Search results for "P3"

showing 10 items of 786 documents

N-acetyl-L-cysteine (NAC) inhibit mucin synthesis and pro-inflammatory mediators in alveolar type II epithelial cells infected with influenza virus A…

2011

64% of chronic obstructive pulmonary disease (COPD) exacerbations are caused by respiratory infections including influenza (strains A and B) and respiratory syncytial virus (RSV). They affect the airway epithelium increasing inflammatory and apoptosis events through mechanisms involving ROS generation, and induce the release of mucins from epithelial cells that are involved in the deterioration of the patient's health during the course of the disease. The antioxidant NAC has proved useful in the management of COPD reducing symptoms, exacerbations and accelerated lung function decline. It has been shown to inhibit influenza virus replication and to diminish the release of inflammatory and ap…

BiologyMucin 5ACmedicine.disease_causeVirus ReplicationBiochemistryp38 Mitogen-Activated Protein KinasesVirusCell LinePulmonary Disease Chronic ObstructivemedicineHumansInterleukin 8PhosphorylationPharmacologyA549 cellMucinNF-kappa BAcetylcysteineRespiratory Syncytial VirusesPulmonary AlveoliInfluenza B virusRespiratory syncytial virus (RSV)Viral replicationApoptosisInfluenza A virusImmunologyRespiratory epitheliumInflammation MediatorsBiochemical pharmacology
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Are IL-10+ regulatory Th17 cells implicated in the sustained response to glucocorticoid treatment in patients with giant cell arteritis? Comment on t…

2013

We have read with interest the recently published paper of Espigol-Frigole et al 1 in which the authors confirmed that interleukin (IL)-17 is highly expressed in giant cell arteritis (GCA) lesions.1–3 They also demonstrated for the first time that IL-17 expression in temporal artery biopsies (TABs) was correlated with a better outcome. Among other interesting results, the identification of Foxp3+IL-17+ T cells by confocal microscopy in TAB made the authors to hypothesize that these cells could be induced regulatory T cells (Treg) that may facilitate the remission of the disease under steroid therapy. …

BiopsyGiant Cell ArteritisImmunologyGeneral Biochemistry Genetics and Molecular Biologylaw.inventionRheumatologyRecurrenceConfocal microscopylawBiopsymedicineHumansImmunology and AllergyGlucocorticoidsmedicine.diagnostic_testbusiness.industryInterleukin-17InterleukinFOXP3Forkhead Transcription Factorsmedicine.diseaseInterleukin-10Temporal ArteriesGiant cell arteritisInterleukin 10ImmunologyTh17 CellsInterleukin 17businessGlucocorticoidmedicine.drugAnnals of the Rheumatic Diseases
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Specific and global regulation of mRNA stability during osmotic stress in Saccharomyces cerevisiae.

2009

Hyperosmotic stress yields reprogramming of gene expression in Saccharomyces cerevisiae cells. Most of this response is orchestrated by Hog1, a stress-activated, mitogen-activated protein kinase (MAPK) homologous to human p38. We investigated, on a genomic scale, the contribution of changes in transcription rates and mRNA stabilities to the modulation of mRNA amounts during the response to osmotic stress in wild-type and hog1 mutant cells. Mild osmotic shock induces a broad mRNA destabilization; however, osmo-mRNAs are up-regulated by increasing both transcription rates and mRNA half-lives. In contrast, mild or severe osmotic stress in hog1 mutants, or severe osmotic stress in wild-type cel…

BioquímicaMessenger RNASaccharomyces cerevisiae ProteinsTranscription GeneticOsmotic shockMRNA destabilizationRNA Stabilityp38 mitogen-activated protein kinasesSaccharomyces cerevisiaeMRNA stabilizationSaccharomyces cerevisiaeBiologybiology.organism_classificationMolecular biologyArticleGenètica molecularCell biologyOsmotic PressureGene Expression Regulation FungalGene expressionOsmotic pressureRNA MessengerMitogen-Activated Protein KinasesMolecular Biology
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Type 1 diabetic mellitus patients with increased atherosclerosis risk display decreased CDKN2A/2B/2BAS gene expression in leukocytes

2019

Background Type 1 diabetes mellitus (T1DM) patients display increased risk of cardiovascular disease (CVD) and are characterized by a diminished regulatory T (Treg) cell content or function. Previous studies have shown an association between decreased CDKN2A/2B/2BAS gene expression and enhanced CVD. In the present study the potential relationship between CDKN2A/2B/2BAS gene expression, immune cell dysfunction and increased cardiovascular risk in T1DM patients was explored. Methods A cross-sectional study was performed in 90 subjects divided into controls and T1DM patients. Circulating leukocyte subpopulations analysis by flow cytometry, expression studies on peripheral blood mononuclear cel…

Blood Glucose0301 basic medicineendocrine system diseasesCellular differentiationlcsh:Medicine0302 clinical medicineRisk FactorsRAR-related orphan receptor gammaimmune system diseasesLeukocytesIL-2 receptorDiabetisFOXP3Cell DifferentiationGeneral MedicineType 1 diabetes030220 oncology & carcinogenesisCytokinesRNA Long Noncodingmedicine.symptomAdultmedicine.medical_specialtyCD14T cellsInflammationPeripheral blood mononuclear cellGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesInternal medicinemedicineHumansRNA MessengerCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p15Glycated HemoglobinInflammationType 1 diabetesbusiness.industryResearchlcsh:RAtherosclerosismedicine.diseaseCardiovascular riskDiabetes Mellitus Type 1030104 developmental biologyEndocrinologyGene Expression RegulationCase-Control StudiesbusinessJournal of Translational Medicine
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Does Glycemic Control Modulate the Impairment of NLRP3 Inflammasome Activation in Type 2 Diabetes?

2019

Since mitochondrial dysfunction is associated with NOD-like receptor family protein 3 (NLRP3) activation in type 2 diabetes (T2D), which can eventually lead to an impaired immune response, we set out to determine if glycemic control modulates the effects of T2D on the NLRP3 inflammasome. We have studied leukocytes from 61 diabetic patients [25 with glycated hemoglobin (HbA(1c)) 7% and 36 with HbA(1c) 8%] and 40 healthy controls. Total and mitochondrial reactive oxygen species (ROS) production was enhanced in T2D patients, and mitochondrial ROS was more pronounced in those with poor glycemic control. Levels of gene and protein expression of NLRP3 were decreased in both diabetic groups and mo…

Blood GlucoseMale0301 basic medicineMitochondrial ROSendocrine system diseasesInflammasomesPhysiologyClinical BiochemistryType 2 diabetesmedicine.disease_causeBiochemistrychemistry.chemical_compoundGene expressionoxidative stressGeneral Environmental Scienceintegumentary systemInterleukinInflammasomeMiddle AgedMitochondriaglycaemic controlCytokinesFemaletype 2 diabetesInflammation MediatorsSignal Transductionmedicine.drugmedicine.medical_specialty03 medical and health sciencesmitochondrial functionInternal medicineNLR Family Pyrin Domain-Containing 3 ProteinmedicineHumansBody Weights and MeasuresMolecular BiologyAgedGlycemicGlycated Hemoglobin030102 biochemistry & molecular biologybusiness.industrynutritional and metabolic diseasesCell Biologymedicine.diseaseNLRP3 inflammasome030104 developmental biologyEndocrinologyDiabetes Mellitus Type 2chemistryGeneral Earth and Planetary SciencesGlycated hemoglobinReactive Oxygen SpeciesbusinessBiomarkersOxidative stressAntioxidants & Redox Signaling
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Dual role of the p38 MAPK/cPLA2 pathway in the regulation of platelet apoptosis induced by ABT-737 and strong platelet agonists.

2013

p38 Mitogen-activated protein (MAP) kinase is involved in the apoptosis of nucleated cells. Although platelets are anucleated cells, apoptotic proteins have been shown to regulate platelet lifespan. However, the involvement of p38 MAP kinase in platelet apoptosis is not yet clearly defined. Therefore, we investigated the role of p38 MAP kinase in apoptosis induced by a mimetic of BH3-only proteins, ABT-737, and in apoptosis-like events induced by such strong platelet agonists as thrombin in combination with convulxin (Thr/Cvx), both of which result in p38 MAP kinase phosphorylation and activation. A p38 inhibitor (SB202190) inhibited the apoptotic events induced by ABT-737 but did not influ…

Blood PlateletsCancer ResearchcPLA2p38 mitogen-activated protein kinasesImmunologyBlotting Westernp38 Mitogen-Activated Protein KinasesPiperazinesNitrophenolsCellular and Molecular NeurosciencePhospholipase A2Crotalid VenomsHumansLectins C-Typeddc:610Cells CulturedMembrane Potential MitochondrialplateletSulfonamidesbiologyKinaseGroup IV Phospholipases A2Biphenyl CompoundsapoptosisConvulxinCell BiologyFlow Cytometryp38 MAP kinaseCell biologyApoptosisMitogen-activated protein kinasebiology.proteinPhosphorylationOriginal ArticleSignal transductionReactive Oxygen SpeciesSignal TransductionCell deathdisease
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Activation of cGMP-dependent Protein Kinase Iβ Inhibits Interleukin 2 Release and Proliferation of T Cell Receptor-stimulated Human Peripheral T Cells

2000

Several major functions of type I cGMP-dependent protein kinase (cGK I) have been established in smooth muscle cells, platelets, endothelial cells, and cardiac myocytes. Here we demonstrate that cGK Ibeta is endogenously expressed in freshly purified human peripheral blood T lymphocytes and inhibits their proliferation and interleukin 2 release. Incubation of human T cells with the NO donor, sodium nitroprusside, or the membrane-permeant cGMP analogs PET-cGMP and 8-pCPT-cGMP, activated cGK I and produced (i) a distinct pattern of phosphorylation of vasodilator-stimulated phosphoprotein, (ii) stimulation of the mitogen-activated protein kinases ERK1/2 and p38 kinase, and, upon anti-CD3 stimu…

Blood PlateletsNitroprussideInterleukin 2Cell Membrane PermeabilityCD3 ComplexT-Lymphocytesp38 mitogen-activated protein kinasesT cellReceptors Antigen T-CellCell SeparationBiologyLymphocyte ActivationBiochemistryJurkat cellsJurkat CellsCyclic AMPCyclic GMP-Dependent Protein KinasesmedicineHumansProtein kinase ACyclic GMPMolecular BiologyCyclic GMP-Dependent Protein Kinase Type IKinaseCell growthMicrofilament ProteinsCell BiologyPhosphoproteinsMolecular biologyCell biologyEnzyme ActivationAlternative Splicingmedicine.anatomical_structureInterleukin-2Mitogen-Activated Protein KinasesCell Adhesion MoleculescGMP-dependent protein kinasemedicine.drugJournal of Biological Chemistry
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SNPs and taxane toxicity in breast cancer patients

2014

Aim: In order to identify genetic variants associated with taxanes toxicity, a panel with 47 SNPs in 20 genes involved in taxane pathways was designed. Patients & methods: Genomic DNA of 113 breast cancer patients was analyzed (70 taking docetaxel, 43 taking paclitaxel). Results: Two SNPs associated with docetaxel toxicity were identified: CYP3A4*1B with infusion-related reactions; and ERCC1 Gln504Lys with mucositis (p ≤ 0.01). Regarding paclitaxel toxicity: CYP2C8 HapC and CYP2C8 rs1934951 were associated with anemia; and ERCC1 Gln504Lys with neuropathy (p ≤ 0.01). Conclusion: Genes involved in DNA repair mechanisms and reactive oxygen species levels influence taxane toxicity in cance…

Bridged-Ring CompoundsMucositisOncologymedicine.medical_specialtyDrug-Related Side Effects and Adverse ReactionsPaclitaxelmedicine.medical_treatmentBreast NeoplasmsDocetaxelPharmacologyPolymorphism Single Nucleotidechemistry.chemical_compoundBreast cancerInternal medicineGeneticsMucositisCytochrome P-450 CYP3AHumansMedicineGenetic Association StudiesAgedPharmacologyChemotherapyTaxanebusiness.industryCancerMiddle AgedEndonucleasesmedicine.diseaseDNA-Binding ProteinsDocetaxelPaclitaxelchemistryMolecular MedicineFemaleTaxoidsERCC1businessmedicine.drugPharmacogenomics
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Th17 immunity in children with allergic asthma and rhinitis: a pharmacological approach

2013

Th17 cells and IL-17A play a role in the development and progression of allergic diseases. We analyzed the IL-17A levels in sputum supernatants (Ss), nasal wash (NW) and plasma (P) from Healthy Controls (HC) and children with Asthma/Rhinitis. We tested the expression of IL-17A, RORγ(t) and FOXP3 in peripheral blood T-lymphocytes from intermittent and mild-moderate asthma. The effect of Budesonide and Formoterol was tested "in vitro" on IL-17A, RORγ(t) and FOXP3 expression in cultured T-lymphocytes from mild-moderate asthma/persistent rhinitis patients, and on nasal and bronchial epithelial cells stimulated with NW and Ss from mild-moderate asthma/persistent rhinitis. Further, the effect of …

BudesonideMalePulmonologyIL 13 and AsthmaGene ExpressionAnti-asthmatic AgentBiochemistryPediatricsimmune system diseasesFormoterol FumarateMolecular Cell BiologyAnti-Asthmatic AgentsBudesonideChildCells CulturedMultidisciplinaryImmune System ProteinsQInterleukin-17RFOXP3Forkhead Transcription FactorsNuclear Receptor Subfamily 1 Group F Member 3EthanolaminesMedicineFemaleInterleukin 17medicine.symptommedicine.drugResearch ArticleRhinitis Allergic PerennialAdolescentScienceImmunologyPediatric PulmonologyInflammationAdministration InhalationmedicineHumansAdrenergic beta-2 Receptor AgonistsBiologyAsthmaInflammationbusiness.industryInterleukin-8SputumImmunityProteinsImmunologic Subspecialtiesmedicine.diseaseNasal Lavage FluidAsthmarespiratory tract diseasesCase-Control StudiesImmunologySputumTh17 CellsClinical ImmunologyFormoterolbusinessPulmonary Immunology
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Cobalt−NHC Catalyzed C(sp2)−C(sp3) and C(sp2)−C(sp2) Kumada Cross‐Coupling of Aryl Tosylates with Alkyl and Aryl Grignard Reagents

2021

The first cobalt‐catalyzed cross‐coupling of aryl tosylates with alkyl and aryl Grignard reagents is reported. The catalytic system uses CoF3 and NHCs (NHC=N‐heterocyclic carbene) as ancillary ligands. The reaction proceeds via highly selective C−O bond functionalization, leading to the corresponding products in up to 98 % yield. The employment of alkyl Grignard reagents allows to achieve a rare C(sp2)−C(sp3) cross‐coupling of C−O electrophiles, circumventing isomerization and β‐hydride elimination problems. The use of aryl Grignards leads to the formation of biaryls. The C−O cross‐coupling sets the stage for a sequential cross‐coupling by exploiting the orthogonal selectivity of the cataly…

C(sp2)−C(sp3) cross-couplingcross-couplingC−O activationsustainabilitycobalt catalysisChemcatchem
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