Search results for "ADAM"

showing 10 items of 372 documents

How to pay for the war in times of imperfect commitment. Adam Smith and David Ricardo on the Sinking Fund

2014

AbstractThe paper proposes a comparative analysis of Smith's and Ricardo's views on the sinking fund. It shows that Smith and Ricardo agreed in stressing the ineffectiveness of the sinking fund as a policy instrument targeted at public debt repayment and tax-burden relief, pointing out that its actual workings had paradoxically helped to increase rather than reduce British total debt-load. Moreover, their explanation of the sinking fund paradox integrates a defective fiscal commitment technology with powerful politicians’ incentives to siphon off the money stored in the sinking fund to meet sudden increases of public expenditure whenever the occasion arose.

Macroeconomics060106 history of social sciencesGeneral Arts and HumanitiesKeynesian economics05 social sciencesEconomics Econometrics and Finance (miscellaneous)Public expenditure06 humanities and the artsDebt repaymentAdam smithAdam Smith David Ricardo Ricardian equivalence sinking fund imperfect commitmentSpanish Civil WarIncentiveHistory and Philosophy of ScienceSettore SECS-P/04 - Storia Del Pensiero Economico0502 economics and businessEconomics0601 history and archaeologySinking fundImperfect050207 economicsSettore SECS-P/01 - Economia Politica
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L’opera in breve: Madama Butterfly

2009

Madama ButterflyoperaSettore L-ART/07 - Musicologia E Storia Della MusicaPuccini
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Belicistas vergonzantes

2003

Mal absolutoVidal-Beneyto JoséArmas atómicasIrakTerrorismoTalibanesPublicaciones: Obra periodística: Columnas y artículos de opiniónPakistánConsejo de SeguridadCasa BlancaAfganistánSeguridadProtectorado USABushGobierno americanoDemocraciaGuerra químicaProgramas humanitariosProsperidadGUERRA CONTRA EL TERRORISMOBin LadenPreguerraGuerra preventivaSeñores de la guerraSadam HuseinOpinión públicaGuerra bacteriológicaOriente PróximoEEUU
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Open ADAMTS13, induced by antibodies, is a biomarker for subclinical immune-mediated thrombotic thrombocytopenic purpura

2020

Recently, we showed that ADAMTS13 circulates in an open conformation during the acute phase of immune-mediated thrombotic thrombocytopenic purpura (iTTP). Although the cause of this conformational change remains elusive, ADAMTS13 is primarily closed in iTTP patients in remission with ADAMTS13 activity >50% and undetectable anti-ADAMTS13 autoantibodies, as well as after rituximab treatment, suggesting a role for anti-ADAMTS13 autoantibodies. Therefore, immunoglobulin G from 18 acute iTTP patients was purified and added to closed ADAMTS13 in healthy donor plasma. This resulted in open ADAMTS13 in 14 of 18 (78%) samples, proving that anti-ADAMTS13 autoantibodies can induce an open ADAMTS13 con…

Male0301 basic medicine[SDV.MHEP.HEM] Life Sciences [q-bio]/Human health and pathology/Hematologymedicine.medical_specialtySettore MED/09 - Medicina InternaProtein ConformationImmunologyThrombotic thrombocytopenic purpuraADAMTS13 ProteinBiochemistryImmunoglobulin G03 medical and health sciences0302 clinical medicineVon Willebrand factorInternal medicinehemic and lymphatic diseasesmedicineHumansAutoantibodiesSubclinical infectionPurpura Thrombocytopenic IdiopathicHematology[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologybiologybusiness.industryAutoantibody[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyCell BiologyHematologyMiddle Agedmedicine.diseaseADAMTS133. Good health030104 developmental biologyImmunologybiology.proteinFemaleRituximabRituximabbusinessBiomarkers[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyFollow-Up Studies030215 immunologymedicine.drug
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SARS CoV2 infection _The longevity study perspectives

2021

Graphical abstract

MaleAgingssRNA single-stranded RNARFLP restriction fragment length polymorphismHSPs heat shock proteinsReviewPTMs post-translational modificationsSevere Acute Respiratory SyndromeBiochemistryHIV-1 human immunodeficiency virus-1TNF-α tumor necrosis factor-αEC endothelial cells0302 clinical medicineFluAV influenza A virusI insertionMedicineIFN-γ interferon-γDIC disseminated intravascular coagulationPCR Polymerase Chain Reactionmedia_commonAged 80 and overLongevityRBD receptor-binding domainNeurologyLongevity modelMI myocardial infarctionNK natural killerhPIV2 human parainfluenza virus type 2media_common.quotation_subjectResearching genetic basis of resistance and potential pharmacological targetsLongevityDBP diastolic blood pressureNF-Kb nuclear transcription factor kBRANTES regulated upon activation normal T cell expressed and secretedMphi human macrophages03 medical and health sciencesCox 2 cyclooxygenase 2ORF open reading framePT prothrombin timeSettore MED/05 - Patologia ClinicaHumansMolecular BiologyInflammatory genesARDS acute respiratory distress syndromeNO nitric oxideD deletionCpGIs CpG islandsT2DM type 2 diabetes mellitusmedicine.diseaseFDP fibrin degradation products030104 developmental biologySARS CoV2 severe acute respiratory syndrome Coronavirus 2 virusImmunologyBMI body max indexItalian nonagenarians/centenariansRSV respiratory syncytial virusComplication030217 neurology & neurosurgeryMAPK mitogen-activated protein kinaseIP-10 IFN-γ -Inducible Protein 1040301 basic medicineAT1R activity of angiotensin 1 receptorsDCs dentritic cellsSSCP single strand conformation polymorphismACE/DD polymorphism of the angiotensin converting enzymeFGF21 fibroblast growth factor 21TLR4 toll-like receptor 4NAD nicotinamide adenine dinucleotideACE angiotensin-I converting enzymeAT2R activity of angiotensin 2 receptorsCOVID-19 Coronavirus disease 2019Respiratory distressACE2 angiotensin converting enzyme 2MKP-1 mitogen-activated protein kinase phosphatase-1 ()PD protease domainSNP single nucleotide polymorphismEH essential hypertensionTNFR tumor necrosis factor receptorINR international normalized ratio of the prothrombin timePAI-1 plasminogen activator inhibitor-1Ang angiotensinLPS lipopolysaccharideMCP1 monocyte chemoattractant protein-1medicine.symptomaPTT partial thromboplastin timeBiotechnologyDUSP1 dual specificity phosphatase 1Coronavirus disease 2019 (COVID-19)PC prostate cancerRAS renin-angiotensin aldosterone systemCCR5Δ32 genetic variant of chemokine receptorCOVID-19 Researching genetic basis of resistance and potential pharmacological targets Italian nonagenarians/centenarians Longevity modelAsymptomaticSARS-1 severe acute respiratory syndrome virus 1SIRT-1 Sirtuin 1Th1 t-helper lymphocyte type 1Immune systemROS reactive oxygen speciesTGF-β transforming growth factor betaET-1 endothelin-1ComputingMethodologies_COMPUTERGRAPHICSADAM-17 metallopeptidase domain 17business.industrySARS-CoV-2SBP systolic blood pressureCOVID-19HDACs histone deacetylasesComorbidityImmune Systembusiness5-LO lipoxygenase 5Ageing Research Reviews
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Extract of Caragana sinica as a potential therapeutic option for increasing alpha-secretase gene expression

2015

Abstract Background Alzheimer's disease represents one of the main neurological disorders in the aging population. Treatment options so far are only of symptomatic nature and efforts in developing disease modifying drugs by targeting amyloid beta peptide-generating enzymes remain fruitless in the majority of human studies. During the last years, an alternative approach emerged to target the physiological alpha-secretase ADAM10, which is not only able to prevent formation of toxic amyloid beta peptides but also provides a neuroprotective fragment of the amyloid precursor protein – sAPPalpha. Purpose To identify novel alpha-secretase enhancers from a library of 313 extracts of medicinal plant…

MaleAmyloid betaADAM10Pharmaceutical ScienceBiologyPharmacologyBlood–brain barrierGene Expression Regulation EnzymologicADAM10 ProteinAmyloid beta-Protein PrecursorMicealpha-Viniferinchemistry.chemical_compoundCell Line TumorDrug DiscoverymedicineAmyloid precursor proteinAnimalsAspartic Acid EndopeptidasesHumansPromoter Regions GeneticBenzofuransMice KnockoutPharmacologyReporter genePlants MedicinalPlant ExtractsCaragana sinicaMembrane Proteinsbiology.organism_classificationCaraganaADAM Proteinsmedicine.anatomical_structureComplementary and alternative medicinechemistryAlpha secretaseBlood-Brain Barrierbiology.proteinMolecular MedicineAmyloid Precursor Protein SecretasesPhytomedicine
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Glia talk back.

2014

This study shows that the activity of neurons can trigger shedding of a protein, NG2, from the surface of oligodendrocyte precursor cells; this protein in turn modulates synaptic transmission, revealing a two-way conversation between neurons and glia.

MaleCell signalingNeural NetworksQH301-705.5AMPA receptorBiologyNeurotransmissionResearch and Analysis MethodsMechanical Treatment of SpecimensGeneral Biochemistry Genetics and Molecular BiologyBehavioral NeuroscienceNeurotransmitter receptormedicineBiological neural networkPremovement neuronal activityAnimalsBiology (General)AntigensNeuronsGeneral Immunology and MicrobiologyGeneral NeuroscienceMembrane ProteinsBiology and Life SciencesLong-term potentiationADAM ProteinsOligodendrogliamedicine.anatomical_structureElectroporationnervous systemSpecimen DisruptionSpecimen Preparation and TreatmentCellular NeuroscienceImmunologyProteoglycansNeuronAmyloid Precursor Protein SecretasesMolecular NeuroscienceGeneral Agricultural and Biological SciencesNeuroscienceResearch ArticleNeurosciencePLoS biology
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Multifocal aplasia cutis congenita, distal limb hemimelia, and cutis marmorata telangiectatica in a patient with Adams-Oliver syndrome.

1992

Summary We describe an 18-month-old boy with multifocal scalp defects over the posterior parietal region combined with an underlying defect of the skull, left lower limb distal hemimelia and generalized cutis marmorata telangiectatica, consistent with a diagnosis of Adams–Oliver syndrome (aplasia cutis congenita with distal transverse limb defects).

MaleCutis marmorataPathologymedicine.medical_specialtyDermatologyAplasia cutis congenitaEctromeliaEctodermal DysplasiamedicineHemimeliaHumansAbnormalities MultipleTelangiectasisSkinLegScalpbusiness.industryInfantAplasiaAnatomySyndromemedicine.diseasebody regionsSkullmedicine.anatomical_structureScalpmedicine.symptombusinessAdams–Oliver syndromeThe British journal of dermatology
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Acitretin, an Enhancer of Alpha-Secretase Expression, Crosses the Blood-Brain Barrier and Is Not Eliminated by P-Glycoprotein

2011

<i>Background:</i> ADAM10 (a disintegrin and metalloproteinase 10) has been demonstrated to act as the main physiological α-secretase. Enzymatic activity of the α-secretase on the one hand prevents the formation of toxic Aβ peptides and on the other hand promotes the secretion of a neurotrophic and neuroprotective amyloid precursor protein fragment (APPs-α) by cleaving the amyloid precursor protein within its Aβ sequence. Enhancement of ADAM10’s gene expression may therefore present a valuable therapeutic approach for the treatment of Alzheimer’s disease (AD), where Aβ peptides are severely involved in the pathogenesis. <i>Objective:</i> In cell culture and in a tran…

MaleGenetically modified mouseATP Binding Cassette Transporter Subfamily BTime FactorsADAM10PharmacologyTransfectionAcitretinADAM10 ProteinMiceNeuroblastomachemistry.chemical_compoundCell Line TumormedicineAmyloid precursor proteinAnimalsHumansATP Binding Cassette Transporter Subfamily B Member 1Chromatography High Pressure LiquidP-glycoproteinMice KnockoutAnalysis of VarianceReporter genebiologyMembrane ProteinsMolecular biologyAcitretinADAM ProteinsGene Expression RegulationNeurologychemistryAlpha secretaseBlood-Brain Barrierbiology.proteinTamibaroteneNeurology (clinical)Amyloid Precursor Protein Secretasesmedicine.drugNeurodegenerative Diseases
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The Carbon Monoxide-Releasing Molecule Tricarbonyldichlororuthenium(II) Dimer Protects Human Osteoarthritic Chondrocytes and Cartilage from the Catab…

2008

We have investigated the effects of a carbon monoxide-releasing molecule, tricarbonyldichlororuthenium(II) dimer (CORM-2), on catabolic processes in human osteoarthritis (OA) cartilage and chondrocytes activated with interleukin-1beta. In these cells, proinflammatory cytokines induce the synthesis of matrix metalloproteinases (MMPs) and aggrecanases, including members of a disintegrin and metalloproteinase with thrombospondin domain (ADAMTS) family, which may contribute to cartilage loss. CORM-2 down-regulated MMP-1, MMP-3, MMP-10, MMP-13, and ADAMTS-5 in OA chondrocytes, and it inhibited cartilage degradation. These effects were accompanied by increased aggrecan synthesis and collagen II e…

MaleInterleukin-1betaDown-RegulationMatrix metalloproteinaseProtective AgentsProinflammatory cytokineExtracellular matrixChondrocytesOsteoarthritisOrganometallic CompoundsmedicineExtracellularHumansAggrecansCollagen Type IIAggrecanAgedPharmacologyCarbon MonoxideThrombospondinChemistryCartilageADAMTSMatrix MetalloproteinasesCell biologyCartilagemedicine.anatomical_structureBiochemistryMolecular MedicineFemaleJournal of Pharmacology and Experimental Therapeutics
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