2023
The serotype-specific prevalence of pneumococci in hospitalized pneumonia patients with COPD: a prospective, multi-center, cohort study
Kim J, Jung J, Kang M, Kim D, Choi H, Cho Y, Jang S, Lee C, Oh Y, Park J. The serotype-specific prevalence of pneumococci in hospitalized pneumonia patients with COPD: a prospective, multi-center, cohort study. The Korean Journal Of Internal Medicine 2023, 38: 714-724. PMID: 37586811, PMCID: PMC10493435, DOI: 10.3904/kjim.2023.152.Peer-Reviewed Original ResearchConceptsCommunity-acquired pneumoniaSerotype-specific prevalencePneumococcal pneumoniaCohort studyS. pneumoniaeChronic obstructive pulmonary disease patientsPneumococcal polysaccharide vaccine 23Obstructive pulmonary disease patientsPCV-13 vaccinationUrine antigen detectionPulmonary disease patientsCommon pneumococcal serotypesPost-vaccination eraPneumococcal vaccinationSerotype 22FCOPD patientsInfluenza vaccinationPCV-13Clinical characteristicsVaccination statusOverall incidencePneumonia patientsPPV-23Pneumococcal serotypesVaccination ratesVISTA (PD-1H) Is a Crucial Immune Regulator to Limit Pulmonary Fibrosis.
Kim S, Adams T, Hu Q, Shin H, Chae G, Lee S, Sharma L, Kwon H, Lee F, Park H, Huh W, Manning E, Kaminski N, Sauler M, Chen L, Song J, Kim T, Kang M. VISTA (PD-1H) Is a Crucial Immune Regulator to Limit Pulmonary Fibrosis. American Journal Of Respiratory Cell And Molecular Biology 2023, 69: 22-33. PMID: 36450109, PMCID: PMC10324045, DOI: 10.1165/rcmb.2022-0219oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisImmune regulatorsTherapeutic potentialHuman idiopathic pulmonary fibrosisCrucial immune regulatorsNovel immune regulatorPulmonary fibrosis micePulmonary fibrosis modelNovel therapeutic targetRole of VISTAWild-type littermatesMonocyte-derived macrophagesT lymphocyte lineageVISTA expressionIPF treatmentAntibody treatmentImmune landscapeFibrotic mediatorsLung fibrosisFibrosis miceInflammatory responseFibrosis modelMyeloid populationsTherapeutic target
2021
Nucleotide‐binding domain and leucine‐rich‐repeat‐containing protein X1 deficiency induces nicotinamide adenine dinucleotide decline, mechanistic target of rapamycin activation, and cellular senescence and accelerates aging lung‐like changes
Shin HJ, Kim S, Park H, Shin M, Kang I, Kang M. Nucleotide‐binding domain and leucine‐rich‐repeat‐containing protein X1 deficiency induces nicotinamide adenine dinucleotide decline, mechanistic target of rapamycin activation, and cellular senescence and accelerates aging lung‐like changes. Aging Cell 2021, 20: e13410. PMID: 34087956, PMCID: PMC8282248, DOI: 10.1111/acel.13410.Peer-Reviewed Original ResearchConceptsCellular senescenceActivation of mTORNucleotide-binding domainCellular senescence responseReplicative cellular senescenceNLR family membersOrganismal agingCellular physiologyMitochondrial moleculesSenescence responseCellular locationProtein X1Crucial regulatorMechanistic targetMitochondrial functionMolecular hallmarksNLRX1 functionRapamycin (mTOR) activationMitochondrial dysfunctionSenescenceMTORPharmacological inhibitionNLRX1BiologyAging Lung
2003
Lung Matrix Metalloproteinase-9 Correlates with Cigarette Smoking and Obstruction of Airflow
Kang M, Oh Y, Lee J, Kim D, Park M, Lee M, Hyun I, Han S, Shim Y, Jung K. Lung Matrix Metalloproteinase-9 Correlates with Cigarette Smoking and Obstruction of Airflow. Journal Of Korean Medical Science 2003, 18: 821-827. PMID: 14676438, PMCID: PMC3055149, DOI: 10.3346/jkms.2003.18.6.821.Peer-Reviewed Original ResearchConceptsChronic obstructive pulmonary diseaseMMP-9 concentrationsCigarette smokingMMP-9Matrix metalloproteinasesTIMP-1Lung parenchymaCharacteristics of COPDPathogenesis of COPDObstructive pulmonary diseaseMatrix metalloproteinase-9 correlatesImportant risk factorMMP-9 expressionObstruction of airflowHuman lung parenchymaFEV1 valuesPulmonary diseaseRisk factorsMMP expressionSmokingTissue inhibitorObstructionGelatinolytic bandsEnzyme immunoassayZymographic analysis