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Ian Woolhouse

Researcher at Queen Elizabeth Hospital Birmingham

Publications -  26
Citations -  1133

Ian Woolhouse is an academic researcher from Queen Elizabeth Hospital Birmingham. The author has contributed to research in topics: Lung cancer & Cancer. The author has an hindex of 10, co-authored 26 publications receiving 914 citations. Previous affiliations of Ian Woolhouse include University Hospitals Birmingham NHS Foundation Trust & Royal College of Physicians.

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Sputum chemotactic activity in chronic obstructive pulmonary disease: effect of α1–antitrypsin deficiency and the role of leukotriene B4 and interleukin 8

TL;DR: The results suggest that the bronchial secretions of COPD patients with α1–AT deficiency have increased neutrophil chemotactic activity, and this relates to the increased levels of IL-8 and, in particular LTB4, which accounted most of the sputum chemistry activity in the patients with COPD as a whole.
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Effect of sputum processing with dithiothreitol on the detection of inflammatory mediators in chronic bronchitis and bronchiectasis

TL;DR: Sputum processing with DTT significantly reduces the detectable concentration of TNFα, LTB4 and MPO, and produces a small but significant increase in median α1-AT levels, recommending that an untreated aliquot of sputum be retained for cytokine analysis.
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Demographics, management and survival of patients with malignant pleural mesothelioma in the National Lung Cancer Audit in England and Wales.

TL;DR: Data collected for the UK National Lung Cancer Audit is used to assess current practice and to highlight regional variation in the management of mesothelioma patients, as well as to describe survival patterns in subgroups.
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Endothelial interactions of neutrophils under flow in chronic obstructive pulmonary disease.

TL;DR: The enhanced endothelial interaction of neutrophils from smokers who have developed chronic obstructive pulmonary disease in the presence of normal levels of α1-antitrypsin deficiency, but not in those with severe α 1-antitsin deficiency is suggests that this is a predisposing factor for the development of the disease, and upregulation of macrophage antigen-1 may be responsible.