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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.

Papers
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Effects of prolonged repeated exposure to ovalbumin in sensitized brown Norway rats.

TL;DR: AHR, present after single or 3-wk repeated exposure, disappears by 8 wk of continuous allergen exposure, and both the enhancement and suppression of AHR may be linked to OA-induced immune and inflammatory mechanisms.
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Increased expression of G protein-coupled receptor kinases in cystic fibrosis lung.

TL;DR: The increase in GRK activity is suggested to be one of the mechanisms underlying alterations in the coupling between beta2-adrenoceptor and adenylyl cyclase via G-protein and may thus contribute to the downregulation of beta2/5 mRNAs and protein expression in cystic fibrosis lung.
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Expression of inducible nitric oxide synthase mRNA in Brown Norway rats exposed to ozone : effect of dexamethasone

TL;DR: It is demonstrated that ozone inhalation induces iNOS expression in vivo, thus providing evidence at the molecular level for the possible involvement of nitric oxide generation in ozone-induced pulmonary inflammation or lung damage.
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Expression of platelet-activating factor receptor mRNA in human and guinea pig lung.

TL;DR: These studies revealed high levels of PAFR mRNA hybridization in blood vessels, moderate levels of Hybridization in alveolar walls and peripheral airway smooth muscle, but no specific signal in airway epithelium.
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Tumour Necrosis Factor-α Regulates Human Eosinophil Apoptosis via Ligation of TNF-Receptor 1 and Balance between NF-κB and AP-1

TL;DR: TNF-α delays human eosinophil apoptosis via TNF-receptor 1 and the resulting changes in longevity depend on yin-yang balance between activation of NF-κB and AP-1.