Catherine A. Shaw

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Diesel exhaust particulate (DEP), a major component of urban air pollution, has been linked to atherogenesis and precipitation of myocardial infarction. We hypothesized that DEP exposure would increase and destabilise atherosclerotic lesions in apolipoprotein E deficient (ApoE−/−) mice. ApoE−/− mice were fed a ‘Western diet’ (8 weeks) to induce ‘complex’(More)
BACKGROUND Diesel exhaust particulate (DEP) is a key arbiter of the adverse cardiovascular effects of air pollution. OBJECTIVES We assessed the in vitro effects of DEP on vascular function, nitric oxide (NO) availability, and the generation of oxygen-centered free radicals. METHODS We assessed the direct vascular effects of DEP (10-100 microg/mL) in(More)
and seminar participants at several universities and institutions for additional comments. All remaining errors are mine. Abstract Estimating the changes in the variance of wages features in two intensively researched areas of economics, one examining changes in residual inequality, the other investigating the link between college attendance and wage(More)
Clinical studies have now confirmed the link between short-term exposure to elevated levels of air pollution and increased cardiovascular mortality, but the mechanisms are complex and not completely elucidated. The present study was designed to investigate the hypothesis that activation of pulmonary sensory receptors and the sympathetic nervous system(More)
Inhalation of diesel exhaust impairs vascular function in man, by a mechanism that has yet to be fully established. We hypothesised that pulmonary exposure to diesel exhaust particles (DEP) would cause endothelial dysfunction in rats as a consequence of pulmonary and systemic inflammation. Wistar rats were exposed to DEP (0.5 mg) or saline vehicle by(More)
The Joseph Rowntree Foundation has supported this project as part of its programme of research and innovative development projects, which it hopes will be of value to policy makers and practitioners. The facts presented and views expressed in this report are, however, those of the authors and not necessarily those of the Foundation. 1 Introduction and(More)
Accelerated thrombus formation induced by exposure to combustion-derived air pollution has been linked to alterations in endogenous fibrinolysis and platelet activation in response to pulmonary and systemic inflammation. We hypothesised that mechanisms independent of inflammation contribute to accelerated thrombus formation following exposure to diesel(More)
BACKGROUND Nitric oxide (NO) can be both pro- and anti-apoptotic in various cell types, including macrophages. This apparent paradox may result from the actions of NO-related species generated in the microenvironment of the cell, for example the formation of peroxynitrite (ONOO-). In this study we have examined the ability of NO and ONOO- to evoke apoptosis(More)