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Showing 1–7 of 7 results
Advanced filters: Author: Ricardo T. Paniagua Clear advanced filters
  • Most Amazon tree species are rare but a small proportion are common across the region. The authors show that different species are hyperdominant in different size classes and that hyperdominance is more phylogenetically restricted for larger canopy trees than for smaller understory ones.

    • Frederick C. Draper
    • Flavia R. C. Costa
    • Christopher Baraloto
    Research
    Nature Ecology & Evolution
    Volume: 5, P: 757-767
  • There has been much speculation on the potential use of kinase inhibitors, such as imatinib mesylate, for the treatment of autoimmune rheumatic diseases. Imatinib inhibits a select set of tyrosine kinases at submicromolar concentrations. In this Viewpoint, the authors discuss how imatinib could provide a potent therapeutic option for a variety of autoimmune and inflammatory diseases, for which current therapies are insufficient.

    • Ricardo T Paniagua
    • William H Robinson
    Reviews
    Nature Clinical Practice Rheumatology
    Volume: 3, P: 190-191
  • Slug supports heart development and tumor metastasis, but its role in blood vessel formation is less clear. Here the authors show that endothelial cell-expressed Slug regulates both physiologic and pathological angiogenesis, at least in part through the modulation of Notch signalling.

    • Nan W. Hultgren
    • Jennifer S. Fang
    • Christopher C. W. Hughes
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-16
  • Several cellular responses, in different cell types, are involved in the pathogenesis of rheumatoid arthritis. Common to many of these responses is signal transduction through tyrosine kinases. Evidence implicating certain tyrosine kinases in the pathogenesis of rheumatoid arthritis, and the potential to inhibit these kinases, is outlined in this Review.

    • Christina D'Aura Swanson
    • Ricardo T. Paniagua
    • William H. Robinson
    Reviews
    Nature Reviews Rheumatology
    Volume: 5, P: 317-324