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Your search keyword '"Lederer, David J"' showing total 14 results
Start Over Author "Lederer, David J" Journal european respiratory journal
14 results on '"Lederer, David J"'

1. Dupilumab leads to better-controlled asthma and quality of life in children: the VOYAGE study

Author

Fiocchi, Alessandro G., primary, Phipatanakul, Wanda, additional, Zeiger, Robert S., additional, Durrani, Sandy R., additional, Cole, Jeremy, additional, Msihid, Jérôme, additional, Gall, Rebecca, additional, Jacob-Nara, Juby A., additional, Deniz, Yamo, additional, Rowe, Paul J., additional, Lederer, David J., additional, Hardin, Megan, additional, Zhang, Yi, additional, and Khan, Asif H., additional

Published
2023
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2. Incidence of Interstitial Lung Abnormalities: The MESA Lung Study

Author

McGroder, Claire F., primary, Hansen, Spencer, additional, Hinckley Stukovsky, Karen, additional, Zhang, David, additional, Nath, P. Hrudaya, additional, Salvatore, Mary M., additional, Sonavane, Sushilkumar K., additional, Terry, Nina, additional, Stowell, Justin T., additional, D'Souza, Belinda M., additional, Leb, Jay S., additional, Dumeer, Shifali, additional, Aziz, Muhammad U., additional, Batra, Kiran, additional, Hoffman, Eric A., additional, Bernstein, Elana J., additional, Kim, John S., additional, Podolanczuk, Anna J., additional, Rotter, Jerome I., additional, Manichaikul, Ani W., additional, Rich, Stephen S., additional, Lederer, David J., additional, Barr, R. Graham, additional, McClelland, Robyn L., additional, and Garcia, Christine Kim, additional

Published
2023
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3. Antinuclear antibodies and subclinical interstitial lung disease in community-dwelling adults: the MESA study

Author

Bernstein, Elana J., primary, Austin, John H.M., additional, Kawut, Steven M., additional, Raghu, Ganesh, additional, Hoffman, Eric A., additional, Newell, John D., additional, Watts, Jubal R., additional, Nath, P. Hrudaya, additional, Sonavane, Sushilkumar K., additional, Barr, R. Graham, additional, and Lederer, David J., additional

Published
2020
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6. Air pollution and subclinical interstitial lung disease: the Multi-Ethnic Study of Atherosclerosis (MESA) air–lung study

Author

Sack, Coralynn, primary, Vedal, Sverre, additional, Sheppard, Lianne, additional, Raghu, Ganesh, additional, Barr, R. Graham, additional, Podolanczuk, Anna, additional, Doney, Brent, additional, Hoffman, Eric A., additional, Gassett, Amanda, additional, Hinckley-Stukovsky, Karen, additional, Williams, Kayleen, additional, Kawut, Steve, additional, Lederer, David J., additional, and Kaufman, Joel D., additional

Published
2017
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9. High attenuation areas on chest computed tomography in community-dwelling adults: the MESA study

Author

Podolanczuk, Anna J., primary, Oelsner, Elizabeth C., additional, Barr, R. Graham, additional, Hoffman, Eric A., additional, Armstrong, Hilary F., additional, Austin, John H.M., additional, Basner, Robert C., additional, Bartels, Matthew N., additional, Christie, Jason D., additional, Enright, Paul L., additional, Gochuico, Bernadette R., additional, Hinckley Stukovsky, Karen, additional, Kaufman, Joel D., additional, Hrudaya Nath, P., additional, Newell, John D., additional, Palmer, Scott M., additional, Rabinowitz, Dan, additional, Raghu, Ganesh, additional, Sell, Jessica L., additional, Sieren, Jered, additional, Sonavane, Sushil K., additional, Tracy, Russell P., additional, Watts, Jubal R., additional, Williams, Kayleen, additional, Kawut, Steven M., additional, and Lederer, David J., additional

Published
2016
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10. Pirfenidone for idiopathic pulmonary fibrosis: analysis of pooled data from three multinational phase 3 trials

Author

Noble, Paul W., primary, Albera, Carlo, additional, Bradford, Williamson Z., additional, Costabel, Ulrich, additional, du Bois, Roland M., additional, Fagan, Elizabeth A., additional, Fishman, Robert S., additional, Glaspole, Ian, additional, Glassberg, Marilyn K., additional, Lancaster, Lisa, additional, Lederer, David J., additional, Leff, Jonathan A., additional, Nathan, Steven D., additional, Pereira, Carlos A., additional, Swigris, Jeffrey J., additional, Valeyre, Dominique, additional, and King, Talmadge E., additional

Published
2015
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13. Pirfenidone for idiopathic pulmonary fibrosis: analysis of pooled data from three multinational phase 3 trials.

Author

Noble PW, Albera C, Bradford WZ, Costabel U, du Bois RM, Fagan EA, Fishman RS, Glaspole I, Glassberg MK, Lancaster L, Lederer DJ, Leff JA, Nathan SD, Pereira CA, Swigris JJ, Valeyre D, and King TE Jr

Subjects
Adult, Aged, Aged, 80 and over, Clinical Trials, Phase III as Topic, Disease Progression, Exercise Test, Female, Forced Expiratory Volume, Humans, Idiopathic Pulmonary Fibrosis physiopathology, International Cooperation, Male, Middle Aged, Pulmonary Diffusing Capacity, Randomized Controlled Trials as Topic, Treatment Outcome, Vital Capacity, Anti-Inflammatory Agents, Non-Steroidal therapeutic use, Idiopathic Pulmonary Fibrosis drug therapy, Pyridones therapeutic use
Abstract

Pirfenidone is an antifibrotic agent that has been evaluated in three multinational phase 3 trials in patients with idiopathic pulmonary fibrosis (IPF). We analysed pooled data from the multinational trials to obtain the most precise estimates of the magnitude of treatment effect on measures of disease progression.All patients randomised to pirfenidone 2403 mg·day(-1) or placebo in the CAPACITY or ASCEND studies were included in the analysis. Pooled analyses of outcomes at 1 year were based on the pre-specified end-points and analytic methods described in the ASCEND study protocol.A total of 1247 patients were included in the analysis. At 1 year, pirfenidone reduced the proportion of patients with a ≥10% decline in per cent predicted forced vital capacity or death by 43.8% (95% CI 29.3-55.4%) and increased the proportion of patients with no decline by 59.3% (95% CI 29.0-96.8%). A treatment benefit was also observed for progression-free survival, 6-min walk distance and dyspnoea. Gastrointestinal and skin-related adverse events were more common in the pirfenidone group, but rarely led to discontinuation.Analysis of data from three phase 3 trials demonstrated that treatment with pirfenidone for 1 year resulted in clinically meaningful reductions in disease progression in patients with IPF., (Copyright ©ERS 2016.)

Published
2016
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14. Pulmonary arteriole gene expression signature in idiopathic pulmonary fibrosis.

Author

Patel NM, Kawut SM, Jelic S, Arcasoy SM, Lederer DJ, and Borczuk AC

Subjects
Adult, Aged, Case-Control Studies, Cell Proliferation, Cluster Analysis, Female, Gene Expression Regulation, Humans, Immunohistochemistry, Laser Capture Microdissection, Lung pathology, Lung Diseases, Interstitial metabolism, Male, Middle Aged, Oligonucleotide Array Sequence Analysis, Transcriptome, Arterioles metabolism, Gene Expression Profiling, Hypertension, Pulmonary metabolism, Idiopathic Pulmonary Fibrosis metabolism, Lung metabolism
Abstract

A third of patients with idiopathic pulmonary fibrosis (IPF) develop pulmonary hypertension (PH-IPF), which is associated with increased mortality. Whether an altered gene expression profile in the pulmonary vasculature precedes the clinical onset of PH-IPF is unknown. We compared gene expression in the pulmonary vasculature of IPF patients with and without PH with controls. Pulmonary arterioles were isolated using laser capture microdissection from 16 IPF patients: eight with PH (PH-IPF) and eight with no PH (NPH-IPF), and seven controls. Probe was prepared from extracted RNA, and hybridised to Affymetrix Hu133 2.0 Plus genechips. Biometric Research Branch array tools and Ingenuity Pathway Analysis software were used for analysis of the microarray data. Univariate analysis revealed 255 genes that distinguished IPF arterioles from controls (p<0.001). Mediators of vascular smooth muscle and endothelial cell proliferation, Wnt signalling and apoptosis were differentially expressed in IPF arterioles. Unsupervised and supervised clustering analyses revealed similar gene expression in PH-IPF and NPH-IPF arterioles. The pulmonary arteriolar gene expression profile is similar in IPF patients with and without coexistent PH. Pathways involved in vascular proliferation and aberrant apoptosis, which may contribute to pulmonary vascular remodelling, are activated in IPF patients.

Published
2013
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