2023
Obesity and Overweight: Probing Causes, Consequences, and Novel Therapeutic Approaches Through the American Heart Association's Strategically Focused Research Network
Clark J, Garvey W, Niswender K, Schmidt A, Ahima R, Aleman J, Battarbee A, Beckman J, Bennett W, Brown N, Chandler‐Laney P, Cox N, Goldberg I, Habegger K, Harper L, Hasty A, Hidalgo B, Kim S, Locher J, Luther J, Maruthur N, Miller E, Sevick M, Wells Q. Obesity and Overweight: Probing Causes, Consequences, and Novel Therapeutic Approaches Through the American Heart Association's Strategically Focused Research Network. Journal Of The American Heart Association 2023, 12: e027693. PMID: 36752232, PMCID: PMC10111504, DOI: 10.1161/jaha.122.027693.Peer-Reviewed Original ResearchConceptsAmerican Heart AssociationHeart AssociationWeight loss interventionNovel therapeutic approachesVanderbilt University Medical CenterUniversity Medical CenterEffective therapeutic interventionsField of obesityResearch NetworkLoss interventionClinical trialsWorldwide prevalenceMedical CenterTherapeutic approachesObesityTherapeutic targetAnimal modelsJohns Hopkins University SchoolTherapeutic interventionsIndividual centersNew targetsUniversity of AlabamaOverweightUniversity SchoolIntervention
2012
Cardiovascular effects of antidiabetic agents: focus on blood pressure effects of incretin-based therapies
Brown NJ. Cardiovascular effects of antidiabetic agents: focus on blood pressure effects of incretin-based therapies. International Journal Of Cardiology Cardiovascular Risk And Prevention 2012, 6: 163-168. PMID: 22433315, PMCID: PMC3422131, DOI: 10.1016/j.jash.2012.02.003.Peer-Reviewed Original ResearchConceptsGlucagon-like peptide-1Cardiovascular eventsDipeptidyl peptidase IV inhibitorsAntidiabetic agentsPeptidase IV inhibitorsBlood pressureClinical trialsPeptide-1Animal modelsType 2 diabetes mellitusIncretin-based agentsBlood pressure effectsIncretin-based therapiesIV inhibitorsLarge clinical trialsFavorable effectIschemia/reperfusionTight glucose controlOverweight diabeticsCardiovascular effectsCardiovascular riskDiabetes mellitusIntensive therapyGlucose controlThiazolidinedione rosiglitazone
2007
Dipeptidyl peptidase IV deficiency increases susceptibility to angiotensin-converting enzyme inhibitor–induced peritracheal edema
Byrd JB, Shreevatsa A, Putlur P, Foretia D, McAlexander L, Sinha T, Does MD, Brown NJ. Dipeptidyl peptidase IV deficiency increases susceptibility to angiotensin-converting enzyme inhibitor–induced peritracheal edema. Journal Of Allergy And Clinical Immunology 2007, 120: 403-408. PMID: 17531305, DOI: 10.1016/j.jaci.2007.04.012.Peer-Reviewed Original ResearchConceptsACE inhibitor-associated angioedemaDPPIV-deficient ratsMagnetic resonance imagingEdema formationSubstance PSerum dipeptidyl peptidase IV activityResonance imagingCaptopril-treated ratsSaline-treated ratsReceptor-dependent mechanismDipeptidyl peptidase IV activityPeptidase IV activityACE inhibitionSerial T2F344 ratsAnimal modelsEdemaAngioedemaDPPIV activityRatsDipeptidyl peptidase activityImpaired degradationSpantideDeficiencyMagnetic resonance
2002
The Renin-Angiotensin-Aldosterone System and Fibrinolysis in Progressive Renal Disease
Brown NJ, Vaughan DE, Fogo AB. The Renin-Angiotensin-Aldosterone System and Fibrinolysis in Progressive Renal Disease. Seminars In Nephrology 2002, 22: 399-406. PMID: 12224047, DOI: 10.1053/snep.2002.34725.Peer-Reviewed Original ResearchConceptsPlasminogen activator inhibitor-1Renal diseaseAldosterone systemProgressive renal diseaseFinal common pathwayActivator inhibitor-1Extracellular matrix accumulationPAI-1 expressionInitiating injuryRenal failureRenin-AngiotensinInterstitial fibrosisClinical managementMajor physiologic inhibitorAnimal modelsProduction of plasminFibrosisMatrix accumulationPlasminogen activatorPhysiologic inhibitorInhibitor-1Common pathwayDiseaseInjuryRAASAldosterone and PAI-1: implications for renal injury.
Brown NJ, Vaughan DE, Fogo AB. Aldosterone and PAI-1: implications for renal injury. Journal Of Nephrology 2002, 15: 230-5. PMID: 12113592.Peer-Reviewed Original ResearchConceptsPlasminogen activator inhibitor-1Activator inhibitor-1Renal injuryAnimal modelsInhibitor-1Aldosterone receptor antagonismPlasminogen activator inhibitor-1 expressionExtracellular matrix accumulationPAI-1 expressionMajor physiological inhibitorRenal diseaseAngiotensin IIReceptor antagonismClinical managementAldosteroneProduction of plasminPAI-1FibrosisMatrix accumulationPlasminogen activatorInjuryPhysiological inhibitorVivoExpressionDisease
1997
Selective Stimulation of Tissue-Type Plasminogen Activator (t-PA) In Vivo by Infusion of Bradykinin
Brown N, Nadeau J, Vaughan D. Selective Stimulation of Tissue-Type Plasminogen Activator (t-PA) In Vivo by Infusion of Bradykinin. Thrombosis And Haemostasis 1997, 77: 522-525. PMID: 9066005, DOI: 10.1055/s-0038-1656000.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAngiotensin-Converting Enzyme InhibitorsAntihypertensive AgentsBlood PressureBradykininCaptoprilFemaleHumansHypertensionIsoquinolinesMalePlasminogen Activator Inhibitor 1QuinaprilRandomized Controlled Trials as TopicTetrahydroisoquinolinesTissue Plasminogen ActivatorConceptsT-PA antigen levelsTissue-type plasminogen activatorMean arterial pressureT-PA levelsAntigen levelsPAI-1 antigen levelsInfusion of bradykininSympathetic nervous systemEffect of bradykininTissue-type plasminogen activator secretionHypertensive patientsHemodynamic effectsArterial pressurePlasminogen activator secretionAngiotensin IIAnimal modelsPotent stimulusNervous systemPAI-1ACEIBradykininBradykinin resultsSelective stimulationPlasminogen activatorSignificant decrease