2001
An anti-CD11/CD18 monoclonal antibody in patients with acute myocardial infarction having percutaneous transluminal coronary angioplasty (the FESTIVAL study)
Rusnak J, Kopecky S, Clements I, Gibbons R, Holland A, Peterman H, Martin J, Saoud J, Feldman R, Breisblatt W, Simons M, Gessler C, Yu A, Investigators F. An anti-CD11/CD18 monoclonal antibody in patients with acute myocardial infarction having percutaneous transluminal coronary angioplasty (the FESTIVAL study). The American Journal Of Cardiology 2001, 88: 482-487. PMID: 11524054, DOI: 10.1016/s0002-9149(01)01723-4.Peer-Reviewed Original ResearchMeSH KeywordsAgedAngioplasty, Balloon, CoronaryAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedChi-Square DistributionCombined Modality TherapyCoronary AngiographyDose-Response Relationship, DrugDouble-Blind MethodDrug Administration ScheduleElectrocardiographyFemaleFollow-Up StudiesHumansInfusions, IntravenousMaleMiddle AgedMyocardial InfarctionNeuroprotective AgentsPilot ProjectsProbabilitySensitivity and SpecificitySeverity of Illness IndexStatistics, NonparametricSurvival RateTomography, Emission-Computed, Single-PhotonTreatment OutcomeConceptsPercutaneous transluminal coronary angioplastyAcute myocardial infarctionIntercellular adhesion molecule-1Hu23F2GTransluminal coronary angioplastyCD11/CD18Monoclonal antibodiesCoronary angioplastyMyocardial infarctionCD11/CD18 monoclonal antibodyMyocardial single photon emissionInitial clinical safetySubsequent cardiac interventionsST-segment elevationHumanized monoclonal antibodyActivation of neutrophilsAdhesion molecule-1CD18 monoclonal antibodySignificant differencesG treatment groupsNear-baseline valuesSingle photon emissionAdverse eventsCoronary reperfusionInflammatory mediators
2000
Inhibition of ubiquitin-proteasome pathway–mediated IκBα degradation by a naturally occurring antibacterial peptide
Gao Y, Lecker S, Post M, Hietaranta A, Li J, Volk R, Li M, Sato K, Saluja A, Steer M, Goldberg A, Simons M. Inhibition of ubiquitin-proteasome pathway–mediated IκBα degradation by a naturally occurring antibacterial peptide. Journal Of Clinical Investigation 2000, 106: 439-448. PMID: 10930447, PMCID: PMC314329, DOI: 10.1172/jci9826.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnti-Infective AgentsAntimicrobial Cationic PeptidesCells, CulturedCysteine EndopeptidasesDNA-Binding ProteinsGene ExpressionHumansI-kappa B ProteinsMaleMiceMice, Inbred ICRMice, TransgenicMultienzyme ComplexesMyocardial InfarctionNF-kappa BNF-KappaB Inhibitor alphaPancreatitisPeptidesProteasome Endopeptidase ComplexSwineUbiquitinsConceptsDependent gene expressionGene expressionNF-kappa BUbiquitin-proteasome pathwayB alpha phosphorylationValosin-containing proteinB alpha degradationNF-kappa B inhibitor ICellular functionsTranscription factorsAlpha phosphorylationBiological processesInhibitor IAlpha 7 subunitSelective regulationProteasome activityB alphaAntibacterial peptidesOverall proteasome activityAlpha degradationNF-kappaBCell culturesIκBα degradationExpressionPeptidesPR39, a peptide regulator of angiogenesis
Li J, Post M, Volk R, Gao Y, Li M, Metais C, Sato K, Tsai J, Aird W, Rosenberg R, Hampton T, Li J, Sellke F, Carmeliet P, Simons M. PR39, a peptide regulator of angiogenesis. Nature Medicine 2000, 6: 49-55. PMID: 10613823, DOI: 10.1038/71527.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntimicrobial Cationic PeptidesAortaCapillariesCattleCell HypoxiaCells, CulturedCoronary VesselsCysteine EndopeptidasesDNA-Binding ProteinsEndothelium, VascularHeartHumansHypoxia-Inducible Factor 1Hypoxia-Inducible Factor 1, alpha SubunitIn Vitro TechniquesMacrophagesMiceMice, Inbred C57BLMice, TransgenicMultienzyme ComplexesMyocardial InfarctionMyocardial IschemiaNeovascularization, PhysiologicNuclear ProteinsPeptidesProteasome Endopeptidase ComplexRecombinant ProteinsSwineTranscription FactorsUbiquitinsUmbilical VeinsVon Willebrand FactorConceptsHypoxia-inducible factor-1α (HIF-1α) degradationMacrophage-derived peptideHypoxia-inducible factor-1α (HIF-1α) proteinCoronary flow studiesInflammation-induced angiogenesisInduction of angiogenesisMyocardial vasculatureTissue injuryPotent inductorFunctional blood vesselsBlood vesselsVascular structuresAngiogenesisSelective inhibitionPR39
1998
Therapeutic Angiogenesis With Basic Fibroblast Growth Factor: Technique and Early Results
Sellke F, Laham R, Edelman E, Pearlman J, Simons M. Therapeutic Angiogenesis With Basic Fibroblast Growth Factor: Technique and Early Results. The Annals Of Thoracic Surgery 1998, 65: 1540-1544. PMID: 9647055, DOI: 10.1016/s0003-4975(98)00340-3.Peer-Reviewed Original ResearchMeSH KeywordsAgedAlginatesAngina PectorisCollateral CirculationCoronary Artery BypassCoronary Artery DiseaseCoronary CirculationCoronary VesselsCreatinineDelayed-Action PreparationsDrug CarriersFeasibility StudiesFemaleFibroblast Growth Factor 2Follow-Up StudiesGlucuronic AcidHeparinHexuronic AcidsHumansMaleMiddle AgedMyocardial ContractionMyocardial InfarctionNeovascularization, PhysiologicPericardiumSafetyStroke VolumeSurvival RateConceptsBasic fibroblast growth factorCoronary artery bypassFibroblast growth factorArtery bypassGrowth factorTherapeutic angiogenesisConventional coronary artery bypassBasic fibroblast growth factor (bFGF) administrationSlow-release devicesStress perfusion scansPerioperative myocardial infarctionSerum creatinine levelsDifficult clinical problemFixed perfusion defectsLong-term resultsMyocardial contractile functionGrowth factor administrationOperative mortalityPatent arteriesMyocardial revascularizationCreatinine levelsEjection fractionClinical efficacyHepatic toxicityPerfusion scan
1997
Macrophage-dependent regulation of syndecan gene expression.
Li J, Brown L, Laham R, Volk R, Simons M. Macrophage-dependent regulation of syndecan gene expression. Circulation Research 1997, 81: 785-96. PMID: 9351452, DOI: 10.1161/01.res.81.5.785.Peer-Reviewed Original ResearchConceptsBlood-derived macrophagesSyndecan expressionSyndecan geneMyocardial infarctionGene expressionRegulation of expressionSyndecan-1Op/op miceGranulocyte-macrophage colony-stimulating factorMacrophage colony-stimulating factorRat infarct modelColony-stimulating factorHeparin-binding growth factorsSyndecan-4 mRNASyndecan-1 mRNABiological processesMacrophage influxCellular responsesMacrophage contentSyndecan-4Right ventricleTissue injuryOp miceExtracellular matrixPrompt increase