P
Peter J. Barnes
Researcher at National Institutes of Health
Publications - 1554
Citations - 177909
Peter J. Barnes is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Asthma & COPD. The author has an hindex of 194, co-authored 1530 publications receiving 166618 citations. Previous affiliations of Peter J. Barnes include University of Nebraska Medical Center & Novartis.
Papers
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Journal ArticleDOI
Increased nitrosothiols in exhaled breath condensate in inflammatory airway diseases.
Massimo Corradi,Paolo Montuschi,Louise E. Donnelly,Alberto Pesci,Sergei A. Kharitonov,Peter J. Barnes +5 more
TL;DR: It is shown that RS-NOs are detectable in exhaled breath condensate of healthy subjects and are increased in patients with inflammatory airway diseases and in current smokers.
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Nuclear localisation of p65 in sputum macrophages but not in sputum neutrophils during COPD exacerbations
Gaetano Caramori,Micaela Romagnoli,Paolo Casolari,Cinzia M. Bellettato,G Casoni,Piera Boschetto,Kian Fan Chung,Peter J. Barnes,Ian M. Adcock,Adalberto Ciaccia,Leonardo M. Fabbri,Alberto Papi +11 more
TL;DR: NF-kappaB appears to be activated in sputum macrophages but not in spUTum neutrophils during exacerbations of COPD, as measured by immunocytochemistry and nuclear staining for p65.
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Elevation of Exhaled Ethane Concentration in Asthma
TL;DR: Exhaled ethane is elevated in asthma, reduced in steroid-treated patients, and correlates with NO and airway obstruction, and may be a useful noninvasive marker of oxidative stress.
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Exhaled nitric oxide from lung periphery is increased in COPD
TL;DR: COPD severity was correlated with an increased Calv,NO regardless of the patient's smoking habit or current treatment and Measurements of nitric oxide at multiple expired flows may be useful in monitoring inflammation and progression of chronic obstructive pulmonary disease, and the response to anti-inflammatory treatment.
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Repression of Cyclooxygenase-2 and Prostaglandin E2Release by Dexamethasone Occurs by Transcriptional and Post-transcriptional Mechanisms Involving Loss of Polyadenylated mRNA
TL;DR: A major role for post-transcriptional mechanisms in the dexamethasone-dependent repression of COX-2 that require de novo glucocorticoid receptor-dependent transcription and translation is indicated.