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
More filters
Journal ArticleDOI
Inhibitory histamine H3-receptors on cholinergic nerves in human airways.
M. Ichinose,Peter J. Barnes +1 more
TL;DR: The results indicate that H3-receptors modulate cholinergic neurotransmission in human airways and cause a dose-dependent inhibition of Cholinergic contractile responses to electrical field stimulation in human bronchi.
Journal ArticleDOI
Alternative mechanisms for tiotropium.
Eric D. Bateman,Stephen I. Rennard,Peter J. Barnes,Peter V. Dicpinigaitis,Reinoud Gosens,Nicholas J. Gross,Jay A. Nadel,Michael Pfeifer,Kurt Racké,Klaus F. Rabe,Bruce K. Rubin,Tobias Welte,Ignaz Wessler +12 more
TL;DR: Data is summarized from a variety of investigations that provide insights into possible mechanisms to account for the effects of tiotropium and the discussion on basic and clinical research in this field is summarized.
Journal ArticleDOI
Steroid resistance in asthma.
Peter J. Barnes,Ian M. Adcock +1 more
TL;DR: Primary steroid resistance in asthma may arise in response to the release of cytokines that activate AP-1 and other transcription factors that bind directly to GR, and a marked reduction in the binding of GR to DNA is demonstrated.
Journal ArticleDOI
Inhibition of neurogenic plasma exudation in guinea-pig airways by CP-96,345, a new non-peptide NK1 receptor antagonist.
TL;DR: A new non‐peptide tachykinin antagonist, CP‐96,345, inhibited airway plasma exudation induced in guinea‐pigs by i.v. capsaicin, but did not inhibit the bronchoconstrictor response to neurokinin A, suggesting selectivity for NK1 receptors.
Journal ArticleDOI
Greater effect of inhaled budesonide on adenosine 5'-monophosphate-induced than on sodium-metabisulfite-induced bronchoconstriction in asthma.
TL;DR: Budesonide reduces AR to MCh and MBS by an action common to the effects of both direct and neural stimuli on airway smooth muscle contraction, which suggests that budesonide may have an additional action by reducing airway mast cell numbers and/or function.