E
Edward M. Schwarz
Researcher at University of Rochester Medical Center
Publications - 424
Citations - 26878
Edward M. Schwarz is an academic researcher from University of Rochester Medical Center. The author has contributed to research in topics: Osteoclast & Arthritis. The author has an hindex of 85, co-authored 400 publications receiving 23861 citations. Previous affiliations of Edward M. Schwarz include Albert Einstein College of Medicine & German Cancer Research Center.
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Journal ArticleDOI
Rel/NF-kappa B/I kappa B family: intimate tales of association and dissociation.
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Cyclooxygenase-2 regulates mesenchymal cell differentiation into the osteoblast lineage and is critically involved in bone repair
Xinping Zhang,Edward M. Schwarz,Donald A. Young,J. Edward Puzas,Randy N. Rosier,Regis J. O'Keefe +5 more
TL;DR: It is demonstrated that COX-2 plays an essential role in both endochondral and intramembranous bone formation during skeletal repair and regulates the induction of cbfa1 and osterix to mediate normal skeletal repair.
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3D printing of composite calcium phosphate and collagen scaffolds for bone regeneration.
Jason A. Inzana,Jason A. Inzana,Diana Olvera,Diana Olvera,Seth M. Fuller,James P. Kelly,James P. Kelly,Olivia A. Graeve,Olivia A. Graeve,Edward M. Schwarz,Edward M. Schwarz,Stephen L. Kates,Stephen L. Kates,Hani A. Awad,Hani A. Awad +14 more
TL;DR: This study demonstrates optimization of material parameters for 3D printed calcium phosphate scaffolds and enhancement of material properties by volumetric collagen incorporation via inkjet printing.
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Cellular and humoral immune responses to adenoviral vectors containing factor IX gene: tolerization of factor IX and vector antigens allows for long-term expression.
TL;DR: It is concluded that currently available adenoviral vectors have serious limitations for use for long-term gene therapy.
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Mechanisms of TNF-α– and RANKL-mediated osteoclastogenesis and bone resorption in psoriatic arthritis
TL;DR: Results suggest a model for understanding the pathogenesis of aggressive bone erosions in PsA, where OCPs arise from TNF-alpha-activated PBMCs that migrate to the inflamed synovium and subchondral bone, where they are exposed to unopposed RANKL and T NF-alpha.