Search results for "Inflammation."

showing 10 items of 2627 documents

TLR4 elimination prevents synaptic and myelin alterations and long-term cognitive dysfunctions in adolescent mice with intermittent ethanol treatment.

2015

The adolescent brain undergoes important dynamic and plastic cell changes, including overproduction of axons and synapses, followed by rapid pruning along with ongoing axon myelination. These developmental changes make the adolescent brain particularly vulnerable to neurotoxic and behavioral effects of alcohol. Although the mechanisms of these effects are largely unknown, we demonstrated that ethanol by activating innate immune receptors toll-like receptor 4 (TLR4), induces neuroinflammation and brain damage in adult mice. The present study aims to evaluate whether intermittent ethanol treatment in adolescence promotes TLR4-dependent pro-inflammatory processes, leading to myelin and synapti…

MAPK/ERK pathwaySynaptic dysfunctionImmunologyNitric Oxide Synthase Type IIBrain damageHMGB1Behavioral NeuroscienceMyelinMiceCognitionmedicineAnimalsTLR4AxonHMGB1 ProteinReceptorNeuroinflammationMyelin SheathMice KnockoutMitogen-Activated Protein Kinase KinasesbiologyBinge ethanol treatmentEthanolEndocrine and Autonomic SystemsNF-kappa BCentral Nervous System DepressantsMyelin alterationsAdolescenceToll-Like Receptor 4medicine.anatomical_structureCyclooxygenase 2SynapsesTLR4biology.proteinmedicine.symptomPsychologyCognition DisordersNeuroscienceCognitive behaviorAlcohol-Related DisordersMyelin ProteinsSignal TransductionBrain, behavior, and immunity
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MARKERS OF INFLAMMATION AND RISK OF VASCULAR EVENTS IN PATIENTS WITH NON-INSULIN DEPENDANT DIABETES

2006

MARKERS OF INFLAMMATION CARDIOVASCULAR RISK
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Serum Amyloid A Is Present in Human Saccular Intracranial Aneurysm Walls and Associates With Aneurysm Rupture

2021

AbstractSaccular intracranial aneurysm (sIA) rupture leads to a disabling subarachnoid hemorrhage. Chronic inflammation and lipid accumulation in the sIA wall contribute to wall degenerative remodeling that precedes its rupture. A better understanding of the pathobiological process is essential for improved future treatment of patients carrying sIAs. Serum amyloid A (SAA) is an acute-phase protein produced in response to acute and chronic inflammation and tissue damage. Here, we studied the presence and the potential role of SAA in 36 intraoperatively resected sIAs (16 unruptured and 20 ruptured), that had previously been studied by histology and immunohistochemistry. SAA was present in all…

MECHANISMPathologybiomarkkeritAneurysm Ruptured3124 Neurology and psychiatrychemistry.chemical_compoundverisuonitaudit0302 clinical medicineMedicineapolipoproteiinitSerum Amyloid A Protein0303 health sciencesbiologytulehdusaneurysmaINDUCTIONGeneral MedicineC-REACTIVE PROTEINSAANeurologyMyeloperoxidaseImmunohistochemistryInflammation Mediatorsmedicine.symptomSaccular intracranial aneurysmEXPRESSIONmedicine.medical_specialtySubarachnoid hemorrhagelipoproteiinitProstaglandinInflammationLDLPathology and Forensic MedicineLIPOPROTEINS03 medical and health sciencesCellular and Molecular NeuroscienceAneurysmHUMAN MAST-CELLSHumansSerum amyloid Akallonsisäinen aneurysma030304 developmental biologyInflammationSerum Amyloid A Proteinbusiness.industry3112 NeurosciencesIntracranial AneurysmCEREBRAL ANEURYSMS3126 Surgery anesthesiology intensive care radiologymedicine.diseaseAneurysmchemistryDENSITYbiology.proteinEndothelium Vascular3111 BiomedicineNeurology (clinical)business030217 neurology & neurosurgerySerum amyloid A
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Resveratrol: preventing properties against vascular alterations and ageing.

2005

International audience; Cardiovascular diseases are the leading cause of death in developed countries where the common pathological substrate underlying this process is atherosclerosis. Several new concepts have emerged in relation to mechanisms that contribute to the regulation of the vascular diseases and associated inflammatory effects. Recently, potential antioxidants (vitamin E, polyphenols) have received much attention as potential anti-atherosclerotic agents. Among the polyphenols with health benefic properties, resveratrol, a phytoalexin of grape, seem to be a good candidate protecting the vascular walls from oxidation, inflammation, platelet aggregation, and thrombus formation. In …

MESH : Oxidative StressAgingAntioxidantPlatelet AggregationArteriosclerosismedicine.medical_treatmentResveratrolPharmacologymedicine.disease_causeMuscle Smooth Vascularchemistry.chemical_compoundMESH : VasodilationMESH : Foam CellsMESH : Platelet AggregationStilbenesMESH : Cardiovascular DiseasesMESH : Macrophageschemistry.chemical_classificationNeovascularization PathologicPhytoalexinfood and beveragesVasodilationBiochemistryCardiovascular Diseasesmedicine.symptomBiotechnologyLipoproteinsInflammationHealth PromotionMESH : LipoproteinsBiologyMESH : StilbenesMESH : ArteriosclerosismedicineHumans[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyReactive oxygen speciesMechanism (biology)MacrophagesMESH : HumansMESH : Neovascularization PathologicMESH : Muscle Smooth VascularMESH : AgingOxidative StresschemistryAgeingResveratrolMESH : Health PromotionOxidative stressFood ScienceFoam Cells
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A follow-up study of a genome-wide association scan identifies a susceptibility locus for venous thrombosis on chromosome 6p24.1.

2010

International audience; To identify genetic susceptibility factors conferring increased risk of venous thrombosis (VT), we conducted a multistage study, following results of a previously published GWAS that failed to detect loci for developing VT. Using a collection of 5862 cases with VT and 7112 healthy controls, we identified the HIVEP1 locus on chromosome 6p24.1 as a susceptibility locus for VT. Indeed, the HIVEP1 rs169713C allele was associated with an increased risk for VT, with an odds ratio of 1.20 (95% confidence interval 1.13-1.27, p = 2.86 x 10(-9)). HIVEP1 codes for a protein that participates in the transcriptional regulation of inflammatory target genes by binding specific DNA …

MESH : Transcription Factors[SDV]Life Sciences [q-bio]Genome-wide association study030204 cardiovascular system & hematologyMESH : Chromosomes Human Pair 60302 clinical medicineGenetics(clinical)Genetics (clinical)GeneticsVenous Thrombosis0303 health sciencesMESH: Polymorphism Single NucleotideMESH : Polymorphism Single NucleotideMESH: Genetic Predisposition to DiseaseMESH: Follow-Up StudiesMESH: Transcription FactorsMESH : Venous ThrombosisMESH: Case-Control StudiesDNA-Binding ProteinsChromosomes Human Pair 6MESH : DNA-Binding ProteinsErratumMESH : Genome-Wide Association StudyMESH : Case-Control StudiesMESH: Chromosomes Human Pair 6Locus (genetics)BiologyPolymorphism Single NucleotideGenetic determinism03 medical and health sciencesReportGenetic predispositionGeneticsHumansGenetic Predisposition to DiseaseAlleleGene030304 developmental biologyMESH: Humans[ SDV ] Life Sciences [q-bio]MESH : Humanslinking inflammation protein atherothrombosis sequence riskCase-control studyChromosomeMESH : Follow-Up StudiesCase-Control StudiesMESH: Genome-Wide Association StudyMESH: Venous ThrombosisMESH : Genetic Predisposition to Disease030217 neurology & neurosurgeryMESH: DNA-Binding ProteinsFollow-Up StudiesGenome-Wide Association StudyTranscription Factors
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Bimodal Recovery Pattern in Human Skeletal Muscle Induced by Exhaustive Stretch-Shortening Cycle Exercise:

2007

Introduction/Purpose: Recovery of force and stretch reflex from exhaustive stretch-shortening cycle (SSC) exercise is usually bimodal, characterized as immediate exercise-induced performance reduction, with its quick recovery followed by a longer-lasting reduction in performance. A clear parallel exists between the respective changes in performance, neural activation, and metabolic or structural exercise-induced changes. This implies the existence of potential coupling between muscle failure and the induced neural adjustments that take place along its recovery. The present study was designed to explore the evidence of this coupling more thoroughly. Methods: H- and stretch reflexes were meas…

MESH: InflammationAdultMaleReflex Stretchmedicine.medical_specialty[SDV.MHEP.PHY] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]Physical Therapy Sports Therapy and RehabilitationInflammationSubstance PPhysical exerciseIsometric exerciseMESH: Bicycling03 medical and health scienceschemistry.chemical_compound0302 clinical medicineMESH: Muscle Stretching ExercisesInternal medicineMuscle Stretching Exercisesmedicine[SDV.MHEP.PHY]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]HumansOrthopedics and Sports MedicineMESH: Reflex Stretch[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Stretch reflexProstaglandin E2Muscle SkeletalExerciseComputingMilieux_MISCELLANEOUSInflammationMESH: Muscle SkeletalMESH: HumansChemistrySkeletal muscleMESH: Adult030229 sport sciencesAnatomyMESH: MaleBicyclingmedicine.anatomical_structureEndocrinologyMESH: Muscle FatigueMESH: ExerciseMuscle FatigueReflex[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]medicine.symptom030217 neurology & neurosurgerymedicine.drug
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Enhanced proinflammatory response to the Candida albicans gpi7 null mutant by murine cells.

2008

International audience; The Candida albicans gpi7/gpi7 null mutant strain (Deltagpi7), which is affected in glycosylphosphatidylinositol (GPI) anchor biosynthesis, showed a reduced virulence following systemic infection of C57BL/6 mice. In vitro production of TNF-alpha, IL-6 and IL-1beta by macrophages in response to Deltagpi7 cells was significantly increased as compared to control (wild type GPI7/GPI7 and revertant gpi7/GPI7) cells; this probably contributes to the enhanced recruitment of neutrophils to the peritoneal cavity in response to Deltagpi7 cells. Survival of knockout mice for Toll-like receptor (TLR) 2 and TLR4 following intravenous injection of Deltagpi7 cells showed no signifi…

MESH: InflammationGlycosylphosphatidylinositolsNeutrophilsmedicine.medical_treatmentInterleukin-1betasourisMESH: NeutrophilsMESH: VirulenceMESH: Mice KnockoutMiceMESH: Interleukin-1betaNull cellMESH: AnimalsCandida albicansPeritoneal CavityCells CulturedMice Knockout0303 health sciencesToll-like receptorbiologyVirulenceMESH: Toll-Like Receptor 2MESH: Peritoneal CavityMESH: Toll-Like Receptor 4MESH: GlycosylphosphatidylinositolsInfectious DiseasesCytokineMESH: Survival AnalysisTumor necrosis factor alphaMESH: Fungal Proteinsprotéine de la paroi cellulaireMESH: Macrophages PeritonealMESH: Cells CulturedVirulence FactorsImmunologyMicrobiologyMicrobiologyProinflammatory cytokineFungal Proteins03 medical and health sciencesMESH: Mice Inbred C57BLmedicineAnimalsMESH: Mice030304 developmental biologyMESH: Virulence FactorsInflammation030306 microbiologyInterleukin-6Tumor Necrosis Factor-alphaMESH: Candida albicans[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologybiology.organism_classificationSurvival AnalysispathogénicitéMESH: Interleukin-6Toll-Like Receptor 2Mice Inbred C57BLToll-Like Receptor 4TLR2GlycosylphosphatidylinositolMESH: Gene DeletionMESH: Tumor Necrosis Factor-alphaTLR4Macrophages Peritonealcandida albicansimmunitéGene Deletion
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The Inflammatory Response in Acyl-CoA Oxidase 1 Deficiency (Pseudoneonatal Adrenoleukodystrophy)

2012

Among several peroxisomal neurodegenerative disorders, the pseudoneonatal adrenoleukodystrophy (P-NALD) is characterized by the acyl-coenzyme A oxidase 1 (ACOX1) deficiency, which leads to the accumulation of very-long-chain fatty acids ( VLCFA) and inflammatory demyelination. However, the components of this inflammatory process in P-NALD remain elusive. In this study, we used transcriptomic profiling and PCR array analyses to explore inflammatory gene expression in patient fibroblasts. Our results show the activation of IL-1 inflammatory pathway accompanied by the increased secretion of two IL-1 target genes, IL-6 and IL-8 cytokines. Human fibroblasts exposed to very-long-chain fatty acids…

MESH: Inflammationperoxisomal disordersMESH: Osteopontinmedicine.medical_treatmentMESH : ImmunohistochemistryMESH : Transcriptomechemokine receptorsVoeding Metabolisme en Genomica0302 clinical medicineEndocrinologyMESH: Reverse Transcriptase Polymerase Chain ReactionAcyl-CoA oxidasemultiple-sclerosis lesionsMESH : OsteopontinMESH : Fatty AcidsCells CulturedOligonucleotide Array Sequence Analysis[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism0303 health sciencesOxidase testMESH : Gene Expression RegulationReverse Transcriptase Polymerase Chain ReactionFatty AcidsMESH: Acyl-CoA OxidaseMESH : Reverse Transcriptase Polymerase Chain ReactionPeroxisome[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismImmunohistochemistryMESH: Gene Expression RegulationMetabolism and Genomics3. Good healthMESH: Fatty AcidsMESH : Oligonucleotide Array Sequence AnalysisCytokineMetabolisme en GenomicaACOX1AdrenoleukodystrophyNutrition Metabolism and GenomicsMESH : Acyl-CoA Oxidasemedicine.symptomInflammation MediatorsMESH: Cells Culturedmedicine.medical_specialtyMESH : Interleukin-8MESH : Interleukin-6MESH: Inflammation MediatorsInflammationBiologyin-vitroMESH : Interleukin-1MESH : Inflammation Mediators03 medical and health sciencesVoedingInternal medicinePeroxisomal disordernf-kappa-bMESH : Cells CulturedMESH : Fibroblastsmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biologygene[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyNutrition030304 developmental biologyVLAGInflammationMESH: HumansMESH : InflammationInterleukin-6MESH: TranscriptomeInterleukin-8MESH : HumansMESH: Interleukin-1MESH: ImmunohistochemistryFibroblastsmedicine.diseaseMESH: Interleukin-6MESH: Interleukin-8EndocrinologyGene Expression RegulationMESH: FibroblastsMESH: Oligonucleotide Array Sequence AnalysiscellsBrief ReportsOsteopontinmicroarray analysisAcyl-CoA OxidaseTranscriptomeinterleukin-1030217 neurology & neurosurgeryx-linked adrenoleukodystrophyInterleukin-1
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Human OX40 tunes the function of regulatory T cells in tumor and nontumor areas of hepatitis C virus-infected liver tissue.

2014

International audience; Regulatory T cells (Tregs) can be considered as a mixed population of distinct subsets, endowed with a diverse extent and quality of adaptation to microenvironmental signals. Here, we uncovered an opposite distribution of Treg expansion, phenotype, and plasticity in different microenvironments in the same organ (liver) derived from patients with chronic hepatitis C: On the one side, cirrhotic and tumor fragments were moderately and highly infiltrated by Tregs, respectively, expressing OX40 and a T-bet high IFN-c – " T-helper (Th)1-suppressing " phenotype; on the other side, noncirrhotic liver specimens contained low frequencies of Tregs that expressed low levels of O…

MESH: Receptors OX40/metabolism*MESH: Interleukin-12/metabolismLiver CirrhosisMaleMacrophagemedicine.disease_causeMESH: Carcinoma Hepatocellular/immunology*T-Lymphocytes RegulatoryMESH: OX40 Ligand/metabolism0302 clinical medicineMESH: Aged 80 and overMESH: T-Lymphocytes Regulatory/physiology*MESH: Up-RegulationOX40MESH: AgedAged 80 and over0303 health scienceseducation.field_of_studyT REGMESH: Middle AgedMedicine (all)MESH: Liver Cirrhosis/immunology*Liver Neoplasmshemic and immune systemsMiddle AgedMESH: Liver Neoplasms/immunology*PhenotypeHepatitis CInterleukin-123. Good healthUp-RegulationPhenotypeLiver Neoplasm[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/VirologyInterleukin 12[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemalemedicine.symptomMESH: Hepatitis C/immunology*OX40; T REG; HEPATITIS C VIRUSHumanmedicine.medical_specialtyCarcinoma HepatocellularHepatitis C virusLiver CirrhosiPopulationInflammationchemical and pharmacologic phenomena[SDV.CAN]Life Sciences [q-bio]/CancerOX40 LigandBiologyMESH: PhenotypeMESH: Liver Neoplasms/virology03 medical and health sciencesIkaros Transcription FactorDownregulation and upregulationInternal medicinemedicineHumansMESH: Macrophages/metabolismeducation030304 developmental biologyAgedMESH: HumansHepatologyMacrophagesHEPATITIS C VIRUSMESH: Carcinoma Hepatocellular/virologyHepatologyReceptors OX40MESH: Ikaros Transcription Factor/metabolismMESH: Hepatitis C/complicationsMESH: MaleOX40 ligandImmunologyMESH: Liver Cirrhosis/virologyMESH: Female030215 immunology
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Semicarbazide-sensitive amine oxidase/vascular adhesion protein-1 deficiency reduces leukocyte infiltration into adipose tissue and favors fat deposi…

2009

1525-2191 (Electronic) Journal Article; Obesity is associated with low-grade inflammation and leukocyte infiltration in white adipose tissue (WAT) and is linked to diabetic complications. Semicarbazide-sensitive amine oxidase, also known as vascular adhesion protein-1 (SSAO/VAP-1), is a membrane protein that is highly expressed in adipocytes and is also present on the endothelial cell surface where it is involved in leukocyte extravasation. We studied fat deposition and leukocyte infiltration in WAT of mice with a null mutation in the amine oxidase copper-containing-3 (AOC3) gene encoding SSAO/VAP-1. Both epididymal and inguinal WATs were larger in 6-month-old AOC3-KO males than in age-matc…

MESH: SemicarbazidesAOC3Obesity/geneticsAdipose tissueMESH: Flow CytometryWhite adipose tissueInbred C57BLMESH: Mice KnockoutTransgenicMiceLeukocytesMESH: ObesityMESH: AnimalsMice KnockoutAmine oxidase (copper-containing)food and beveragesNatural killer T cellFlow CytometryLeukocyte extravasationSemicarbazidesCell Adhesion Molecules/*deficiency/*geneticsAdipose TissueMESH: Cell Adhesion MoleculesLeukocytes/*physiologyAmine Oxidase (Copper-Containing)medicine.symptomInfiltration (medical)MESH: Adipose Tissuemedicine.medical_specialtyMESH: Mice TransgenicKnockoutMice TransgenicInflammation[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyMESH: Monoamine OxidasePathology and Forensic MedicineMESH: LeukocytesMonoamine Oxidase/*deficiencyMESH: Mice Inbred C57BLInternal medicinemedicineAnimalsHumansObesityMonoamine OxidaseMESH: Mice[SDV.BC] Life Sciences [q-bio]/Cellular BiologyMESH: HumansAmine Oxidase (Copper-Containing)/*deficiency/*geneticsmedicine.diseaseAdipose Tissue/pathology/*physiologyMice Inbred C57BLEndocrinologyImmunologyMESH: Amine Oxidase (Copper-Containing)Semicarbazides/*pharmacologyCell Adhesion MoleculesRegular Articles
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