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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Capsaicin and sensory neuropeptide stimulation of goblet cell secretion in guinea-pig trachea.
TL;DR: In guinea‐pig trachea, goblet cell secretion is under the control of capsaicin‐sensitive sensory nerves and release of neuropeptides from these nerves may induce mucus discharge via tachykinin receptors of the NK‐1 subtype.
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Cytokine modulators as novel therapies for asthma.
TL;DR: Because so many cytokines are involved in asthma, drugs that inhibit the synthesis of multiple cytokines may prove to be more useful and the risk of side effects with these nonspecific inhibitors may be reduced by the inhaled route of delivery.
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Breath condensate pH in children with cystic fibrosis and asthma: a new noninvasive marker of airway inflammation?
Giovanna Elisiana Carpagnano,Peter J. Barnes,Jackie Francis,Nicola Wilson,Andrew Bush,Sergei A. Kharitonov +5 more
TL;DR: The measurement of EBC pH may be useful in the evaluation of airway inflammation in children with asthma and CF and to try to determine whether pH could be used as a marker ofAirway inflammation.
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Oxidative stress dependent microRNA-34a activation via PI3Kα reduces the expression of sirtuin-1 and sirtuin-6 in epithelial cells
Jonathan R. Baker,Chaitanya Vuppusetty,Thomas Colley,Andriana I. Papaioannou,Peter Fenwick,Louise E. Donnelly,K. Ito,Peter J. Barnes +7 more
TL;DR: It is shown that oxidative stress selectively elevates microRNA-34a but not the related miR-34b/c, with concomitant reduction of SIRT1/-6 in bronchial epithelial cells (BEAS2B), which was also observed in peripheral lung samples from patients with COPD.
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Interleukin-5 induces CD34(+) eosinophil progenitor mobilization and eosinophil CCR3 expression in asthma.
TL;DR: Systemic IL-5 increased circulating eosinophil progenitors, suggesting a key role for systemic IL- 5 in eos inophil mobilization, and causes terminal maturation of the eosInophil by increasing CCR3 expression, potentially affecting C CR3-dependent chemotaxis by eOSinophils and lymphocytes.