2022
Activation of the transcription factor NRF2 mediates the anti-inflammatory properties of a subset of over-the-counter and prescription NSAIDs
Eisenstein A, Hilliard BK, Pope SD, Zhang C, Taskar P, Waizman DA, Israni-Winger K, Tian H, Luan HH, Wang A. Activation of the transcription factor NRF2 mediates the anti-inflammatory properties of a subset of over-the-counter and prescription NSAIDs. Immunity 2022, 55: 1082-1095.e5. PMID: 35588739, PMCID: PMC9205175, DOI: 10.1016/j.immuni.2022.04.015.Peer-Reviewed Original ResearchConceptsNonsteroidal anti-inflammatory drugsAnti-inflammatory propertiesMyeloid cellsPrescription nonsteroidal anti-inflammatory drugsGrowth/differentiation factor 15Anti-inflammatory effectsDifferentiation factor 15Myeloid-specific deletionAnti-inflammatory activityAnti-inflammatory drugsNrf2-dependent mechanismKelch-like ECHTranscription factor Nrf2NSAID usageClinical outcomesCOX inhibitionPharmacologic approachesFactor 15Murine modelTissue protectionMurine myeloid cellsNuclear factorPrimary humanFactor Nrf2Nrf2
2021
Pain Management During Vaginal Childbirth
Jin J, Son M. Pain Management During Vaginal Childbirth. JAMA 2021, 326: 450-450. PMID: 34342617, DOI: 10.1001/jama.2021.10702.Peer-Reviewed Educational Materials
2015
Novel pharmacologic approach to enhance the epigenetic and immune priming effect of decitabine in patients with advanced non-small cell lung cancer
Velcheti V, Pennell N, Rakshit S, Stevenson J, Shapiro M, Almeida F, Gurajala R, Schalper K, Saunthararajah Y. Novel pharmacologic approach to enhance the epigenetic and immune priming effect of decitabine in patients with advanced non-small cell lung cancer. Journal For ImmunoTherapy Of Cancer 2015, 3: p178. PMCID: PMC4645121, DOI: 10.1186/2051-1426-3-s2-p178.Peer-Reviewed Original Research
2013
Pharmacologic inhibition of PKCα and PKCθ prevents GVHD while preserving GVL activity in mice
Haarberg K, Li J, Heinrichs J, Wang D, Liu C, Bronk C, Kaosaard K, Owyang A, Holland S, Masuda E, Tso K, Blazar B, Anasetti C, Beg A, Yu X. Pharmacologic inhibition of PKCα and PKCθ prevents GVHD while preserving GVL activity in mice. Blood 2013, 122: 2500-2511. PMID: 23908466, PMCID: PMC3790515, DOI: 10.1182/blood-2012-12-471938.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell SeparationDisease Models, AnimalEnzyme InhibitorsFlow CytometryGraft vs Host DiseaseGraft vs Leukemia EffectHematopoietic Stem Cell TransplantationIsoenzymesLeukemiaLymphocyte ActivationLymphomaMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutProtein Kinase CProtein Kinase C-alphaProtein Kinase C-thetaT-LymphocytesConceptsHematopoietic cell transplantationDonor T cell proliferationAllogeneic hematopoietic cell transplantationT cell proliferationGVL activityGVL effectCytokine productionT cellsPharmacologic inhibitionChemokine/cytokine productionT-cell cytotoxicDonor T cellsPreclinical murine modelsPotential therapeutic targetT cell activationGVHD inductionGVHD preventionPrevents GVHDHost diseaseLeukemia effectSevere graftTherapeutic optionsCell transplantationEffective therapyPharmacologic approaches
2008
Pharmacologic approaches to cognitive rehabilitation
McAllister T, Arnsten A. Pharmacologic approaches to cognitive rehabilitation. 2008, 298-320. DOI: 10.1017/cbo9781316529898.022.Peer-Reviewed Original ResearchCognitive rehabilitationCognitive neuroscienceCognitive changesEfficacy of interventionsVariety of populationsSuccessful interventionsRehabilitation successDifferent disordersNeuroscienceInterventionRehabilitationMemoryExternal factorsRole of imagingLanguagePharmacologic approachesDisordersNew findingsLatest developmentsClinical applicationPractical guidanceFindingsResearchEdition
2007
Inhibition of NF-κB Activation Reduces the Tissue Effects of Transgenic IL-13
Chapoval SP, Al-Garawi A, Lora JM, Strickland I, Ma B, Lee PJ, Homer RJ, Ghosh S, Coyle AJ, Elias JA. Inhibition of NF-κB Activation Reduces the Tissue Effects of Transgenic IL-13. The Journal Of Immunology 2007, 179: 7030-7041. PMID: 17982094, DOI: 10.4049/jimmunol.179.10.7030.Peer-Reviewed Original ResearchMeSH KeywordsAdenoviridaeAnimalsApoptosisCaspasesHeterocyclic Compounds, 3-RingI-kappa B KinaseInflammationInhibitor of Apoptosis ProteinsInterleukin-13MiceMice, Mutant StrainsMice, TransgenicMucusNF-kappa B p50 SubunitPeptidesPulmonary AlveoliPulmonary FibrosisPyridinesReceptors, Cell SurfaceRespiratory HypersensitivitySignal TransductionTh2 CellsConceptsTransgenic IL-13IL-13Alveolar remodelingIL-13 transgenic miceNF-kappaBMajor Th2 cytokinesExcessive mucus productionTissue effectsNF-κB activationNF-kappaB activationNF-kappaB activityNF-kappaB componentsAirway hyperresponsivenessTh2 cytokinesTissue inflammationPharmacologic approachesMucus productionIL-13Ralpha1Murine lungSmall molecule inhibitorsTissue alterationsNF-kappaB.MiceCell apoptosisDiminished levels
2000
Cocaine, HIV, and their cardiovascular effects: is there a role for ACE-inhibitor therapy?
Margolin A, Avants S, Setaro J, Rinder H, Grupp L. Cocaine, HIV, and their cardiovascular effects: is there a role for ACE-inhibitor therapy? Drug And Alcohol Dependence 2000, 61: 35-45. PMID: 11064182, DOI: 10.1016/s0376-8716(00)00124-1.Peer-Reviewed Original ResearchConceptsACE inhibitor therapyCocaine abuseCocaine useAngiotensin converting enzyme (ACE) inhibitorsDiastolic heart functionNew pharmacologic approachesLevels of dopamineConverting Enzyme InhibitorsCocaine-abusing populationCocaine-abusing patientsConsiderable clinical utilityClass of agentsPlatelet activation studiesCardiovascular sequelaeHIV patientsCardiovascular effectsHIV diseaseHIV-positiveACE inhibitorsHIV serostatusRisk factorsPharmacologic approachesPlatelet abnormalitiesClinical utilityHeart function
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply