B
Brendan F. Boyce
Researcher at University of Rochester Medical Center
Publications - 255
Citations - 30591
Brendan F. Boyce is an academic researcher from University of Rochester Medical Center. The author has contributed to research in topics: Osteoclast & Bone resorption. The author has an hindex of 81, co-authored 241 publications receiving 28028 citations. Previous affiliations of Brendan F. Boyce include United States Department of Veterans Affairs & University of Texas at Austin.
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Journal ArticleDOI
Stimulation of bone formation in vitro and in rodents by statins.
Gregory R. Mundy,R I Garrett,Stephen E. Harris,J. Chan,David J. Chen,G. Rossini,Brendan F. Boyce,Ming Zhao,Gloria Gutierrez +8 more
TL;DR: It is shown that the statins, drugs widely used for lowering serum cholesterol, also enhance new bone formation in vitro and in rodents, and may have therapeutic applications for the treatment of osteoporosis.
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Increased bone formation in osteocalcin-deficient mice
Patricia Ducy,Christelle Desbois,Brendan F. Boyce,Gerald J. Pinero,Beryl Story,Colin R. Dunstan,Erica Smith,Jeffrey Bonadio,Steven A. Goldstein,Caren M. Gundberg,Allan Bradley,Gerard Karsenty +11 more
TL;DR: This study provides the first evidence that osteocalcin is a determinant of bone formation, and generates osteocalin-deficient mice that develop a phenotype marked by higher bone mass and bones of improved functional quality.
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Functions of RANKL/RANK/OPG in bone modeling and remodeling.
Brendan F. Boyce,Lianping Xing +1 more
TL;DR: The current understanding of the role of the RANKL/RANK/OPG system in bone modeling and remodeling is reviewed to show that the relative concentration of RankL and OPG in bone is a major determinant of bone mass and strength.
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Increased osteoclast development after estrogen loss: mediation by interleukin-6
Robert L. Jilka,Giao Hangoc,Giuseppe Girasole,Giovanni Passeri,Daniel C. Williams,John S. Abrams,Brendan F. Boyce,Hal E. Broxmeyer,Stavros C. Manolagas +8 more
TL;DR: Estrogen loss results in an interleukin-6-mediated stimulation of osteoclastogenesis, which suggests a mechanism for the increased bone resorption in postmenopausal osteoporosis.
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Bisphosphonates promote apoptosis in murine osteoclasts in vitro and in vivo
David E. Hughes,Kenneth R. Wright,Harry L. Uy,Harry L. Uy,Akira Sasaki,Toshiyuki Yoneda,David G. Roodman,David G. Roodman,Gregory R. Mundy,Brendan F. Boyce +9 more
TL;DR: Osteoclast apoptosis may be a major mechanism whereby bisphosphonates reduce osteoclast numbers and activity, and induction of apoptosis could be a therapeutic goal for new antiosteoclast drugs.