D
Deva D. Chan
Researcher at Rensselaer Polytechnic Institute
Publications - 43
Citations - 788
Deva D. Chan is an academic researcher from Rensselaer Polytechnic Institute. The author has contributed to research in topics: Cartilage & Medicine. The author has an hindex of 15, co-authored 32 publications receiving 635 citations. Previous affiliations of Deva D. Chan include Rush University Medical Center & University of California, Berkeley.
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Journal ArticleDOI
In vivo articular cartilage deformation: noninvasive quantification of intratissue strain during joint contact in the human knee.
Deva D. Chan,Luyao Cai,Kent D. Butz,Stephen B. Trippel,Eric A. Nauman,Corey P. Neu,Corey P. Neu +6 more
TL;DR: The MRI-based approach may accelerate the development of regenerative therapies for diseased or damaged cartilage, which is currently limited by the lack of reliable in vivo methods for noninvasive assessment of functional changes following treatment.
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Development of residual strains in human vertebral trabecular bone after prolonged static and cyclic loading at low load levels.
TL;DR: The concept that non-traumatic vertebral fractures may be related to long-term creep effects because the trabecular bone does not have sufficient time to recover mechanically from creep deformations accumulated by prolonged static or cyclic loading is supported.
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Stress distributions and material properties determined in articular cartilage from MRI-based finite strains
TL;DR: The results demonstrate the feasibility of a new and computationally efficient technique incorporating MRI-based deformation with mathematical modeling to non-invasively evaluate the mechanical behavior of biological tissues and materials.
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Deficiency of hyaluronan synthase 1 (Has1) results in chronic joint inflammation and widespread intra-articular fibrosis in a murine model of knee joint cartilage damage.
TL;DR: It is concluded that the ineffective repair of injured cartilage in Has1(-/-) joints can be at least partly explained by the markedly enhanced expression of particular genes in pathways linked to ECM turnover, IL-17/IL-6 cytokine signaling, and apoptosis.
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Human genome-wide expression analysis reorients the study of inflammatory mediators and biomechanics in osteoarthritis
TL;DR: The article provides a data-driven perspective, which concludes that IL-1β should be replaced by soluble mediators such as IL-17 or TGF-β1, which are much more likely to mimic the disease in OA model systems.