M
Malcolm R. DeBaun
Researcher at Stanford University
Publications - 66
Citations - 805
Malcolm R. DeBaun is an academic researcher from Stanford University. The author has contributed to research in topics: Medicine & Internal fixation. The author has an hindex of 7, co-authored 51 publications receiving 397 citations. Previous affiliations of Malcolm R. DeBaun include Harborview Medical Center & University of Washington.
Papers
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Journal ArticleDOI
Treatment of critical-sized bone defects: clinical and tissue engineering perspectives.
TL;DR: This review provides an overview of the current operative treatment strategies of critical-sized bone defects as well as the current state of tissue engineering for such defects.
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Current Clinical Recommendations for Use of Platelet-Rich Plasma.
TL;DR: Evidence of its efficacy has been highly variable depending on the specific indication, and additional high-quality clinical trials with longer follow-up will be critical in shaping the perspective of this treatment option.
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Platelet-Rich Plasma.
TL;DR: Evidence of PRP efficacy has been mixed and highly variable depending on the specific indication, and sweeping recommendations about its utility impossible to make are likely to make.
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Quantitation of progenitor cell populations and growth factors after bone marrow aspirate concentration.
Richard Schäfer,Malcolm R. DeBaun,Erika Fleck,Christopher J. Centeno,Daniela Kraft,Johannes Leibacher,Karen Bieback,Erhard Seifried,Jason L. Dragoo +8 more
TL;DR: Assessment of the enrichment of stem/progenitor cells and growth factors in BM aspirate by two different commercial concentration devices versus standard BM aspiration contributed to the development of BMAC quality control assays as both BMAC systems concentrated platelets, growth factors and non-hematopoietic stem cell subpopulations with distinct phenotypes without loss of cell viability.
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The Intracellular Effect of Relaxin on Female Anterior Cruciate Ligament Cells
TL;DR: In this article, relaxin binding to receptors on female ACL cells was shown to result in an increase in matrix metalloproteinase (MMP) and decrease in tissue inhibitor of TIMP gene expression, a decrease in collagen and alpha smooth muscle actin (αSMA) expression, inhibition of transforming growth factor β1 (TGFβ1)induced fibrosis, and an increase of cyclic adenosine 3′,5′-monophosphate (cAMP) production.