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 Exhaled 8-Isoprostane in Childhood Asthma
Eugenio Baraldi,L. Ghiro,Vania Piovan,Silvia Carraro,Giovanni Ciabattoni,Peter J. Barnes,Paolo Montuschi +6 more
TL;DR: Lung oxidative stress is increased in children who are in stable condition with asthma, as reflected by increased exhaled 8-isoprostane concentrations, which seems to be relatively resistant to treatment with ICSs.
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Relationship between exhaled nitric oxide and mucosal eosinophilic inflammation in mild to moderately severe asthma.
TL;DR: Exhaled NO levels do not reflect airway mucosal eosinophilia and these markers reflect different aspects of airway inflammation, and the clinical usefulness of exhaled NO needs to be determined in prospective longitudinal studies.
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Increased p21CIP1/WAF1 and B Cell Lymphoma Leukemia-xL Expression and Reduced Apoptosis in Alveolar Macrophages from Smokers
Katsuyuki Tomita,Gaetano Caramori,Sam Lim,Kazuhiro Ito,Toyoyuki Hanazawa,Timothy Oates,Irena Chiselita,Elen Jazrawi,K. Fan Chung,Peter J. Barnes,Ian M. Adcock +10 more
TL;DR: Results suggested that AM and bronchial epithelial cells from smokers, in contrast to those from normal subjects and subjects with asthma, have reduced cell death, and oxidative stress induced by cigarette smoking may contribute to the chronicity of inflammation in the airway, through a reduction of apoptosis.
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Molecular mechanisms and cellular effects of glucocorticosteroids
TL;DR: There is now a better understanding of how the responsiveness to GCSs is reduced in patients who have severe asthma, who have asthma and smoke, and who have COPD, and an important mechanism now emerging is a reduction in HDAC2 activity as a result of oxidative stress.
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Interaction of Pattern Recognition Receptors with Mycobacterium Tuberculosis
Esmaeil Mortaz,Ian M. Adcock,Payam Tabarsi,Mohammad Reza Masjedi,Davood Mansouri,Ali Akbar Velayati,Jean-Laurent Casanova,Peter J. Barnes +7 more
TL;DR: An update on PRR signaling during M. tuberculosis infection is provided and how greater knowledge of these pathways may lead to new therapeutic opportunities is indicated.