Search results for "inflammation"

showing 10 items of 2662 documents

Polymorphisms of pro-inflammatory genes and Alzheimer's disease risk: A pharmacogenomic approach.

2006

Clinically and pathologically Alzheimer's disease (AD) represents a sequential progressive neurodegenerative disorder. AD is etiologically heterogeneous and accounts for a majority of dementia in western societies. Inflammation clearly occurs in pathologically vulnerable regions of the AD brain and the search for genetic factors influencing the pathogenesis of AD has lead to the identification of numerous gene polymorphisms that might act as susceptibility modifiers. Accordingly, several reports have indicated that the risk of AD is substantially influenced by several genetic polymorphisms in the promoter region, or other untranslated regions, of genes encoding inflammatory mediators, altho…

RiskAgingDiseaseBiologyBioinformaticsPathogenesisDegenerative diseaseGeneticAlzheimer DiseaseGenetic variationmedicineDementiaSettore MED/05 - Patologia ClinicaAnimalsHumansGeneGeneticsInflammationSettore MED/04 - Patologia GeneraleGenomePolymorphism Geneticmedicine.diseasePharmacogeneticsPharmacogenomicsAlzheimer's diseaseInflammation MediatorsPharmacogenomicsAlzheimer’s diseaseDevelopmental Biology
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Therapeutic modulation of lipoprotein-associated phospholipase A2 (Lp-PLA2)

2011

Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a calcium-independent phospholipase A2 that circulates in plasma in association with lipoprotein particles, whereas in atherosclerotic plaques it is co-localized with macrophages. Lp-PLA2 generates two proinflammatory mediators, lysophosphatidylcholine and oxidized nonesterified fatty acids, which play a role in the development of atherosclerotic lesions and formation of a necrotic core, leading to more vulnerable plaques. Epidemiologic studies demonstrate that increased circulating levels of Lp-PLA2 predict an increased risk of myocardial infarction, stroke and cardiovascular mortality. Furthermore, histologic examination of diseased hum…

RiskPathologymedicine.medical_specialtycoronary-artery-diseasecardiovascular-diseasePharmacologyatherosclerotic plaqueProinflammatory cytokinechemistry.chemical_compoundPhospholipase A2cardiovascular diseaseDarapladibOximesDrug DiscoveryHyperlipidemiamedicineHumansMyocardial infarctionPharmacologyClinical Trials as Topicbiologylow-density-lipoproteinLipoprotein-associated phospholipase A2risk-assessmentCardiovascular AgentsAtherosclerosismedicine.diseaselp-pla2heart-diseaselipoproteinsLysophosphatidylcholinechemistryCardiovascular DiseasesinflammationBenzaldehydes1-Alkyl-2-acetylglycerophosphocholine Esterasebiology.proteindarapladibrheumatoid-arthritislipids (amino acids peptides and proteins)atherosclerosisfactor-acetylhydrolase activityAtherosclerosis Cardiovascular disease Darapladib Inflammation Lipoproteins Lp-PLA2.platelet-activating-factorsecondary preventionLipoprotein
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Effect of two prophylaxis methods on adherence of Streptococcus mutans to microfilled composite resin and giomer surfaces

2010

Objectives: Surface attributes of a restoration play an important role in adherence of plaque bacteria. Prophylaxis methods may be involved in modification of or damaging the restoration surface. The aim of the present study was to evaluate the effect of two prophylaxis methods on adherence of Streptococcus mutans to the surface of two restorative materials. Study design: A total of 60 specimens were prepared from each material; a microfilled composite resin (HelioProgress) and a giomer (Beautifil II). For each material, the specimens were randomly divided into three groups (n=20). Group 1: no prophylaxis treatment (control); Group 2: prophylaxis with pumice and rubber cup; Group 3: prophyl…

Rubber CupPost hocbiologySurface PropertiesAtomic force microscopybusiness.industryComposite numberDentistryHelioprogress:CIENCIAS MÉDICAS [UNESCO]biology.organism_classificationComposite ResinsStreptococcus mutansBacterial AdhesionStreptococcus mutansOtorhinolaryngologyGlass Ionomer CementsUNESCO::CIENCIAS MÉDICASRestorative materialMicroscopy Electron ScanningMedicineSurgerybusinessGeneral DentistryPlaque inflammationMedicina Oral Patología Oral y Cirugia Bucal
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Die allergisch-hyperergische Entzündung von Haut und Gelenken unter dem Einflu\ von Hyaluronidase und Rutin

1954

Es wurde der Einflu\ von Hyaluronidase und Rutin auf die allergisch-hyperergische Entzundung der Haut und der Gelenke beim Kaninchen untersucht. Hyaluronidase allein ruft lediglich ein entzundliches odem hervor. Hyaluronidase am Ort der Antigenreinjektion appliziert fuhrt in der Haut zu einer AbschwAchung und im Gelenk zu einer VerstArkung der Entzundung. Intravenose Hyaluronidasegaben verstArken die Entzundung in der Haut, wAhrend die Arthritis keine wesentliche Beeinflussung erfAhrt. Rutin intravenos gegeben fuhrt zu einer deutlichen Herabminderung der Entzundungserscheinungen an Haut und Gelenken.

Rutinchemistry.chemical_compoundchemistrybusiness.industryHyaluronidaseMedicineInflammationGeneral Medicinemedicine.symptombusinessMolecular biologymedicine.drugZeitschrift für Die Gesamte Experimentelle Medizin
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MiR-29b antagonizes the pro-inflammatory tumor-promoting activity of multiple myeloma-educated dendritic cells

2017

Dendritic cells (DCs) have a key role in regulating tumor immunity, tumor cell growth and drug resistance. We hypothesized that multiple myeloma (MM) cells might recruit and reprogram DCs to a tumor-permissive phenotype by changes within their microRNA (miRNA) network. By analyzing six different miRNA-profiling data sets, miR-29b was identified as the only miRNA upregulated in normal mature DCs and significantly downregulated in tumor-associated DCs. This finding was validated in primary DCs co-cultured in vitro with MM cell lines and in primary bone marrow DCs from MM patients. In DCs co-cultured with MM cells, enforced expression of miR-29b counteracted pro-inflammatory pathways, includin…

STAT3 Transcription Factor0301 basic medicineCancer Researchdendritic cellDown-RegulationInflammationMice SCIDBiologyMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationBone MarrowCell Line Tumorhemic and lymphatic diseasesmicroRNAmedicineAnimalsHumanstumor immunologyMultiple myelomaCell ProliferationInflammationmicroRNA.Cell growthNF-kappa BDendritic CellsHematologySTAT3 Transcription Factormedicine.diseaseNFKB1Up-RegulationGene Expression Regulation Neoplasticmultiple myelomaMicroRNAs030104 developmental biologymedicine.anatomical_structureOncologyCancer researchOriginal ArticleFemaleBone marrowTh17medicine.symptom030215 immunology
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PKM2 promotes Th17 cell differentiation and autoimmune inflammation by fine-tuning STAT3 activation

2019

Th17 cells undergo metabolic reprogramming towards glycolysis to support their differentiation and pathogenicity. Damasceno et al. report that PKM2, a glycolytic enzyme, plays a nonmetabolic role in mediating Th17 cell differentiation and autoimmune neuroinflammation by fine-tuning STAT3 activation.

STAT3 Transcription Factor0301 basic medicineEncephalomyelitis Autoimmune ExperimentalCellular differentiationEncephalomyelitisPyruvate KinaseImmunologyFluorescent Antibody TechniqueAutoimmunityInflammationPKM2Real-Time Polymerase Chain ReactionArticleMice03 medical and health sciences0302 clinical medicineNeuroinflammationmedicineAnimalsImmunology and AllergySTAT3InflammationbiologyChemistryExperimental autoimmune encephalomyelitisCell Differentiationhemic and immune systemsFlow Cytometrymedicine.diseaseCell biologyMice Inbred C57BL030104 developmental biologyTumor progression030220 oncology & carcinogenesisbiology.proteinTh17 Cellsmedicine.symptomREAÇÃO EM CADEIA POR POLIMERASEPyruvate kinaseJournal of Experimental Medicine
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STAT3 links IL-22 signaling in intestinal epithelial cells to mucosal wound healing.

2009

Signal transducer and activator of transcription (STAT) 3 is a pleiotropic transcription factor with important functions in cytokine signaling in a variety of tissues. However, the role of STAT3 in the intestinal epithelium is not well understood. We demonstrate that development of colonic inflammation is associated with the induction of STAT3 activity in intestinal epithelial cells (IECs). Studies in genetically engineered mice showed that epithelial STAT3 activation in dextran sodium sulfate colitis is dependent on interleukin (IL)-22 rather than IL-6. IL-22 was secreted by colonic CD11c+ cells in response to Toll-like receptor stimulation. Conditional knockout mice with an IEC-specific d…

STAT3 Transcription FactorAnimals; Colitis/chemically induced; Colitis/immunology; Dextran Sulfate/pharmacology; Epithelial Cells/cytology; Epithelial Cells/physiology; Gene Expression Profiling; Inflammation/immunology; Inflammation/pathology; Interleukin-6/genetics; Interleukin-6/immunology; Interleukins/genetics; Interleukins/immunology; Intestinal Mucosa/cytology; Intestinal Mucosa/pathology; Mice; Mice Inbred C57BL; Mice Knockout; Oligonucleotide Array Sequence Analysis; STAT3 Transcription Factor/genetics; STAT3 Transcription Factor/metabolism; Signal Transduction/physiology; Wound HealingImmunologyInterleukin 22Mice03 medical and health sciences0302 clinical medicineIntestinal mucosaConditional gene knockoutImmunology and AllergyAnimalsIntestinal MucosaSTAT3Oligonucleotide Array Sequence Analysis030304 developmental biologyInflammationMice KnockoutWound Healing0303 health sciencesbiologyInterleukin-6Gene Expression ProfilingInterleukinsDextran SulfateBrief Definitive ReportEpithelial CellsCell BiologySTAT3 Transcription FactorColitisIntestinal epithelium3. Good healthMice Inbred C57BLbiology.proteinCancer researchSTAT proteinWound healingSignal Transduction030215 immunology
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Signaling molecules: the pathogenic role of the IL-6/STAT-3 trans signaling pathway in intestinal inflammation and in colonic cancer.

2008

Although the precise etiology of inflammatory bowel diseases (IBD) still remains unclear, considerable progress has been made in the identification of novel signal transduction pathways that elucidate the immunopathogenesis involved in the perpetuation of the inflammatory process. As both ulcerative colitis and Crohn's disease are associated with an increased risk for developing colorectal cancer (CRC) and precancerous dysplastic epithelial changes, further studies have concentrated on finding a common signaling pathway that could serve as a mechanistic link between inflammation and associated colonic cancer in IBD. This review presents the current data concerning the pathogenic role of the…

STAT3 Transcription FactorCell signalingColorectal cancerClinical BiochemistryAnti-Inflammatory AgentsInflammationAntineoplastic AgentsDiseaseSuppressor of cytokine signallingDrug DiscoverymedicineAnimalsHumansAutocrine signallingPharmacologybusiness.industryInterleukin-6medicine.diseaseInflammatory Bowel DiseasesUlcerative colitisdigestive system diseasesCell Transformation NeoplasticColonic NeoplasmsCancer researchMolecular Medicinemedicine.symptomSignal transductionbusinessSignal TransductionCurrent drug targets
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Activation of Intestinal Epithelial Stat3 Orchestrates Tissue Defense during Gastrointestinal Infection

2015

Gastrointestinal infections with EHEC and EPEC are responsible for outbreaks of diarrheal diseases and represent a global health problem. Innate first-line-defense mechanisms such as production of mucus and antimicrobial peptides by intestinal epithelial cells are of utmost importance for host control of gastrointestinal infections. For the first time, we directly demonstrate a critical role for Stat3 activation in intestinal epithelial cells upon infection of mice with Citrobacter rodentium - a murine pathogen that mimics human infections with attaching and effacing Escherichia coli. C. rodentium induced transcription of IL-6 and IL-22 in gut samples of mice and was associated with activat…

STAT3 Transcription FactorColonAntimicrobial peptideslcsh:MedicineInflammation-digestive systemMicrobiologyMiceMedizinische FakultätmedicineCitrobacter rodentiumAnimalsHumansddc:610Intestinal Mucosalcsh:ScienceSTAT3PathogenMice KnockoutGastrointestinal tractMultidisciplinarybiologylcsh:REnterobacteriaceae InfectionsEpithelial CellsColitisMucusEpitheliumIntestinesMice Inbred C57BLmedicine.anatomical_structureImmunologybiology.proteinCitrobacter rodentiumlcsh:Qmedicine.symptomResearch ArticlePLoS ONE
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Socs3 induction by PPARγ restrains cancer-promoting inflammation

2013

The presence of proinflammatory cytokines in the tumor microenvironment can support further growth of established cancers. Docosahexaenoic acid (DHA), a peroxisome proliferator-activated receptor-gamma (PPARγ) ligand, has been shown to suppress inflammation and limit tumor progression in vivo. Are the anticancer properties of DHA relying on its ability to prevent inflammation? If so, what are the molecular links between the anti-inflammatory properties of DHA and its anticancer effects? DHA is an n-3 polyinsaturated fatty acid mainly found in fish oil that was shown to contribute to inflammation resolution by preventing the release of proinflammatory mediators in vivo.1 DHA has also been as…

STAT3 Transcription FactorDocosahexaenoic AcidsCellular differentiationPeroxisome proliferator-activated receptorInflammationSuppressor of Cytokine Signaling ProteinsBiologyEditorials: Cell Cycle FeaturesProinflammatory cytokineMicemedicineAnimalsHumansPhosphorylationPromoter Regions GeneticMolecular BiologyCells Culturedchemistry.chemical_classificationInflammationTumor microenvironmentInterleukin-17TroglitazoneCell DifferentiationCell BiologyPPAR gammaCell Transformation NeoplasticchemistryGene Expression RegulationSuppressor of Cytokine Signaling 3 ProteinImmunologyCancer cellCancer researchTh17 CellsInterleukin 17medicine.symptomDevelopmental Biologymedicine.drugProtein BindingSignal TransductionCell Cycle
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