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David A. Hume

Researcher at University of Queensland

Publications -  612
Citations -  66127

David A. Hume is an academic researcher from University of Queensland. The author has contributed to research in topics: Macrophage & Macrophage colony-stimulating factor. The author has an hindex of 113, co-authored 573 publications receiving 59932 citations. Previous affiliations of David A. Hume include University of California, San Diego & University of Oxford.

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Resting and injury-induced inflamed periosteum contain multiple macrophage subsets that are located at sites of bone growth and regeneration.

TL;DR: Observations confirm that osteomacs are key components of both osteal tissues, in spite of salient differences between endosteal and periosteal structure and that multiple macrophage subsets are involved in peruosteal bone dynamics.
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Regulation of the plasminogen activator inhibitor-2 (PAI-2) gene in murine macrophages. Demonstration of a novel pattern of responsiveness to bacterial endotoxin.

TL;DR: PAI‐2 mRNA levels generally varied inversely from those of its target, urokinase‐type plasminogen activator (uPA), and the macrophage growth factor CSF‐1, which induces uPA, inhibited PAI‐ 2 expression in cells treated subsequently with LPS.
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Effector ExoU from the Type III Secretion System Is an Important Modulator of Gene Expression in Lung Epithelial Cells in Response to Pseudomonas aeruginosa Infection

TL;DR: A detailed insight is provided into the response of epithelial cells to infection and the significant role played by the type III virulence mechanism in the initial host response is indicated.
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S100A8 chemotactic protein is abundantly increased, but only a minor contributor to LPS-induced, steroid resistant neutrophilic lung inflammation in vivo

TL;DR: S100A8, despite its abundance, resistance to steroids and known chemotactic activity, is unlikely to be an important determinant of LPS-induced neutrophilic lung inflammation in vivo, and the need for extensive in vivo profiling of proteomically identified candidate molecules is demonstrated.
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Network Analysis Reveals Distinct Clinical Syndromes Underlying Acute Mountain Sickness

TL;DR: The results challenge the accepted paradigm that AMS is a single disease process and describe at least two distinct syndromes following acute ascent to high altitude, and have potential utility in other clinical Syndromes.