2025
Late Permissive Hypercapnia for Mechanically Ventilated Preterm Infants: A Randomized Trial
Travers C, Gentle S, Shukla V, Aban I, Yee A, Armstead K, Benz R, Laney D, Ambalavanan N, Carlo W. Late Permissive Hypercapnia for Mechanically Ventilated Preterm Infants: A Randomized Trial. Pediatric Pulmonology 2025, 60: e71165. PMID: 40525736, PMCID: PMC12172392, DOI: 10.1002/ppul.71165.Peer-Reviewed Original ResearchConceptsPostnatal day 7Permissive hypercapniaPreterm infantsInstitutional review boardDay 7Ventilator-freeMechanically ventilated preterm infantsSingle-center randomized clinical trialReduced mechanical ventilation durationWeeks postmenstrual ageMechanical ventilation durationRespiratory distress syndromeVentilator-free daysRandomized clinical trialsPostmenstrual ageGestational ageWeeks gestationDistress syndromeVentilation durationBirth weightLung protectionRandomized trialsClinical trialsPrimary outcomeInfants
2015
An endothelial TLR4‐VEGFR2 pathway mediates lung protection against oxidant‐induced injury
Takyar S, Zhang Y, Haslip M, Jin L, Shan P, Zhang X, Lee PJ. An endothelial TLR4‐VEGFR2 pathway mediates lung protection against oxidant‐induced injury. The FASEB Journal 2015, 30: 1317-1327. PMID: 26655705, PMCID: PMC4750407, DOI: 10.1096/fj.15-275024.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisEndothelial CellsHydrogen PeroxideHyperoxiaLungLung InjuryMAP Kinase Signaling SystemMiceMice, Inbred C57BLMice, TransgenicOxidantsOxygenProto-Oncogene Proteins c-aktSignal TransductionToll-Like Receptor 4Vascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2ConceptsVEGF receptor 2Primary endothelial cellsLung protectionEndothelial cellsC57/BL6 miceEffect of TLR4VEGF transgenic miceRole of TLR4Bone marrow chimerasLung cell apoptosisTLR4 knockdownTLR4 deficiencyLung injuryTLR4 expressionBL6 miceProtective effectLung compartmentsReceptor 2TLR4Transgenic miceHuman TLR4LDH releaseTransgenic modelingCell apoptosisInjury
2014
The Mitochondrial Cardiolipin Remodeling Enzyme Lysocardiolipin Acyltransferase Is a Novel Target in Pulmonary Fibrosis
Huang LS, Mathew B, Li H, Zhao Y, Ma SF, Noth I, Reddy SP, Harijith A, Usatyuk PV, Berdyshev EV, Kaminski N, Zhou T, Zhang W, Zhang Y, Rehman J, Kotha SR, Gurney TO, Parinandi NL, Lussier YA, Garcia JG, Natarajan V. The Mitochondrial Cardiolipin Remodeling Enzyme Lysocardiolipin Acyltransferase Is a Novel Target in Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2014, 189: 1402-1415. PMID: 24779708, PMCID: PMC4098083, DOI: 10.1164/rccm.201310-1917oc.Peer-Reviewed Original ResearchMeSH Keywords1-Acylglycerol-3-Phosphate O-AcyltransferaseAcyltransferasesAnimalsBiomarkersCardiolipinsCohort StudiesDisease Models, AnimalHumansIdiopathic Pulmonary FibrosisIn Situ HybridizationLeukocytes, MononuclearMiceMitochondriaPredictive Value of TestsPulmonary FibrosisRNA, MessengerSensitivity and SpecificitySeverity of Illness IndexConceptsPeripheral blood mononuclear cellsIdiopathic pulmonary fibrosisPulmonary fibrosisMurine modelAlveolar epithelial cellsOverall survivalReactive oxygen species generationLysocardiolipin acyltransferaseOxygen species generationCarbon monoxide diffusion capacityRadiation-induced pulmonary fibrosisPulmonary function outcomesEpithelial cellsBlood mononuclear cellsPreclinical murine modelsNovel therapeutic approachesSpecies generationBleomycin challengeLung inflammationLung protectionPulmonary functionFunction outcomesLung fibrosisMononuclear cellsFibrotic lungs
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply