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.
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TGFβ1 allele association with asthma severity
TL;DR: It is shown that the –509T variant on haplotype 1 is the most informative marker of the TGFβ1 contribution to asthma severity.
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Oxidative stress-based therapeutics in COPD.
TL;DR: Treating oxidative stress by antioxidants or enhancing endogenous antioxidants should be an effective strategy to treat the underlying pathogenetic mechanisms of COPD.
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An in vitro study of the properties of single vagal afferents innervating guinea-pig airways.
TL;DR: It is demonstrated that single vagal afferents may be studied in vitro and the first examination of the properties of sensory fibres innervating guinea‐pig airways is provided, to show marked differences in terms of their chemosensitivity.
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Diagnostic Performance of an Electronic Nose, Fractional Exhaled Nitric Oxide, and Lung Function Testing in Asthma
Paolo Montuschi,Marco Santonico,Chiara Mondino,Giorgio Pennazza,Giulia Mantini,Eugenio Martinelli,Rosamaria Capuano,Giovanni Ciabattoni,Roberto Paolesse,Corrado Di Natale,Peter J. Barnes,Arnaldo D'Amico +11 more
TL;DR: The electronic nose has a high diagnostic performance that can be increased when combined with FENO and MS fingerprints of VOCs could discriminate between patients with asthma and healthy subjects.
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Induction of cyclo‐oxygenase‐2 by cytokines in human cultured airway smooth muscle cells: novel inflammatory role of this cell type
Maria G. Belvisi,Michael A. Saunders,El-Bdaoui Haddad,S. J. Hirst,Magdi H. Yacoub,Peter J. Barnes,Jane A. Mitchell +6 more
TL;DR: The findings suggest that the increased expression of COX‐2 is intimately involved in the exaggerated release of prostanoids from HASM cells exposed to pro‐inflammatory cytokines, indicating a role for airway smooth muscle cells, in addition to their contractile function, as inflammatory cells involved inThe production of mediators which may contribute to the inflammatory response seen in diseases such as asthma.