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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Mechanisms and resistance in glucocorticoid control of inflammation
TL;DR: Several molecular mechanisms of glucocorticoid resistance have now been identified and HDAC2 is markedly reduced in activity and expression as a result of oxidative/nitrative stress so that inflammation becomes resistant to the anti-inflammatory actions of glucOCorticoids.
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Corticosteroids: The drugs to beat
TL;DR: Corticosteroids are likely to remain the mainstay of asthma therapy and new therapeutic strategies may reverse the corticosteroid insensitivity in COPD and severe asthma.
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The effect of airway epithelium on smooth muscle contractility in bovine trachea.
TL;DR: It is concluded that the bronchial epithelium may produce a relaxant factor which is not a cyclo‐oxygenase or lipoxygenases product and the production of this factor may be reduced or lost following epithelial damage and this may be important in the pathogenesis of bronchia hyperresponsiveness in asthma.
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Exhaled ethane, a marker of lipid peroxidation, is elevated in chronic obstructive pulmonary disease.
TL;DR: Exhaled ethane is elevated, correlates with FEV(1), and is significantly lower in patients treated with steroids, so it may be complementary to the use of NO and CO in assessing and monitoring oxidative stress in COPD.
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Relative Corticosteroid Insensitivity of Peripheral Blood Mononuclear Cells in Severe Asthma
Mark Hew,Pankaj K. Bhavsar,Alfons Torrego,Sally Meah,Nadia Khorasani,Peter J. Barnes,Ian M. Adcock,Kian Fan Chung +7 more
TL;DR: Patients with severe asthma have diminished corticosteroid sensitivity of PBMCs when compared with patients with nonsevere asthma, associated with a reduction in HDAC activity that parallels the impaired corticOSToid sensitivity.