Search results for "Enos"

showing 10 items of 1576 documents

The nuclear autoantigen La/SS-associated antigen B: One gene, three functional mRNAs

1997

Transcription of the gene encoding for the nuclear autoantigen La resulted in three mRNA forms. A promoter switching combined with an alternative splicing pathway replaced exon 1 with either exon 1´ or exon 1´´. The exon 1´´ donor splice site was located 4 nts downstream of the exon 1´ donor splice site. All three La mRNA forms were expressed in all the tissues analysed including peripheral blood lymphocytes, liver, fetal spleen, cultured primary endothelial cells, and mouse LTA cell lines permanently transfected with the human La gene. Both the exons 1´ and 1´´ had unusual structures. They contained GC-rich regions and an oligo(U)-tail of 23 uridine residues. Moreover, they encoded for thr…

Molecular Sequence DataBiologyAutoantigensPolymerase Chain ReactionBiochemistryMiceExonExon trappingAnimalsHumansAmino Acid SequenceRNA MessengerMolecular BiologyGeneRibonucleoproteinAdenosine TriphosphatasesMessenger RNASplice site mutationBase SequenceAlternative splicingExonsSequence Analysis DNACell BiologyMolecular biologyOpen reading frameGenetic TechniquesRibonucleoproteinsResearch ArticleTranscription Factors
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Mapping of a binding site for ATP within the extracellular region of the Torpedo nicotinic acetylcholine receptor beta-subunit.

1997

Using 2,8,5'-[H-3]ATP as a direct photoaffinity label for membrane-bound nicotinic acetylcholine receptor (nAChR) from Torpedo marmorata, we have identified a binding site for ATP in the extracellular region of the beta-subunit of the receptor. Photolabeling was completely inhibited in the presence of saturating concentrations of nonradioactive ATP, whereas neither the purinoreceptor antagonists suramin, theophyllin, and caffeine nor the nAChR antagonists alpha-bungarotoxin and d-tubocurarine affected the labeling reaction. Competitive and noncompetitive nicotinic agonists and Ca2+ increased the yield of the photoreaction by up to 50%, suggesting that the respective binding sites are allost…

Molecular Sequence DataPhotoaffinity LabelsReceptors NicotinicTorpedoTritiumBiochemistryPeptide Mappingchemistry.chemical_compoundGanglion type nicotinic receptorAdenosine TriphosphateAdenine nucleotideAnimalsChymotrypsinTrypsinAmino Acid SequenceBinding siteBinding SitesbiologyHydrolysisCell MembranePeptide FragmentsNicotinic acetylcholine receptorNicotinic agonistBiochemistrychemistrybiology.proteinAlpha-4 beta-2 nicotinic receptorExtracellular SpaceAdenosine triphosphateSequence AnalysisATP synthase alpha/beta subunitsBiochemistry
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Inhibition of Eimeria tenella CDK-related kinase 2: From target identification to lead compounds.

2010

Apicomplexan parasites encompass several human- and animal-pathogenic protozoans such as Plasmodium falciparum, Toxoplasma gondii, and Eimeria tenella. E. tenella causes coccidiosis, a disease that afflicts chickens, leading to tremendous economic losses to the global poultry industry. The considerable increase in drug resistance makes it necessary to develop new therapeutic strategies against this parasite. Cyclin-dependent kinases (CDKs) are key molecules in cell-cycle regulation and are therefore prominent target proteins in parasitic diseases. Bioinformatics analysis revealed four potential CDK-like proteins, of which one—E. tenella CDK-related kinase 2 (EtCRK2)—has already been charact…

Molecular Sequence DataProtozoan ProteinsBiochemistryEimeriaArticleAdenosine TriphosphateCyclin-dependent kinaseDrug Discoveryparasitic diseasesAnimalsHumansComputer SimulationHomology modelingAmino Acid SequenceGeneral Pharmacology Toxicology and PharmaceuticsProtein Kinase InhibitorsPharmacologyVirtual screeningBinding SitesbiologyDrug discoveryKinaseCoccidiosisOrganic ChemistryCyclin-dependent kinase 2Cyclin-Dependent Kinase 2Plasmodium falciparumbiology.organism_classificationMolecular biologyBiochemistrybiology.proteinMolecular MedicineBenzimidazolesChickensSequence AlignmentEimeria tenellaChemMedChem
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Preparation of monolithic polymer-magnetite nanoparticle composites into poly(ethylene-co-tetrafluoroethylene) tubes for uses in micro-bore HPLC sepa…

2021

[EN] This paper describes the fabrication of a novel microbore monolithic column modified with magnetite nanoparticles (MNPs) prepared in a poly(ethylene-co-tetrafluoroethylene) (EFTE) tubing, and its application as stationary phase for the chromatographic separation of phosphorylated compounds. In order to obtain the composite column, a two-step procedure was performed. The formation of a glycidyl methacrylate-based monolith inside the activated ETFE tube was firstly carried out. Then, two incorporation approaches of MNPs in monoliths were investigated. The generic polymer was modified with 3-aminopropyltrimethoxysilane (APTMS) to be subsequently attached to MNP surfaces. Alternatively, AP…

Monolithic columnGlycidyl methacrylateMonolithic HPLC column02 engineering and technologyEFTE tubing01 natural sciencesAnalytical Chemistrychemistry.chemical_compoundETFEAdsorptionQUIMICA ANALITICAHybrid monolithsHILICMonolithAdenosine phosphatesMagnetite nanoparticleschemistry.chemical_classificationgeographygeography.geographical_feature_categoryHydrophilic interaction chromatography010401 analytical chemistryExtraction (chemistry)Polymer021001 nanoscience & nanotechnology0104 chemical scienceschemistryChemical engineering0210 nano-technologyTalanta
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2013

Graft-versus-host disease (GvHD) is a key contributor to the morbidity and mortality after allogeneic hematopoetic stem cell transplantation (HSCT). Regulatory Foxp3(+) CD4(+) T cells (Treg) suppress conventional T cell activation and can control GvHD. In our previous work, we demonstrate that a basic mechanism of Treg mediated suppression occurs by the transfer of cyclic adenosine monophosphate (cAMP) to responder cells. Whether this mechanism is relevant for Treg mediated suppression of GvHD is currently unknown. To address this question, bone marrow and T cells from C57BL/6 mice were transferred into lethally irradiated BALB/c recipients, and the course of GvHD and survival were monitore…

MultidisciplinaryT cellFOXP3chemical and pharmacologic phenomenaBiologymedicine.diseaseTransplantationchemistry.chemical_compoundsurgical procedures operativemedicine.anatomical_structureGraft-versus-host diseasechemistryImmunologymedicineCytotoxic T cellCyclic adenosine monophosphateStem cellRoliprammedicine.drugPLOS ONE
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Using FFR to Detect Ischemia in Myocardial Bridge Lesions

2016

Beyond atherosclerosis, a number of other phenomena may result in cardiac ischemia. Among these, extracoronary compression due to myocardial bridges may cause a dynamic stenosis and typical angina. The assessment of the hemodynamic relevance and the treatment of such lesions have unique characteristics that are due to the fact that extracoronary compression from myocardial bridges is mostly a systolic phenomenon and is dependent on the inotropic state. The consequence is that other hyperemic stimuli, such as dobutamine, may be more adequate to unveil ischemia in these settings.

Myocardial bridgeInotropemedicine.medical_specialtybusiness.industryCardiac ischemiaIschemiaHemodynamicsmedicine.diseaseTypical anginaStenosisInternal medicineCardiologyMedicineDobutaminebusinessmedicine.drug
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Dexamethasone dipropionate loaded nanoparticles of α-elastin-g-PLGA for potential treatment of restenosis.

2013

A graft copolymer of α-elastin with poly(lactic-co-glycolic) acid (PLGA) has been synthesized and successfully employed to produce nanoparticles. Exploiting the known biological activity of α-elastin to promote the maintenance of smooth muscle cells (SMCs) contractile phenotype and the antiproliferative effect of glucocorticoids, the aim of this research was to produce drug-loaded nanoparticles suitable for potential treatment of restenosis. In particular, nanoparticles of α-elastin-g-PLGA with a mean size of 200 nm have been produced and loaded with dexamethasone dipropionate (10% w/w), chosen as a model drug that inhibits proliferation of vascular SMCs. These nanoparticles are able to pro…

Myocytes Smooth MusclePharmaceutical ScienceDexamethasoneMuscle Smooth VascularCoronary Restenosischemistry.chemical_compoundPolylactic Acid-Polyglycolic Acid CopolymerDrug DiscoveryMyocyteAnimalsHumansLactic AcidParticle SizeCells CulturedCell ProliferationDrug CarriersbiologyCell growthElastaseBiological activityCell DifferentiationElastinBlotPLGAchemistryBiochemistryBiophysicsbiology.proteinMolecular MedicineNanoparticlesCattleDrug carrierElastinPolyglycolic AcidMolecular pharmaceutics
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Nitric oxide synthase inhibition and oxidative stress in cardiovascular diseases: Possible therapeutic targets?

2013

International audience; Nitric oxide (• NO) is synthetized enzymatically from L-arginine (L-Arg) by three NO synthase isoforms, iNOS, eNOS and nNOS. The synthesis of NO is selectively inhibited by guanidino-substituted analogs of L-Arg or methylarginines such as asymmetric dimethylarginine (ADMA), which results from protein degradation in cells. Many disease states, including cardiovascular diseases and diabetes, are associated with increased plasma levels of ADMA. The N-terminal catalytic domain of these NOS isoforms binds the heme prosthetic group as well as the redox cofactor, tetrahydrobiopterin (BH 4) associated with a regulatory protein, calmodulin (CaM). The enzymatic activity of NOS…

NO inhibitorsfree radicals030204 cardiovascular system & hematologyProtein degradationPharmacologyNitric OxideNitric oxide03 medical and health scienceschemistry.chemical_compoundBH 40302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemcardiovascular diseaseEnosmedicineAnimalsHumansPharmacology (medical)Enzyme InhibitorsEndothelial dysfunctionReactive nitrogen species030304 developmental biologyPharmacologyNO synthases0303 health sciencesbiologyTetrahydrobiopterinbiology.organism_classificationmedicine.disease[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system3. Good healthADMANitric oxide synthaseOxidative StresschemistryBiochemistryCardiovascular Diseasesbiology.proteinNitric Oxide SynthaseAsymmetric dimethylargininemedicine.drugPharmacology & Therapeutics
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Conjugados poliméricos y su utilización como nanomedicinas anticancerígenas

2009

Independientemente del descubrimiento de nuevos fármacos para dianas farmacológicas bien establecidas, el compromiso de la ciencia con la sociedad demanda del desarrollo de análogos macromoleculares que mejoren las posibilidades terapéuticas de los fármacos existentes aportando una mayor actividad biológica y una mayor especificidad. Se postula, cada vez con más fuerza, que la aplicación de la nanotecnología a la medicina es la clave para conseguir las mejoras necesarias tanto en diagnosis como en terapia anticancerígeno [1]. Para poder distinguirlos de otros productos biotecnológicos como proteínas y anticuerpos, los nanofármacos han sido definidos como “... sistemas complejos de escala na…

NanomedicinasConjugados poliméricos:CIENCIAS MÉDICAS ::Farmacología [UNESCO]AnticancerígenosUNESCO::CIENCIAS MÉDICAS ::FarmacologíaConjugados poliméricos; Nanomedicinas; Anticancerígenos
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Intracellular glutathione in human hepatocytes incubated with S-adenosyl-L-methionine and GSH-depleting drugs

1991

Abstract The present study was undertaken to investigate (a) whether S- adenosyl- L -methionine (SAMe) added to culture medium can increase intracellular glutathione (GSH) levels in human hepatocytes and (b) whether SAMe can prevent the GSH depletion found in human hepatocytes incubated with GSH-depleting drugs (paracetamol, opiates, ethanol). Incubation of hepatocytes with increasing concentrations of SAMe resulted in a dose-dependent elevation of intracellular GSH content, which reached its maximum (35% increase) at 30 μM after 20 h. SAMe, as the only sulfur source in the medium, was efficient in repleting GSH-depleted hepatocytes following treatment with diethyl maleate. Incubation of hu…

NarcoticsS-Adenosylmethioninemedicine.medical_treatmentPharmacologyToxicologychemistry.chemical_compoundmedicineHumansAntidoteIncubationCells CulturedAcetaminophenEthanolMethionineDose-Response Relationship DrugEthanolGlutathioneGlutathioneHeroinmedicine.anatomical_structureLiverchemistryBiochemistryHepatocyteToxicityMethadoneIntracellularToxicology
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