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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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Mitogen-activated protein kinases mediate peroxynitrite-induced cell death in human bronchial epithelial cells

TL;DR: MAPKs may mediate signal transduction pathways induced by peroxynitrite in lung epithelial cells leading to cell death, and this was increased with the inclusion of SB-239063.
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Inhaled prazosin in asthma.

TL;DR: There was no significant difference between prazosin and placebo, suggesting that alpha-adrenergic receptors are not important in the control of bronchial tone in asthma, and the weak bronchodilatation ascribed to alpha-antagonists in previous studies could be explained by other pharmacological actions of the drugs used.
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Up-regulation of airway smooth muscle histamine H(1) receptor mRNA, protein, and function by beta(2)-adrenoceptor activation.

TL;DR: Fenoterol increases the expression of airway smooth muscle H(1) receptors via activation of the cAMP system through increased gene transcription and mRNA stability, which may be involved in the adverse responses encountered with the clinical use of short-acting beta(2)-agonists.
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The problem of cough and development of novel antitussives.

TL;DR: There is a pressing need to develop novel and safe antitussive therapies for cough, likely to arise from better understanding of the sensory nerves involved in cough and the signalling pathways that are activated.
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Increased vitronectin and endothelin-1 in the breath condensate of patients with fibrosing lung disease.

TL;DR: The presence of two profibrotic markers, the vitronectin and the endothelin-1 (ET-1) in the airways of NSIP and FASSc patients is investigated to justify further studies of vitronECTin and ET-1 levels in exhaled breath condensate, as a means of monitoring activity and predicting progression of pulmonary fibrosis.