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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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Determination of mass changes in phosphatidylinositol 4,5-bisphosphate and evidence for agonist-stimulated metabolism of inositol 1,4,5-trisphosphate in airway smooth muscle.

TL;DR: These findings strongly suggest the occurrence of persistent receptor-mediated increases in PtdIns(4,5)P2 hydrolysis and Ins(1,4,3,4)P3 formation, and provide evidence that regulation of the metabolism of Ins (1, 4,5),P3 is a major determinant of Ins( 1,2,5,5]P3 concentration in this tissue under agonist-stimulated conditions.
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Safety of regadenoson, an adenosine A2A receptor agonist for myocardial perfusion imaging, in mild asthma and moderate asthma patients: a randomized, double-blind, placebo-controlled trial

TL;DR: In this pilot safety study of 48 patients with mild or moderate asthma who had bronchial reactivity to adenosine monophosphate, regadenoson was safe and well tolerated.
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Inhibitors of protein kinase C (PKC) prevent activated transcription: role of events downstream of NF-kappaB DNA binding.

TL;DR: Bergmann et al. as mentioned in this paper showed that protein kinase C (PKC) inhibitor, Ro 31-8220, and the phosphotidylcholine-specific phospholipase C inhibitor, D609, prevent NF-kappaB-dependent transcription, yet DNA binding is unaffected.
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The airway vasculature: recent advances and clinical implications

TL;DR: Advances in the development of non-invasive assessment of bronchial blood flow and the study of angiogenesis have provided a tool to investigate airway physiology in vivo, which will contribute to a better understanding of inflammatory airway diseases.
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Restoration of Corticosteroid Sensitivity in Chronic Obstructive Pulmonary Disease by Inhibition of Mammalian Target of Rapamycin

TL;DR: In this article, the role of mammalian target of rapamycin (mTOR) in corticosteroid sensitivity in COPD was investigated by using Western blotting to quantify the dexamethasone concentration required to achieve 30% inhibition of tumor necrosis factor-α-induced CXCL8 production.