2023
An AI-powered patient triage platform for future viral outbreaks using COVID-19 as a disease model
Charkoftaki G, Aalizadeh R, Santos-Neto A, Tan W, Davidson E, Nikolopoulou V, Wang Y, Thompson B, Furnary T, Chen Y, Wunder E, Coppi A, Schulz W, Iwasaki A, Pierce R, Cruz C, Desir G, Kaminski N, Farhadian S, Veselkov K, Datta R, Campbell M, Thomaidis N, Ko A, Thompson D, Vasiliou V. An AI-powered patient triage platform for future viral outbreaks using COVID-19 as a disease model. Human Genomics 2023, 17: 80. PMID: 37641126, PMCID: PMC10463861, DOI: 10.1186/s40246-023-00521-4.Peer-Reviewed Original ResearchConceptsCOVID-19 patientsDisease severityViral outbreaksFuture viral outbreaksLength of hospitalizationIntensive care unitWorse disease prognosisLife-threatening illnessEffective medical interventionsCOVID-19Clinical decision treeGlucuronic acid metabolitesNew potential biomarkersHospitalization lengthCare unitComorbidity dataSerotonin levelsDisease progressionHealthy controlsPatient outcomesDisease prognosisPatient transferPatientsHealthcare resourcesPotential biomarkers
2022
Longitudinal lung function and gas transfer in individuals with idiopathic pulmonary fibrosis: a genome-wide association study
Allen RJ, Oldham JM, Jenkins DA, Leavy OC, Guillen-Guio B, Melbourne CA, Ma SF, Jou J, Kim JS, Cooperative C, Fahy WA, Oballa E, Hubbard RB, Navaratnam V, Braybrooke R, Saini G, Roach KM, Tobin MD, Hirani N, Whyte MKB, Kaminski N, Zhang Y, Martinez FJ, Linderholm AL, Adegunsoye A, Strek ME, Maher TM, Molyneaux PL, Flores C, Noth I, Jenkins R, Wain LV. Longitudinal lung function and gas transfer in individuals with idiopathic pulmonary fibrosis: a genome-wide association study. The Lancet Respiratory Medicine 2022, 11: 65-73. PMID: 35985358, PMCID: PMC10077113, DOI: 10.1016/s2213-2600(22)00251-x.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisLung capacityAmerican Thoracic Society/European Respiratory Society guidelinesDiagnosis of IPFEuropean Respiratory Society guidelinesPotential novel therapeutic approachHealth-National HeartLongitudinal lung functionRespiratory Society guidelinesGenetic variantsNovel therapeutic approachesIncurable lung diseaseMedical Research CouncilProgressive scarringFVC declineLung functionVital capacityBlood InstituteSociety guidelinesLung diseaseNational HeartDisease progressionTherapeutic approachesSignificant associationCD38 Mediates Lung Fibrosis by Promoting Alveolar Epithelial Cell Aging.
Cui H, Xie N, Banerjee S, Dey T, Liu RM, Antony VB, Sanders YY, Adams TS, Gomez JL, Thannickal VJ, Kaminski N, Liu G. CD38 Mediates Lung Fibrosis by Promoting Alveolar Epithelial Cell Aging. American Journal Of Respiratory And Critical Care Medicine 2022, 206: 459-475. PMID: 35687485, DOI: 10.1164/rccm.202109-2151oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisLung fibrosisCD38 expressionAlveolar epithelial cell injuryEpithelial cell injuryEffective therapeutic strategyHuman lung parenchymaIPF lungsLung functionPulmonary fibrosisDisease progressionFibrotic lungsReal-time PCRYoung miceLung parenchymaOld miceCell injuryTherapeutic strategiesFibrosisPharmacological inactivationCD38Single-cell RNA sequencingFlow cytometryWestern blottingOld animalsLung Microenvironments and Disease Progression in Fibrotic Hypersensitivity Pneumonitis.
De Sadeleer LJ, McDonough JE, Schupp JC, Yan X, Vanstapel A, Van Herck A, Everaerts S, Geudens V, Sacreas A, Goos T, Aelbrecht C, Nawrot TS, Martens DS, Schols D, Claes S, Verschakelen JA, Verbeken EK, Ackermann M, Decottignies A, Mahieu M, Hackett TL, Hogg JC, Vanaudenaerde BM, Verleden SE, Kaminski N, Wuyts WA. Lung Microenvironments and Disease Progression in Fibrotic Hypersensitivity Pneumonitis. American Journal Of Respiratory And Critical Care Medicine 2022, 205: 60-74. PMID: 34724391, PMCID: PMC8865586, DOI: 10.1164/rccm.202103-0569oc.Peer-Reviewed Original ResearchConceptsFibrotic hypersensitivity pneumonitisIdiopathic pulmonary fibrosisHypersensitivity pneumonitisLung zonesMolecular traitsUnused donor lungsInterstitial lung diseaseLocal disease extentProgression of fibrosisSevere fibrosis groupGene co-expression network analysisCo-expression network analysisExplant lungsDonor lungsLung involvementEndothelial functionLung findingsDisease extentPulmonary fibrosisLung diseaseFibrosis groupLung microenvironmentClinical behaviorDisease progressionBAL samples
2021
S65 Genome-wide association study of survival times after diagnosis of idiopathic pulmonary fibrosis
Allen R, Oldham J, Lorenzo-Salazar J, Molyneaux P, Ma S, Stockwell A, Joseph C, Kim J, Guillen-Guio B, Hernandez-Beeftink T, Kropski J, Huang Y, Lee C, Adegunsoye A, Pugashetti J, Linderholm A, Vo V, Strek M, Hubbard R, Hirani N, Whyte M, Hart S, Nicholson A, Parfrey H, Rassl D, Wallace W, Fahy W, Valenzi E, Zhang Y, Kaminski N, Wolters P, Molina-Molina M, Martinez F, Hall I, Tobin, Maher T, Blackwell T, Yaspan B, Jenkins R, Flores C, Wain L, Noth I. S65 Genome-wide association study of survival times after diagnosis of idiopathic pulmonary fibrosis. Thorax 2021, 76: a43-a43. DOI: 10.1136/thorax-2021-btsabstracts.71.Peer-Reviewed Original ResearchGenome-wide analysisIdiopathic pulmonary fibrosisAssociation studiesGenome-wide association studiesGenetic variantsImportant biological processesWide association studyTwo-stage GWASIPF casesIPF survivalSurvival timeDisease progressionDNA regionsFirst GWASLikely genePulmonary fibrosisGene expressionBiological processesDiagnosis of IPFGenetic principal componentsProgression of IPFDisease riskStage 1Genetic determinantsCox proportional hazards model
2017
Local and Systemic CD4+ T Cell Exhaustion Reverses with Clinical Resolution of Pulmonary Sarcoidosis
Hawkins C, Shaginurova G, Shelton DA, Herazo-Maya JD, Oswald-Richter KA, Rotsinger JE, Young A, Celada LJ, Kaminski N, Sevin C, Drake WP. Local and Systemic CD4+ T Cell Exhaustion Reverses with Clinical Resolution of Pulmonary Sarcoidosis. Journal Of Immunology Research 2017, 2017: 3642832. PMID: 29234685, PMCID: PMC5695030, DOI: 10.1155/2017/3642832.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedApoptosisCD4-Positive T-LymphocytesCell ProliferationCells, CulturedClonal AnergyCytokinesDisease ProgressionFemaleGene Expression RegulationHumansLymphocyte ActivationMaleMiddle AgedProgrammed Cell Death 1 ReceptorReceptors, Antigen, T-Cell, alpha-betaSarcoidosis, PulmonaryTh1 CellsYoung AdultConceptsT cell exhaustionTh1 cytokine expressionPD-1 expressionCell exhaustionCytokine expressionT cellsHealthy controlsInhibitory cell surface receptorsT cell immune functionTh1 immune responseChronic antigenic stimulationCell immune functionProliferative capacityT cell functionSarcoidosis subjectsSystemic CD4Pulmonary sarcoidosisDisease resolutionProgressive diseaseClinical resolutionCytokine productionAntigenic stimulationDisease progressionImmune responseCD4Transcriptome profiles in sarcoidosis and their potential role in disease prediction
Schupp JC, Vukmirovic M, Kaminski N, Prasse A. Transcriptome profiles in sarcoidosis and their potential role in disease prediction. Current Opinion In Pulmonary Medicine 2017, 23: 487-492. PMID: 28590292, PMCID: PMC5637542, DOI: 10.1097/mcp.0000000000000403.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsGenome-wide expression studiesWide expression studiesTranscriptome profilesTranscriptomic dataRNA sequencingExpression studiesGene expressionMolecular mechanismsLarge prospective followTh1 immune responseTranscriptomeNonnecrotizing granulomasProspective followSystemic diseaseDisease progressionTreatment outcomesImmune responseSarcoidosisPotential roleControl tissuesProgressive sarcoidosisKey roleDiseaseTranscriptomicsGranulomasExtracellular Mitochondrial DNA Is Generated by Fibroblasts and Predicts Death in Idiopathic Pulmonary Fibrosis
Ryu C, Sun H, Gulati M, Herazo-Maya J, Chen Y, Osafo-Addo A, Brandsdorfer C, Winkler J, Blaul C, Faunce J, Pan H, Woolard T, Tzouvelekis A, Antin-Ozerkis DE, Puchalski JT, Slade M, Gonzalez AL, Bogenhagen DF, Kirillov V, Feghali-Bostwick C, Gibson K, Lindell K, Herzog RI, Dela Cruz CS, Mehal W, Kaminski N, Herzog EL, Trujillo G. Extracellular Mitochondrial DNA Is Generated by Fibroblasts and Predicts Death in Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2017, 196: 1571-1581. PMID: 28783377, PMCID: PMC5754440, DOI: 10.1164/rccm.201612-2480oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisNormal human lung fibroblastsExtracellular mitochondrial DNABronchoalveolar lavageIPF fibroblastsPulmonary fibrosisInnate immune ligandsEvent-free survivalSmooth muscle actin expressionMtDNA concentrationsSmooth muscle actin-expressing myofibroblastsGrowth factor-β1Muscle actin expressionHuman lung fibroblastsTGF-β1 stimulationExtracellular mtDNAIPF cohortClinical outcomesControl subjectsDisease progressionGlycolytic reprogrammingSoluble mediatorsTGF-β1Factor-β1Immune ligands
2015
Update in Diffuse Parenchymal Lung Disease 2013
Rosas IO, Kaminski N. Update in Diffuse Parenchymal Lung Disease 2013. American Journal Of Respiratory And Critical Care Medicine 2015, 191: 270-274. PMID: 25635490, PMCID: PMC4351573, DOI: 10.1164/rccm.201405-0856up.Peer-Reviewed Original ResearchMeSH KeywordsAnti-Inflammatory Agents, Non-SteroidalClinical Trials, Phase III as TopicDisease ProgressionDrug ApprovalEnzyme InhibitorsGenomicsHumansIdiopathic Pulmonary FibrosisIndolesLung Diseases, InterstitialPolymorphism, GeneticPyridonesTreatment OutcomeUnited StatesUnited States Food and Drug AdministrationConceptsMajority of patientsDistinct clinical presentationsSignificant clinical implicationsClinical presentationPulmonary fibrosis researchDisease progressionClinical implicationsGenetic biomarkersPatientsFibrosis researchGenetic variantsBiological mechanismsIPFNew biological mechanismsNintedanibPirfenidonePeriodHistoric approval
2014
Wnt Coreceptor Lrp5 Is a Driver of Idiopathic Pulmonary Fibrosis
Lam AP, Herazo-Maya JD, Sennello JA, Flozak AS, Russell S, Mutlu GM, Budinger GR, DasGupta R, Varga J, Kaminski N, Gottardi CJ. Wnt Coreceptor Lrp5 Is a Driver of Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2014, 190: 185-195. PMID: 24921217, PMCID: PMC4226053, DOI: 10.1164/rccm.201401-0079oc.Peer-Reviewed Original ResearchMeSH KeywordsAgedAnimalsBeta CateninBiomarkersDisease ProgressionFemaleHumansIdiopathic Pulmonary FibrosisLeukocytes, MononuclearLow Density Lipoprotein Receptor-Related Protein-5Low Density Lipoprotein Receptor-Related Protein-6MaleMiceMice, KnockoutMiddle AgedProspective StudiesSeverity of Illness IndexSignal TransductionTransforming Growth Factor betaWnt ProteinsConceptsIdiopathic pulmonary fibrosisPeripheral blood mononuclear cellsBlood mononuclear cellsLung fibrosisPulmonary fibrosisDisease progressionMononuclear cellsDisease severityNull miceAlveolar type 2 cellsTGF-β productionWild-type miceActivation of TGFType 2 cellsWnt pathway inhibitorsWnt/β-catenin signalingWnt coreceptors LRP5Role of LRP5Bone marrow cellsLrp5 lossΒ-catenin signalingPatient selectionSmall molecular inhibitorsAdditional cohortFibrosis
2013
Serum lysyl oxidase-like 2 levels and idiopathic pulmonary fibrosis disease progression.
Chien JW, Richards TJ, Gibson KF, Zhang Y, Lindell KO, Shao L, Lyman SK, Adamkewicz JI, Smith V, Kaminski N, O'Riordan T. Serum lysyl oxidase-like 2 levels and idiopathic pulmonary fibrosis disease progression. European Respiratory Journal 2013, 43: 1430-8. PMID: 24177001, DOI: 10.1183/09031936.00141013.Peer-Reviewed Original ResearchConceptsIPF disease progressionDisease progressionIdiopathic pulmonary fibrosis patientsCarbon monoxide diffusion capacityPulmonary fibrosis patientsDisease progression eventsGAP subjectsIPF studiesPathological stromaVital capacityLOXL2 levelsProgression eventsDiffusion capacityFibrosis patientsSpirometric dataDisease severityPhysiological surrogatesProgressionPatientsRiskMultiple limitationsSubjectsLevelsProteomic analysisCohort
2009
MMP activation peptide detection in biological samples as a diagnostic marker of idiopathic pulmonary fibrosis
Voeghtly L, Kaminski N, Oury T. MMP activation peptide detection in biological samples as a diagnostic marker of idiopathic pulmonary fibrosis. The FASEB Journal 2009, 23: 572.11-572.11. DOI: 10.1096/fasebj.23.1_supplement.572.11.Peer-Reviewed Original ResearchIdiopathic pulmonary fibrosisPulmonary fibrosisAcute exacerbationMatrix metalloproteasesMMP activationChronic interstitial lung diseaseInterstitial lung diseaseUrine of miceMechanism of clearanceActivation peptideExtracellular matrix turnoverProgressive diseaseLung functionWT miceLung diseaseUnknown etiologyDisease progressionHealthy controlsHuman patientsDiagnostic markerUrine detectionFibrosisDiseaseEarly detectionMatrix turnover
2008
Cross Talk between Id1 and Its Interactive Protein Dril1 Mediate Fibroblast Responses to Transforming Growth Factor-β in Pulmonary Fibrosis
Lin L, Zhou Z, Zheng L, Alber S, Watkins S, Ray P, Kaminski N, Zhang Y, Morse D. Cross Talk between Id1 and Its Interactive Protein Dril1 Mediate Fibroblast Responses to Transforming Growth Factor-β in Pulmonary Fibrosis. American Journal Of Pathology 2008, 173: 337-346. PMID: 18583319, PMCID: PMC2475772, DOI: 10.2353/ajpath.2008.070915.Peer-Reviewed Original ResearchConceptsLung fibrosisPulmonary fibrosisGrowth factorSuppression of fibrosisTranscriptional regulator inhibitorIdiopathic pulmonary fibrosisProgressive lung fibrosisEffects of Id1Activation of TGFInhibited DNA bindingProfibrotic functionsDisease progressionFibrosisFibrotic diseasesDifferentiation 1TGFPotential mechanismsId1FibroblastsNovel binding partnerHuman fibroblastsDRIL1Target genesPatientsLung
2007
A Patient-Gene Model for Temporal Expression Profiles in Clinical Studies
Kaminski N, Bar-Joseph Z. A Patient-Gene Model for Temporal Expression Profiles in Clinical Studies. Journal Of Computational Biology 2007, 14: 324-338. PMID: 17563314, DOI: 10.1089/cmb.2007.0001.Peer-Reviewed Original ResearchConceptsClinical studiesResponse ratePatient expression dataDisease progressionPatient levelPatient responseExpression profilesResponse patternsBaseline expressionPatient dataCommon response patternExpression levelsPatientsCell linesSpecific response patternsTemporal expression levelsLab animalsExpression patternsGene levelSpecific expression patternsImportant pathwayLevelsTemporal expression profiles
2006
A Patient-Gene Model for Temporal Expression Profiles in Clinical Studies
Kaminski N, Bar-Joseph Z. A Patient-Gene Model for Temporal Expression Profiles in Clinical Studies. Lecture Notes In Computer Science 2006, 3909: 69-82. DOI: 10.1007/11732990_6.Peer-Reviewed Original ResearchClinical studiesResponse ratePatient expression dataDisease progressionPatient levelPatient responseResponse patternsExpression profilesBaseline expressionPatient dataCommon response patternExpression levelsPatientsCell linesSpecific response patternsTemporal expression levelsLab animalsExpression patternsGene levelSpecific expression patternsImportant pathwayLevelsInterferonTemporal expression profiles