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Ronald G. Tompkins

Researcher at Harvard University

Publications -  531
Citations -  44641

Ronald G. Tompkins is an academic researcher from Harvard University. The author has contributed to research in topics: Burn injury & Poison control. The author has an hindex of 93, co-authored 526 publications receiving 41859 citations. Previous affiliations of Ronald G. Tompkins include University of Toronto & Tulane University.

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Isolation of rare circulating tumour cells in cancer patients by microchip technology.

TL;DR: The CTC-chip successfully identified CTCs in the peripheral blood of patients with metastatic lung, prostate, pancreatic, breast and colon cancer in 115 of 116 samples, with a range of 5–1,281CTCs per ml and approximately 50% purity.
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Genomic responses in mouse models poorly mimic human inflammatory diseases

TL;DR: This study shows that, although acute inflammatory stresses from different etiologies result in highly similar genomic responses in humans, the responses in corresponding mouse models correlate poorly with the human conditions and also, one another.
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Detection of Mutations in EGFR in Circulating Lung-Cancer Cells

TL;DR: Molecular analysis of circulating tumor cells from the blood of patients with lung cancer offers the possibility of monitoring changes in epithelial tumor genotypes during the course of treatment, and shows that a reduction in the number of captured cells was associated with a radiographic tumor response; an increase in theNumber of cells wasassociated with tumor progression, with the emergence of additional EGFR mutations in some cases.
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Continuous inertial focusing, ordering, and separation of particles in microchannels

TL;DR: The ability to differentially order particles of different sizes, continuously, at high rates, and without external forces in microchannels is expected to have a broad range of applications in continuous bioparticle separation, high-throughput cytometry, and large-scale filtration systems.
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A network-based analysis of systemic inflammation in humans

TL;DR: This work explores the known genome-wide interaction network to identify significant functional modules perturbed in response to an inflammatory stimulus and reveals that the human blood leukocyte response to acute systemic inflammation includes the transient dysregulation of leukocytes bioenergetics and modulation of translational machinery.