2016
465 Protein S-Acylation in Pulmonary Disease
Randall M, Ather J, Hoyt L, Dixon A, Poynter M. 465 Protein S-Acylation in Pulmonary Disease. Free Radical Biology And Medicine 2016, 100: s193. DOI: 10.1016/j.freeradbiomed.2016.10.528.Peer-Reviewed Original ResearchHigh-fat dietHouse dust miteNasal epithelial cellsLung tissueMurine lung tissueWhole lung tissueReactive oxygen speciesEpithelial cellsPrimary nasal epithelial cellsPoor symptom controlHuman nasal epithelial cellsNon-asthmatic patientsPathophysiology of asthmaMajor risk factorFrequent exacerbationsObese asthmaticsSymptom controlComorbid diseasesObese controlsPulmonary diseaseC57BL/6 miceLung diseaseDust miteRisk factorsWestern diet
2012
Impaired NLRP3 inflammasome activity in elderly hosts contributes to the prevalence of primary and secondary Streptococcus pneumoniae infection. (114.4)
Stout-Delgado H, Shirali A, Jaramillo R, Harrod K. Impaired NLRP3 inflammasome activity in elderly hosts contributes to the prevalence of primary and secondary Streptococcus pneumoniae infection. (114.4). The Journal Of Immunology 2012, 188: 114.4-114.4. DOI: 10.4049/jimmunol.188.supp.114.4.Peer-Reviewed Original ResearchSecondary bacterial infectionSecondary S. pneumoniae infectionS. pneumoniae infectionElderly miceNLRP3 inflammasome activityPneumoniae infectionInfluenza infectionBacterial infectionsIL-1βInflammasome activitySecondary Streptococcus pneumoniae infectionStreptococcus pneumoniae infectionInfluenza viral infectionWhole lung tissueExpression of ASCHigher bacterial titersCapase-1Elderly hostsIL-18NLRP3 inflammasomeLung tissueYoung miceCellular infiltrationElderly populationLethal pneumonia
2004
Burn Injury and Pulmonary Sepsis: Development of a Clinically Relevant Model
Davis KA, Santaniello JM, He LK, Muthu K, Sen S, Jones SB, Gamelli RL, Shankar R. Burn Injury and Pulmonary Sepsis: Development of a Clinically Relevant Model. Journal Of Trauma And Acute Care Surgery 2004, 56: 272-278. PMID: 14960967, DOI: 10.1097/01.ta.0000108995.64133.90.Peer-Reviewed Original ResearchConceptsColony-stimulating factorPulmonary sepsisCytokine tumor necrosisSystemic sepsisInterleukin-6Tumor necrosisProinflammatory cytokine tumor necrosisInflammatory cytokine tumor necrosisAlveolar macrophage releaseBurn/traumaDorsal scald burnGram stainMultiple organ failureDevelopment of pneumoniaGranulocyte-macrophage (GM) CSFFemoral bone marrow cellsEnd-organ responseIsolated alveolar macrophagesPositive tissue culturesPseudomonas aeruginosaWhole lung tissueMale B6D2F1 miceTissue Gram stainMacrophage colony-stimulating factorBone marrow cells
2003
Mesenchymal stem cell engraftment in lung is enhanced in response to bleomycin exposure and ameliorates its fibrotic effects
Ortiz LA, Gambelli F, McBride C, Gaupp D, Baddoo M, Kaminski N, Phinney DG. Mesenchymal stem cell engraftment in lung is enhanced in response to bleomycin exposure and ameliorates its fibrotic effects. Proceedings Of The National Academy Of Sciences Of The United States Of America 2003, 100: 8407-8411. PMID: 12815096, PMCID: PMC166242, DOI: 10.1073/pnas.1432929100.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBleomycinBone Marrow TransplantationCollagenDrug ResistanceEnzyme InductionFemaleFibrosisGene Expression RegulationGraft SurvivalHydroxyprolineIn Situ Hybridization, FluorescenceLungMaleMatrix MetalloproteinasesMesodermMiceMice, Inbred BALB CMice, Inbred C57BLOsteopontinPolymerase Chain ReactionPulmonary FibrosisRNA, MessengerSialoglycoproteinsStem Cell TransplantationTransplantation, HeterotopicConceptsLung tissueMesenchymal stem cellsCollagen depositionResistant BALB/c miceMesenchymal stem cell engraftmentBALB/c miceTotal lung DNAControl-treated miceDonor-derived cellsWhole lung tissueStem cell engraftmentType II epithelial cellsTransplant recipientsC57BL/6 recipientsMSC administrationEpithelium-like morphologyFibrotic effectsIntracranial transplantationMSC transplantationC miceBleomycin exposureLung DNAMurine bone marrowReal-time PCRBone marrow
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