Search results for "Dexamethasone"

showing 10 items of 246 documents

LATE-BREAKING ABSTRACT: Anti-inflammatory effect of RP6557, a dual PI3K δ/γ inhibitor, in glucocorticoid insensitive human neutrophils from chronic o…

2015

Rationale: Glucocorticoid function is markedly impaired in patients with chronic obstructive pulmonary disease (COPD). Class I PI3K enzymes play a key role in chronic lung inflammation of COPD patients. This study explored differential inhibitory effects of dexamethasone and RP6557, a dual PI3K δ/γ inhibitor, on inflammatory responses in human neutrophils from healthy and COPD patients. Methods: Peripheral blood neutrophils were isolated from COPD patients andhealthy subjects and pre-incubated with dexamethasone (DEX) or RP6557 for 1 h. Neutrophils were stimulated with 5% cigarette smoke extract (CSE) for 6 h. Supernatants were used to measure IL-8 while RNA from neutrophils was analyzed fo…

COPDmedicine.medical_specialtyLungmedicine.drug_classbusiness.industryInflammationmedicine.diseaseAnti-inflammatoryEndocrinologymedicine.anatomical_structureInternal medicineImmunologymedicineSecretionmedicine.symptomRespiratory systembusinessGlucocorticoidDexamethasonemedicine.drug5.1 Airway Pharmacology and Treatment
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Induction of carbonic anhydrase in SaOS-2 cells, exposed to bicarbonate and consequences for calcium phosphate crystal formation.

2013

Ca-phosphate/hydroxyapatite crystals constitute the mineralic matrix of vertebrate bones, while Ca-carbonate dominates the inorganic matrix of otoliths. In addition, Ca-carbonate has been identified in lower percentage in apatite crystals. By using the human osteogenic SaOS-2 cells it could be shown that after exposure of the cells to Ca-bicarbonate in vitro, at concentrations between 1 and 10 mm, a significant increase of Ca-deposit formation results. The crystallite nodules formed on the surfaces of SaOS-2 cells become denser and larger in the presence of bicarbonate if simultaneously added together with the mineralization activation cocktail (β-glycerophosphate/ascorbic acid/dexamethason…

Calcium Phosphatesmedicine.drug_classBicarbonateBiophysicschemistry.chemical_elementBioengineering02 engineering and technologyAscorbic AcidCalciumDexamethasoneCell LineBiomaterials03 medical and health scienceschemistry.chemical_compoundCarbonic anhydrasemedicineEscherichia coliHumansCarbonic anhydrase inhibitorBone ResorptionCarbonic Anhydrase InhibitorsSaos-2 cells030304 developmental biologyCarbonic Anhydrases0303 health sciencesbiologyX-RaysGene Expression Regulation Developmental021001 nanoscience & nanotechnologyPhosphateAscorbic acidUp-RegulationAcetazolamideBicarbonatesMicroscopy ElectronchemistryBiochemistryMechanics of MaterialsGlycerophosphatesCeramics and Compositesbiology.protein0210 nano-technologyAcetazolamidemedicine.drugBiomaterials
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Induction of the alkyltransferase (MGMT) gene by DNA damaging agents and the glucocorticoid dexamethasone and comparison with the response of base ex…

1996

Repair of alkylated bases in DNA is performed by O6-methylguanine-DNA methyltransferase (MGMT) and a set of enzymes of the base excision repair pathway involving N-methylpurine-DNA glycosylase (MPG), apurinic endonuclease (APE), DNA polymerase beta (Pol beta) and DNA ligase. The level of expression of these enzymes may exert a profound effect on resistance of cells towards alkylating drugs. We have comparatively analyzed the expression of MGMT and the different base excision repair genes in rat hepatoma cells (line H4IIE) after exposure to alkylating agents, X-rays and the glucocorticoid hormone dexamethasone. Furthermore, the effect of these agents on the activity of the cloned human MGMT …

Cancer ResearchAlkylationDNA RepairDNA damageDNA polymerase betaBiologyDexamethasoneGene Expression Regulation Enzymologicchemistry.chemical_compoundO(6)-Methylguanine-DNA MethyltransferaseLiver Neoplasms ExperimentalAnimalsRNA MessengerPromoter Regions GeneticneoplasmsAntineoplastic Agents AlkylatingGlucocorticoidschemistry.chemical_classificationDNA ligaseO-6-methylguanine-DNA methyltransferaseGeneral MedicineBase excision repairDNA NeoplasmMethyltransferasesMolecular biologyDNA-(apurinic or apyrimidinic site) lyasedigestive system diseasesRatsUp-RegulationGene Expression Regulation NeoplasticKineticschemistryDNA glycosylaseEnzyme InductionAlkyltransferaseDNA DamageCarcinogenesis
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Bortezomib: a new pro-apoptotic agent in cancer treatment.

2010

Bortezomib is a proteasome inhibitor. It targets the ubiquitin-proteasome pathway with subsequent inhibition of the degradation of proteins involved in cell cycle regulation and cancer cell survival. The best known molecular mechanism concerns the inhibition of IkappaB breakdown and the related stabilization of NFkappaB, thus preventing its translocation to the nucleus for the activation of downstream pathways. Bortezomib is the only drug in this class which has been approved for clinical use. It has shown an efficient antitumor effect in a phase III clinical trial (APEX) involving relapsed multiple myeloma patients. Response rate, time to progression and overall survival have been improved…

Cancer ResearchCell cycle checkpointSettore MED/06 - Oncologia MedicaAntineoplastic AgentsApoptosisPharmacologyDexamethasoneBortezomibMiceNeoplasmshemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsDrug DiscoverymedicineAnimalsHumansDexamethasoneMultiple myelomaPharmacologyproteasome inhibitionClinical Trials as TopicNeovascularization Pathologicbusiness.industryBortezomibCell CycleNF-kappa Bsolid tumorsmedicine.diseaseBoronic AcidsClinical trialBortezomib; solid tumors; proteasome inhibition.OncologyApoptosisPyrazinesCancer cellProteasome inhibitorCancer researchMultiple MyelomabusinessProteasome InhibitorsBortezomib solid tumors proteasome inhibitionmedicine.drug
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Elotuzumab plus lenalidomide and dexamethasone in relapsed/refractory multiple myeloma: Extended 3‐year follow‐up of a multicenter, retrospective cli…

2022

: The combination of elotuzumab, lenalidomide, and dexamethasone (EloRd) enhanced the clinical benefit over Rd with a manageable toxicity profile in the ELOQUENT-2 trial, leading to its approval in relapsed/refractory multiple myeloma (RRMM). The present study is a 3-year follow-up update of a previously published Italian real-life RRMM cohort of patients treated with EloRd. This revised analysis entered 319 RRMM patients accrued in 41 Italian centers. After a median follow-up of 36 months (range 6-55), 236 patients experienced disease progression or died. Median progression-free survival (PFS) and overall survival (OS) were 18.4 and 34 months, respectively. The updated multivariate analyse…

Cancer Researchlenalidomidedexamethasone; elotuzumab; lenalidomide; multiple myeloma; salvage therapydexamethasoneHematologyGeneral MedicineAntibodies Monoclonal HumanizedelotuzumabThalidomidemultiple myelomaOncologyAntineoplastic Combined Chemotherapy ProtocolsHumanssalvage therapySettore MED/15 - Malattie del SangueFollow-Up StudiesRetrospective StudiesHematological Oncology
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Dexamethasone lacks effect on blood pressure in mice with a disrupted endothelial NO synthase gene.

2003

Cushing's syndrome and systemic administration of glucocorticoids are associated with hypertension, but the underlying molecular mechanism is only partially understood. We have shown previously that dexamethasone downregulates the expression of the endothelial NO synthase (eNOS) gene in human endothelial cells and in the rat and that this may contribute to the blood pressure-raising effect of the steroid [Proc. Natl. Acad. Sci. USA 96 (1999) 13357]. In the current communication, we demonstrated that dexamethasone increased mean arterial blood pressure in wild-type C-57 Bl6 mice (eNOS+/+ mice), but had no effect on blood pressure in mice with a disrupted eNOS gene (eNOS-/- mice) derived from…

Cancer Researchmedicine.medical_specialtyEndotheliumNitric Oxide Synthase Type IIIPhysiologyClinical BiochemistryNitric Oxide Synthase Type IIBlood PressureBiologyKidneyNitric OxideBiochemistryDexamethasoneMiceDownregulation and upregulationEnosInternal medicinemedicineAnimalsEnzyme InhibitorsDexamethasoneMice KnockoutKidneyMyocardiumNitric Oxide Synthase Type IIIbiology.organism_classificationmedicine.anatomical_structureBlood pressureEndocrinologyLiverPharmacogeneticsHypertensionSystemic administrationNitric Oxide Synthasemedicine.drugNitric oxide : biology and chemistry
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Dificultad en el tratamiento del hipertiroidismo por amiodarona: Presentación de un caso

2007

La amiodarona puede alterar la función tiroidea en un 15-20% de los pacientes que la toman, dando lugar a hipotiroidismo o hipertiroidismo. La sobrecarga de yodo y la toxicidad directa sobre el tiroides inducida por amiodarona pueden provocar hipertiroidismo. Describimos un caso de tirotoxicosis grave por amiodarona que se diagnosticó buscando la causa que descompensó la cardiopatía de base del paciente, condicionando ésta el pronóstico y el manejo terapéutico. El tratamiento precisó un estrecho seguimiento y se basó en dosis elevadas de propiltiouracilo y dexametasona que no controlaron las consecuencias del hipertiroidismo a nivel cardiaco necesitando la tiroidectomia total. Creemos, con …

Cardiac function curveendocrine systemmedicine.medical_specialtyendocrine system diseasesmedicine.diagnostic_testbusiness.industryHipertiroidismo por amiodaronaCorticoterapiaAmiodaronemedicine.diseaseGastroenterologyThyroid function testsThyroiditisSurgeryAntitiroideos de síntesisRefractoryInternal medicineTiroidectomia totalInternal MedicinemedicinePropylthiouracilThyroid functionbusinessDexamethasonemedicine.drugAnales de Medicina Interna
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Multiple signal transduction pathways regulate clusterin (gp 80) gene expression in MDCK cells

1996

ABSTRACT Clusterin (gp 80, apolipoprotein J, TRPM-2) is a widely expressed multifunctional glycoprotein. Its demonstrated and proposed functions include the transport of lipids and membrane fragments, the inhibition of the cytolytic action of the terminal complement complex and the modulation of cell—cell interactions. The expression of the gene is enhanced during tissue injury and remodelling and by hormone-withdrawal-induced apoptosis of prostate and mammary cells. We show here that, in the kidney-derived epithelial cell line MDCK, clusterin mRNA is repressed by glucocorticoids and by progesterone. Treatment with epidermal growth factor also represses clusterin gene expression in MDCK cel…

Cell typeTranscription GeneticKidneyDexamethasoneEpitheliumCell LineAlkaloidsDogsEndocrinologyEpidermal growth factor1-Methyl-3-isobutylxanthineGene expressionCyclic AMPAnimalsRNA MessengerEnzyme InhibitorsAldosteroneMolecular BiologyProgesteroneProtein Kinase CProtein kinase CGlycoproteinsBenzophenanthridinesMessenger RNAEpidermal Growth FactorClusterinbiologyChemistryMolecular biologyeye diseasesPhenanthridinesCell biologyKineticsClusterinCell culturebiology.proteinTetradecanoylphorbol Acetatesense organsSignal transductionMolecular ChaperonesSignal TransductionJournal of Molecular Endocrinology
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Regulation of the type II oncostatin M receptor expression in lung-derived epithelial cells

1998

AbstractOncostatin M (OSM) is a potent modulator of human lung-derived epithelial cell function. This cytokine binds two distinct receptor complexes: type I OSM receptor which is also a functional receptor for leukemia inhibitory factor (LIF), and type II OSM-specific receptor. The role of these two distinct receptors in mediating the response of individual cell types to OSM has not been delineated. In contrast to LIF, OSM induces synthesis of α1-antichymotrypsin and α1-antiproteinase inhibitor in lung-derived epithelial cells. The differential responsiveness to LIF and OSM suggested that the response of lung epithelial cells to OSM may be mediated by the OSM-specific receptor. Therefore, w…

Cell typemedicine.medical_treatmentTransforming growth factor β1Respiratory SystemBronchial epitheliumBiophysicsBronchiOncostatin MInterleukin 1 receptor type IILeukemia Inhibitory FactorBiochemistryDexamethasoneAntigens CDStructural BiologyCytokine Receptor gp130GeneticsmedicineHumansReceptors CytokineReceptorLungMolecular BiologyLymphokinesMembrane GlycoproteinsbiologyInterleukin-6ChemistryfungiOncostatin MOncostatin M receptorEpithelial CellsReceptors Oncostatin MCell BiologyGrowth InhibitorsCell biologyInterleukin 31CytokineGene Expression Regulationbiology.proteinCancer researchCytokinesInflammation MediatorsPeptidesLeukemia inhibitory factorFEBS Letters
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Differential Promotion of Glutamate Transporter Expression and Function by Glucocorticoids in Astrocytes from Various Brain Regions

2005

Steroids that activate glucocorticoid receptors (GRs) and mineralocorticoid receptors have important regulatory effects on neural development, plasticity, and the body's stress response. Here, we investigated the role of corticosteroids in regulating the expression of the glial glutamate transporters glial glutamate transporter-1 (GLT-1) and glutamate-aspartate transporter (GLAST) in rat primary astrocytes. The synthetic glucocorticoid dexamethasone provoked a marked increase of GLT-1 transcription and protein levels in cortical astrocytes, whereas GLAST expression remained unaffected. Up-regulation of GLT-1 expression was accompanied by an enhanced glutamate uptake, which could be blocked …

Central Nervous SystemTime FactorsAmino Acid Transport System X-AGLigandsBiochemistryDexamethasoneRats Sprague-Dawleychemistry.chemical_compoundGlucocorticoid receptorMineralocorticoid receptorAdrenal Cortex HormonesCorticosteroneCerebellumGene expressionLuciferasesReceptorDNA Modification MethylasesKainic AcidReverse Transcriptase Polymerase Chain ReactionGlutamate receptorBrainImmunohistochemistryUp-RegulationMifepristoneAzacitidineNeurogliaGlucocorticoidmedicine.drugmedicine.medical_specialtymedicine.drug_classBlotting WesternDetergentsBiologyDecitabineTransfectionMembrane MicrodomainsInternal medicinemedicineAnimalsGlucocorticoidsMolecular BiologyDNA PrimersFluorescent DyesDose-Response Relationship DrugCell BiologyDNA MethylationRatsReceptors MineralocorticoidEndocrinologychemistryMineralocorticoidAstrocytesCorticosteroneJournal of Biological Chemistry
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