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Peter S. Gilmour

Researcher at University of Edinburgh

Publications -  39
Citations -  4372

Peter S. Gilmour is an academic researcher from University of Edinburgh. The author has contributed to research in topics: Oxidative stress & A549 cell. The author has an hindex of 30, co-authored 39 publications receiving 4243 citations. Previous affiliations of Peter S. Gilmour include University of Nebraska Medical Center & Edinburgh Napier University.

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Journal ArticleDOI

Oxidative stress and calcium signaling in the adverse effects of environmental particles (PM10).

TL;DR: Oxidative stress arising from PM(10) has been shown to activate a number of redox-responsive signaling pathways in lung target cells that play a role in responses relevant to inflammation and pathological change, including MAPKs, NF-kappaB, AP-1, and histone acetylation.
Journal ArticleDOI

Free radical activity and pro-inflammatory effects of particulate air pollution (PM10) in vivo and in vitro.

TL;DR: Evidence is provided that PM10 has free radical activity and causes lung inflammation and epithelial injury, and the proposed hypothesis for the mechanism by which particulate air pollution causes adverse effects in patients with airways diseases is supported.
Journal ArticleDOI

Calcium and ROS-mediated activation of transcription factors and TNF-α cytokine gene expression in macrophages exposed to ultrafine particles

TL;DR: In this article, the effect of Uf particles on rat alveolar macrophages and human blood monocytes was investigated with reference to the roles of calcium and reactive oxygen species (ROS).
Journal ArticleDOI

Free radical activity associated with the surface of particles: a unifying factor in determining biological activity?

TL;DR: Using a sensitive phi X174 RF plasmid DNA assay, free radical activity was detected at the surface of normal and ultrafine titanium dioxide (TiO2), environmental particles (PM-10), asbestos and a range of man-made fibres.
Book ChapterDOI

Oxidative stress and TNF-alpha induce histone acetylation and NF-kappaB/AP-1 activation in alveolar epithelial cells: potential mechanism in gene transcription in lung inflammation

TL;DR: This study shows that the oxidant H2O2 and the pro-inflammatory mediator, TNF-a induce histone acetylation which is associated with decreased GSH levels and increased AP-1 and NF-kappaB activation leading to enhanced proinflammatory IL-8 release in alveolar epithelial cells.