Search results for "adenosine"

showing 10 items of 542 documents

Inhibitory responses to exogenous adenosine in murine proximal and distal colon”

2006

The aims of the present study were firstly, to characterize pharmacologically the subtypes of P(1) purinoreceptors involved in the inhibitory effects induced by exogenous adenosine in longitudinal smooth muscle of mouse colon, and secondly, to examine differences in the function and distribution of these receptors between proximal and distal colon. Adenosine (100 microM-3 mM) caused a concentration-dependent reduction of the amplitude of spontaneous contractions in the proximal colon, and muscular relaxation in the distal colon. In the proximal colon, adenosine effects were antagonized by a selective A(1) receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 10 nM), but were not m…

MaleAdenosineNitric Oxide Synthase Type IIIColonmouse colonadenosine A2B receptorNitric OxideSettore BIO/09 - FisiologiaMiceP1 purinoreceptorAnimalsadenosine A3 receptorEnzyme InhibitorsDose-Response Relationship Drugadenosine A1 receptorReceptors Purinergic P1Muscle SmoothTriazolesnitrergic nervesMice Inbred C57BLNG-Nitroarginine Methyl Esteradenosine A2 receptorPurinergic P1 Receptor AntagonistsXanthinesPapersQuinazolinesTheobrominemechanical activityMuscle ContractionSignal Transduction
researchProduct

p38 MAPK Controls Prothrombin Expression by Regulated RNA 3′ End Processing

2011

Thrombin is a key protease involved in blood coagulation, complement activation, inflammation, angiogenesis, and tumor invasion. Although induced in many (patho-)physiological conditions, the underlying mechanisms controlling prothrombin expression remained enigmatic. We have now discovered that prothrombin expression is regulated by a posttranscriptional regulatory mechanism responding to stress and inflammation. This mechanism is triggered by external stimuli that activate p38 MAPK. In turn, p38 MAPK upmodulates canonical 3' end processing components and phosphorylates the RNA-binding proteins FBP2 and FBP3, which inhibit 3' end processing of mRNAs, such as prothrombin mRNA, that bear a d…

MaleAdenosinePolymersp38 mitogen-activated protein kinasesInflammationPlasma protein bindingBiologyp38 Mitogen-Activated Protein KinasesGene Expression Regulation EnzymologicMiceThrombinCell Line TumormedicineAnimalsHumansNeoplasm InvasivenessRNA MessengerMolecular BiologyRegulation of gene expressionMessenger RNARNACell BiologyXenograft Model Antitumor AssaysCell biologyRibonucleoproteinsImmunologyPhosphorylationRNAProthrombinmedicine.symptomRNA 3' End Processingmedicine.drugProtein BindingMolecular Cell
researchProduct

Apremilast, a novel phosphodiesterase 4 (PDE4) inhibitor, regulates inflammation through multiple cAMP downstream effectors

2015

Introduction This work was undertaken to delineate intracellular signaling pathways for the PDE4 inhibitor apremilast and to examine interactions between apremilast, methotrexate and adenosine A2A receptors (A2AR). Methods After apremilast and LPS incubation, intracellular cAMP, TNF-α, IL-10, IL-6 and IL-1α were measured in the Raw264.7 monocytic murine cell line. PKA, Epac1/2 (signaling intermediates for cAMP) and A2AR knockdowns were performed by shRNA transfection and interactions with A2AR and A2BR, as well as with methotrexate were tested in vitro and in the murine air pouch model. Statistical differences were determined using one or two-way ANOVA or Student’s t test. The alpha nominal…

MaleAdenosineReceptor Adenosine A2AImmunologyBlotting WesternAdenosine A2A receptorGene ExpressionPharmacologyBiologyCell LineMiceRheumatologyPhenethylaminesmedicineCyclic AMPImmunology and AllergyAnimalsGuanine Nucleotide Exchange FactorsReceptorIC50ArtritisReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaMacrophagesAdenosineMolecular biologyCyclic AMP-Dependent Protein KinasesThalidomideMethotrexateMechanism of actionAntirheumatic AgentsCytokinesTumor necrosis factor alphaRNA InterferenceApremilastPhosphodiesterase 4 Inhibitorsmedicine.symptomInflammation MediatorsIntracellularMedicamentsmedicine.drugResearch Article
researchProduct

Prevalence and prognostic impact of nonischemic late gadolinium enhancement in stress cardiac magnetic resonance

2020

Aim To assess the prevalence and prognostic significance of NI-LGE in patients undergoing stress-CMR. Methods Stress-CMR with either dipyridamole or adenosine was performed in 283 patients (228 men, 81%) including perfusion imaging, wall motion evaluation and LGE. Follow-up was completed in all enrolled patients (median time: 1850 days; interquartile range: 1225-2705 days). Composite endpoint included cardiac death, ventricular tachycardia, myocardial infarction, stroke, hospitalization for cardiac cause and coronary revascularization performed beyond 90 days from stress-CMR scans. Results One hundred and twelve patients (40%) had negative LGE (no-LGE), 140 patients (49%) I-LGE and 31 patie…

MaleAdenosineTime FactorsVasodilator AgentsContrast MediaPerfusion scanning030204 cardiovascular system & hematologyVentricular tachycardia0302 clinical medicineRisk FactorsInterquartile rangePrevalence030212 general & internal medicineMyocardial infarctionStrokenonischemic fibrosislate gadolinium enhancement; nonischemic cardiac findings; nonischemic fibrosis; prognosis; stress perfusion cardiac magnetic resonanceDipyridamoleGeneral MedicineMiddle AgedMagnetic Resonance ImagingDipyridamolelate gadolinium enhancementstress perfusion cardiac magnetic resonanceembryonic structurescardiovascular systemCardiologyFemaleCardiology and Cardiovascular MedicinePerfusionmedicine.drugnonischemic cardiac findingsmedicine.medical_specialtyHeart DiseasesPerfusion ImagingRisk Assessment03 medical and health sciencesPredictive Value of TestsInternal medicinemedicineHumanscardiovascular diseasesSurvival analysisAgedRetrospective Studiesbusiness.industryMyocardiummedicine.diseaseFibrosisLate gadolinium enhancement Nonischemic cardiac findings Nonischemic fibrosis Prognosis Stress perfusion cardiac magnetic resonanceprognosisbusinessJournal of Cardiovascular Medicine
researchProduct

Differential expression of PGC-1α and metabolic sensors suggest age-dependent induction of mitochondrial biogenesis in Friedreich ataxia fibroblasts.

2011

11 pages, 6 figures. PMID:21687738[PubMed] PMCID: PMC3110204

MaleAgingMitochondrial DiseasesMitochondrial MyopathyUbiquinoneCardiomyopathylcsh:MedicineMitochondrionAMP-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesAntioxidantsAdenosine TriphosphateAMP-activated protein kinaseTrinucleotide RepeatsFibrosisMolecular Cell BiologyChildlcsh:ScienceHeat-Shock ProteinsRegulation of gene expressionMultidisciplinaryMovement DisordersbiologyNeuromuscular DiseasesMiddle AgedCatalasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaCell biologyMitochondriaDNA-Binding ProteinsNeurologyDisease ProgressionMedicineFemalemedicine.symptomSignal TransductionResearch ArticleAdultcongenital hereditary and neonatal diseases and abnormalitiesAtaxiaAdolescentMitochondrial ProteinsmedicineGeneticsHumansBiologyAllelesGlutathione PeroxidaseSuperoxide Dismutaselcsh:RHuman GeneticsFibroblastsmedicine.diseaseMolecular biologyOxidative StressMitochondrial biogenesisGene Expression RegulationFriedreich Ataxiabiology.proteinFrataxinlcsh:QEnergy MetabolismReactive Oxygen SpeciesTranscription FactorsPLoS ONE
researchProduct

Neurotransmitters involved in the fast inhibitory junction potentials in mouse distal colon

2003

We investigated, in murine colon circular muscle, the role of adenosine 5′-triphosphate (ATP) and pituitary adenylate cyclase activating peptide (PACAP) as inhibitory neurotransmitters of the fast component of nerve-evoked inhibitory junction potential (fast IJP). Fast IJP was antagonised by apamin or suramin, abolished by desensitisation with the P2Y receptor agonist, adenosine 5′-O-2-thiodiphosphate (ADPβS), unaffected by desensitisation with P2X receptor agonist, α,β-methylene ATP (α,β-meATP), and reduced by PACAP-(6-38), a PACAP receptor antagonist. ATP induced membrane hyperpolarization resistant to tetrodotoxin, Nω-nitro-L-arginine methyl ester (L-NAME) or PACAP-(6-38), but antagonise…

MaleAgonistendocrine systemmedicine.medical_specialtyP2Y receptorColonmedicine.drug_classPurinoceptorNeuromuscular JunctionSuraminTetrodotoxinBiologyApaminSettore BIO/09 - FisiologiaMembrane PotentialsCellular and Molecular NeuroscienceMicechemistry.chemical_compoundAdenosine TriphosphateInternal medicinemedicineAnimalsMurinePharmacologyNeurotransmitter AgentsDose-Response Relationship Drugmusculoskeletal neural and ocular physiologyNeuropeptidesMembrane hyperpolarizationThionucleotidesHyperpolarization (biology)Receptor antagonistAdenosinePeptide FragmentsATPAdenosine DiphosphatePituitary adenylate cyclase-activating peptideNG-Nitroarginine Methyl EsterEndocrinologyApaminchemistryPituitary Adenylate Cyclase-Activating PolypeptideFast inhibitory junction potentialPACAP (pituitary adenylate cyclase activating peptide)hormones hormone substitutes and hormone antagonistsmedicine.drugEuropean Journal of Pharmacology
researchProduct

The interaction of Fe(III), adriamycin and daunomycin with nucleotides and DNA and their effects on cell growth of fibroblasts (NIH-3T3)

1996

The interactions of the iron complexes of the anthracycline antitumour drugs daunomycin (DN) and adriamycin (ADM) with the mononucleotide AMP, herring sperm DNA, plasmic pBR322 and immortalized 3T3 fibroblasts were studied. By means of Mössbauer spectroscopy it was demonstrated that DNA is a powerful ferric iron chelator as compared with AMP, which is not able to compete with DN or acetohydroxamic acid for ferric iron. The difference between AMP and DNA is postulated to be based on the chelate effect. The Mössbauer spectra of the ternary Fe-anthracycline-DNA systems differ from Fe-anthracycline binary complexes, indicating rearrangement reactions. Dialysis experiments clearly disclose the f…

MaleBase pairStereochemistryIronIntercalation (chemistry)General Biochemistry Genetics and Molecular BiologyBiomaterialsMiceSpectroscopy Mossbauerchemistry.chemical_compoundmedicineAnimalsNucleotideCytotoxicitychemistry.chemical_classificationChemistryCell growthAcetohydroxamic acidDaunorubicinFishesMetals and AlloysBiological Transport3T3 CellsDNASpermatozoaAdenosine MonophosphateDoxorubicinFerricGeneral Agricultural and Biological SciencesCell DivisionDNAPlasmidsmedicine.drugBiometals
researchProduct

Inhibition of iNOS activity by 1400W decreases glutamate release and ameliorates stroke outcome after experimental ischemia

2005

Background and purpose. It has been shown that the reversed operation of glutamate transporters when ATP levels fall accounts for most glutamate release induced by severe cerebral ischemia. Nitric oxide (NO) is formed after ischemia and causes ATP depletion. Our purpose is to test if NO release from inducible NO synthase (iNOS) after stroke may cause a delayed glutamate release due to ATP depletion that might underlie progression of the ischemic infarct. We have studied the effect of the highly selective inhibitor of iNOS activity 1400W on brain ATP levels, extracellular glutamate, and stroke outcome after transient focal cerebral ischemia in rats. Methods. To induce focal ischemia, the mid…

MaleBenzylaminesAmino Acid Transport System X-AGIschemiaAmidinesInfarctionDown-RegulationGlutamic AcidNitric Oxide Synthase Type IIL-argininePharmacologyNeuroprotectionNitric oxidelcsh:RC321-571chemistry.chemical_compoundAdenosine TriphosphateWestern blotmedicine.arteryStroke outcomeMedicineAnimalscardiovascular diseasesEnzyme InhibitorsRats Wistarlcsh:Neurosciences. Biological psychiatry. Neuropsychiatrymedicine.diagnostic_testbusiness.industryGlutamate receptorBrainInfarction Middle Cerebral ArteryNitric oxideCerebral Infarctionmedicine.diseaseNeuroprotectionRatsATPStrokeDisease Models AnimalNeuroprotective AgentsTreatment OutcomeNeurologychemistryCytoprotectionIschemic Attack TransientAnesthesiaMiddle cerebral arteryNitric Oxide SynthaseGlutamatebusinessNeurobiology of Disease
researchProduct

Characterization of DNA adducts at the bay region of dibenz[a,h]anthracene formed in vitro

1993

Bay region diolepoxide-DNA adducts of dibenz[a,h]anthracene (DBA) formed in vitro were identified and their absolute stereochemistry was assigned. After activation of [5,12-14C]DBA with liver microsomes obtained from Aroclor 1254 treated male Sprague-Dawley rats in the presence of calf thymus DNA for 1 h, the amount of DNA adducts was found to be 9.9 +/- 2.4 pmol/mg DNA, calculated on the basis of the portion of radioactivity eluted from the HPLC reversed-phase column with a water/acetonitrile gradient. Bay region diolepoxide-DNA adducts represented 27.5% of radioactivity associated with DNA adducts. The absolute configuration of the various adducts was determined from the reaction of the (…

MaleCancer ResearchAnthraceneMetaboliteAbsolute configurationStereoisomerismDNAGeneral MedicineIn Vitro TechniquesHigh-performance liquid chromatographyMedicinal chemistryRatsAdductRats Sprague-DawleyDNA Adductschemistry.chemical_compoundchemistryBiochemistryDeoxyadenosineBenz(a)AnthracenesMicrosomes LiverAnimalsDeoxyguanosineDibenz(ah)anthraceneBiotransformationCarcinogenesis
researchProduct

Quantitative changes of metabolic and bioenergetic parameters in experimental tumors during fractionated irradiation.

1999

Abstract Purpose: Previous studies with rat rhabdomyosarcomas indicate that during fractionated irradiation profound alterations of the tumor microvasculature and the oxygenation status occur when the total dose exceeds 45 Gy. At this dose a destruction which included all structures of the vessels and a significant worsening in tumor oxygenation were found. The aim of the present study was to analyze whether these effects of fractionated irradiation on the microvasculature and on tumor oxygenation also induce changes in the bioenergetic and metabolic status in the tumors during radiation treatment. Methods and Materials: R1H rhabdomyosarcomas of the rat implanted into the flank were irradia…

MaleCancer ResearchPathologymedicine.medical_specialtyRadiobiologyTime Factorsmedicine.medical_treatmentAdenosine TriphosphateRhabdomyosarcomaMedicineAnimalsRadiology Nuclear Medicine and imagingIrradiationLactic AcidCobalt RadioisotopesRhabdomyosarcomaRadiationbusiness.industryDose fractionationRadiobiologyOxygenationTumor Oxygenationmedicine.diseaseRatsRadiation therapyGlucoseOncologySarcomaDose Fractionation RadiationNuclear medicinebusinessNeoplasm TransplantationInternational journal of radiation oncology, biology, physics
researchProduct