0000000000156675

AUTHOR

Ramos M

showing 2 related works from this author

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

2017

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, …

0301 basic medicine030204 cardiovascular system & hematologylaw.invention0302 clinical medicinec-reactive proteinRandomized controlled triallawCardiovascular Diseasemiddle ageddouble-blind methodantibodiesMyocardial infarctionhumansStrokeinterleukin-1betabiologyAntibodies MonoclonaldrugGeneral MedicineLipidAged; anti-inflammatory agents; antibodies; monoclonal; antibodies; monoclonal; humanized; atherosclerosis; c-reactive protein; cardiovascular diseases; dose-response relationship; drug; double-blind method; female; humans; incidence; infections; interleukin-1beta; lipids; male; middle aged; myocardial infarction; neutropenia; secondary prevention; strokestrokeAnti-Inflammatory AgentagedEditorialfemalemyocardial infarctionAtherosclerosiMonoclonalsecondary preventionHumanmedicine.drugmedicine.medical_specialtymonoclonalNeutropeniaAntibodies Monoclonal HumanizedInfectionsPlaceboaged; anti-inflammatory agents; antibodies monoclonal; atherosclerosis; c-reactive protein; cardiovascular diseases; dose-response relationship drug; double-blind method; female; humans; incidence; infection; interleukin-1beta; lipids; male; middle aged; myocardial infarction; neutropenia; secondary prevention; stroke; medicine (all)anti-inflammatory agentsdose-response relationshiplipids03 medical and health sciencesmaleInternal medicinemedicineneutropeniamedicine (all)Dose-Response Relationship Drugbusiness.industryAntiinflammatory Therapy Canakinumab for Atherosclerotic DiseaseC-reactive proteinmedicine.diseaseinfectioncardiovascular diseasesSurgeryCanakinumab030104 developmental biologyincidencebiology.proteinatherosclerosisbusinessNew England journal of medicine
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Oxidative stress induces the expression of the major histocompatibility complex in murine tumor cells.

2001

The effect of t-butyl hydroperoxide (t-BOOH) on the induction of the Major Histocompatibility Complex (MHC) class I genes has been studied in two cell clones (B9 and G2) of the methylcholanthrene-induced murine fibrosarcoma GR9. These two clones were selected based on their different biological and biochemical behavior specially related to their tumor induction capability when injected into a BALB/c mouse. t-BOOH (0.125 mM) induced the expression of H-2 molecules in both cell clones. In B9 cell clone, in which MHC basal expression is very low or absent, t-BOOH significantly induced H-2Kd, H-2Dd and H-2Ld molecules. In G2 cell clone the expression of MHC class I genes was also enhanced by th…

FibrosarcomaCellElectrophoretic Mobility Shift AssayBiologyMajor histocompatibility complexBiochemistryMajor Histocompatibility ComplexTransactivationMiceAntigentert-ButylhydroperoxideCell CloneMalondialdehydeMHC class ImedicineTumor Cells CulturedAnimalsGlutathione PeroxidaseMice Inbred BALB CSuperoxide DismutaseMHC Class I GeneHistocompatibility Antigens Class INF-kappa BDeoxyguanosineGeneral Medicine3T3 CellsCatalaseFlow CytometryMolecular biologyGlutathioneOxidative Stressmedicine.anatomical_structureGene Expression Regulation8-Hydroxy-2'-Deoxyguanosinebiology.proteinCD8MethylcholanthreneFree radical research
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