has limited efficacy due to poor penetration in some organs and tissues. Here, we investigated the potential of the β-D-xyloside derivative odiparcil as an oral GAG clearance therap…

0301 basic medicineMaleMucopolysaccharidosis type VIRespiratory SystemAdministration OralGlycosaminoglycanRats Sprague-DawleyWhite Blood CellsMice0302 clinical medicineOral administrationAnimal CellsMedicine and Health SciencesGlycosidesCells CulturedConnective Tissue CellsGlycosaminoglycansMultidisciplinaryMucopolysaccharidosis VIChemistryChondroitin SulfatesQRMucopolysaccharidosis VIAnimal Models3. Good healthTracheamedicine.anatomical_structureExperimental Organism SystemsConnective Tissue[SDV.SP.PHARMA] Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyMedicineFemaleBiological CulturesCellular TypesAnatomyCellular Structures and OrganellesResearch Articlemedicine.medical_specialtyImmune CellsScienceImmunologyDermatan SulfateMouse ModelsIn Vitro TechniquesResearch and Analysis Methods03 medical and health sciencesModel OrganismsIn vivoInternal medicinemedicineAnimalsHumansBlood CellsCartilageBiology and Life SciencesEndothelial CellsKidneysCell BiologyRenal SystemFibroblastsCell CulturesIn vitroMice Mutant StrainsRatsMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyBiological TissueCartilageCell cultureAnimal Studies[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyCattleLysosomes030217 neurology & neurosurgery
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Oligodendrocytes support axonal transport and maintenance via exosome secretion

2020

Neurons extend long axons that require maintenance and are susceptible to degeneration. Long-term integrity of axons depends on intrinsic mechanisms including axonal transport and extrinsic support from adjacent glial cells. The mechanisms of support provided by myelinating oligodendrocytes to underlying axons are only partly understood. Oligodendrocytes release extracellular vesicles (EVs) with properties of exosomes, which upon delivery to neurons improve neuronal viability in vitro. Here, we show that oligodendroglial exosome secretion is impaired in 2 mouse mutants exhibiting secondary axonal degeneration due to oligodendrocyte-specific gene defects. Wild-type oligodendroglial exosomes …

0301 basic medicineMaleMutantHippocampusCentrifugationExosomesAxonal TransportHippocampusMass SpectrometryAnalytical ChemistryMiceMyelin0302 clinical medicineNerve FibersSpectrum Analysis TechniquesAnimal CellsMedicine and Health SciencesBiology (General)Myelin SheathNeuronsLiquid ChromatographyGeneral NeuroscienceChromatographic TechniquesBrainCell biologyChemistrySeparation ProcessesOligodendrogliamedicine.anatomical_structureCell ProcessesPhysical SciencesFemaleCellular TypesCellular Structures and OrganellesAnatomyGeneral Agricultural and Biological SciencesNeurogliaResearch ArticleSignal TransductionMaintenanceQH301-705.5Liquid Chromatography-Mass SpectrometryBiologyResearch and Analysis MethodsExosomeGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesExtracellular VesiclesmedicineAnimalsHumansSecretionVesiclesGeneral Immunology and MicrobiologyWild typeBiology and Life SciencesCell BiologyIn vitroAxonsMicrovesiclesMice Inbred C57BL030104 developmental biologyHEK293 Cellsnervous systemCellular NeuroscienceAxoplasmic transportNeuronUltracentrifugation030217 neurology & neurosurgeryNeuroscience
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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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