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Chandrika D Mahalingam Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA

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Tanuka Datta Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA

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Rashmi V Patil Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA

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Jaclynn Kreider Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA

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R Daniel Bonfil Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA
Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA

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Keith L Kirkwood Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA

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Steven A Goldstein Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA

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Abdul B Abou-Samra Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA

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Nabanita S Datta Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA
Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA
Division of Endocrinology, Department of Orthopedic Surgery, Department of Urology and Pathology, Departments of Craniofacial Biology and Microbiology and Immunology, Barbara Ann Karmanos Cancer Institute, Cardiovascular Research Institute, Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA

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%). Tibial cortical parameters were also significantly affected in the KO mice showing decrease in cortical BMC (10%), and TMD (3%). Bone histomorphometry revealed a reduced trabecular bone formation in Mkp1 KO compared with WT female mice (KO 4

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Katherine A Staines The Roslin Institute and Royal (Dick) School of Veterinary Studies, The University of Edinburgh, Easter Bush, Edinburgh, Midlothian EH25 9RG, UK

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Vicky E MacRae The Roslin Institute and Royal (Dick) School of Veterinary Studies, The University of Edinburgh, Easter Bush, Edinburgh, Midlothian EH25 9RG, UK

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Colin Farquharson The Roslin Institute and Royal (Dick) School of Veterinary Studies, The University of Edinburgh, Easter Bush, Edinburgh, Midlothian EH25 9RG, UK

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extracellular acidification ( Palokangas et al . 1997 , Mellis et al . 2011 ). Like bone formation, this is under tight control by a variety of autocrine, paracrine, and endocrine factors and is thought to be primarily regulated by the terminally

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Aijaz A John Division of Endocrinology and Centre for Research in Anabolic Skeletal Targets in Health and Illness (ASTHI), CSIR-Central Drug Research Institute, Lucknow, India

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Ravi Prakash Division of Endocrinology and Centre for Research in Anabolic Skeletal Targets in Health and Illness (ASTHI), CSIR-Central Drug Research Institute, Lucknow, India

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Divya Singh Division of Endocrinology and Centre for Research in Anabolic Skeletal Targets in Health and Illness (ASTHI), CSIR-Central Drug Research Institute, Lucknow, India

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osteoblast functions. In this study, we establish that miR-487b-3p negatively controls osteogenesis by obstructing Notch-regulated ankyrin-repeat protein (Nrarp) which blocks Notch signaling and promotes bone formation. Materials and methods

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Natalie K Y Wee Bone Cell Biology and Disease Unit, St Vincent’s Institute of Medical Research, Fitzroy, Australia

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Thaísa F C de Lima Bone Cell Biology and Disease Unit, St Vincent’s Institute of Medical Research, Fitzroy, Australia
Department of Genetics and Molecular Biology, University of Campinas, São Paulo, Brazil

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Narelle E McGregor Bone Cell Biology and Disease Unit, St Vincent’s Institute of Medical Research, Fitzroy, Australia

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Emma C Walker Bone Cell Biology and Disease Unit, St Vincent’s Institute of Medical Research, Fitzroy, Australia

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Ingrid J Poulton Bone Cell Biology and Disease Unit, St Vincent’s Institute of Medical Research, Fitzroy, Australia

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Martha Blank Bone Cell Biology and Disease Unit, St Vincent’s Institute of Medical Research, Fitzroy, Australia
Department of Medicine, The University of Melbourne, St. Vincent’s Hospital, Melbourne, Australia

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Natalie A Sims Bone Cell Biology and Disease Unit, St Vincent’s Institute of Medical Research, Fitzroy, Australia
Department of Medicine, The University of Melbourne, St. Vincent’s Hospital, Melbourne, Australia

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consolidation and did not rescue the phenotype of Dmp1cre.Socs3 fl/fl mice. Leptin receptor deficiency delayed bone consolidation only in female mice. One explanation for this may arise from the sex-dependent levels of bone formation and resorption in male

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Claire L Wood Division of Developmental Biology, Roslin Institute, University of Edinburgh, Edinburgh, UK

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Ondrej Soucek Department of Paediatrics, 2nd Faculty of Medicine, Charles University in Prague and Motol University Hospital, Prague, Czech Republic
Department of Women’s and Children’s Health, Karolinska Institutet and Pediatric Endocrinology Unit, Karolinska University Hospital, Stockholm, Sweden

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Sze C Wong Developmental Endocrinology Research Group, School of Medicine, University of Glasgow, Glasgow, UK

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Farasat Zaman Department of Women’s and Children’s Health, Karolinska Institutet and Pediatric Endocrinology Unit, Karolinska University Hospital, Stockholm, Sweden

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Colin Farquharson Division of Developmental Biology, Roslin Institute, University of Edinburgh, Edinburgh, UK

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Lars Savendahl Department of Women’s and Children’s Health, Karolinska Institutet and Pediatric Endocrinology Unit, Karolinska University Hospital, Stockholm, Sweden

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S Faisal Ahmed Developmental Endocrinology Research Group, School of Medicine, University of Glasgow, Glasgow, UK

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rates of bone growth, their skeleton is particularly vulnerable to the adverse effects of GCs on bone formation. GC-induced growth retardation was first described 60 years ago after an equivalent cortisone dose of only 1.5 mg/kg/day ( Blodgett et al

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Colin Farquharson Bone Biology Group, The Roslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Edinburgh EH25 9RG, UK

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changes in bone were a result of impaired bone formation, whilst resorption was normal. The reduced formation may be a consequence of altered signalling pathways such as the GH/IGF1 axis that is known to be anabolic to the skeleton. These changes resemble

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Niklas Andersson Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Ulrika Islander Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Emil Egecioglu Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Elin Löf Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Charlotte Swanson Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Sofia Movérare-Skrtic Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Klara Sjögren Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Marie K Lindberg Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Hans Carlsten Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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Claes Ohlsson Center for Bone Research at the Sahlgrenska Academy, Division of Endocrinology, Department of Internal Medicine, Göteborg University, Gröna stråket 8 SE-413 45 Göteborg, Sweden
Department of Rheumatology and Inflammation Research at the Sahlgrenska Academy, Göteborg University, Guldhedsgatan 10, SE-413 46 Göteborg, Sweden
Department of Physiology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden
Department of Pharmacology, Göteborg University, Medicinaregatan 9, Box 434 SE-405 30 Göteborg, Sweden

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compartment. The bone sparing effects of estrogen in rodents are believed not only to be mediated through inhibition of bone resorption, but also through stimulation of bone formation ( Chow et al. 1992 ). However, some studies indicate that the effects of

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Urszula T Iwaniec Skeletal Biology Laboratory, School of Biological and Population Health Sciences, Oregon State University, Corvallis, Oregon, USA
Center for Healthy Aging Research, Oregon State University, Corvallis, Oregon, USA

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Russell T Turner Skeletal Biology Laboratory, School of Biological and Population Health Sciences, Oregon State University, Corvallis, Oregon, USA
Center for Healthy Aging Research, Oregon State University, Corvallis, Oregon, USA

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surface. Modeling refers to changes in bone architecture where bone is added to a preexisting bone surface without a requirement for prior bone resorption or by which bone is resorbed from a bone surface without initiating subsequent bone formation

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Jonathan J Nicholls Molecular Endocrinology Group, Department of Medicine, Imperial College London, Hammersmith Campus, Room 7N2b, Commonwealth Building, Du Cane Road, London W12 0NN, UK

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Mary Jane Brassill Molecular Endocrinology Group, Department of Medicine, Imperial College London, Hammersmith Campus, Room 7N2b, Commonwealth Building, Du Cane Road, London W12 0NN, UK

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Graham R Williams Molecular Endocrinology Group, Department of Medicine, Imperial College London, Hammersmith Campus, Room 7N2b, Commonwealth Building, Du Cane Road, London W12 0NN, UK

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J H Duncan Bassett Molecular Endocrinology Group, Department of Medicine, Imperial College London, Hammersmith Campus, Room 7N2b, Commonwealth Building, Du Cane Road, London W12 0NN, UK

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chondrocytes synthesise type X collagen, which induces cartilage mineralisation, thus generating a template for osteoblastic bone formation. Epiphyseal growth plates form at either end of the anlage and consist of organised columns of proliferating

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Mone Zaidi The Mount Sinai Bone Program, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA

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Maria I New The Mount Sinai Bone Program, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA

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Harry C Blair The Pittsburgh VA Medical Center and Departments of Pathology and of Cell Biology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA

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Alberta Zallone Department of Histology, University of Bari, Bari, Italy

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Ramkumarie Baliram The Mount Sinai Bone Program, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA

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Terry F Davies The Mount Sinai Bone Program, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA

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Christopher Cardozo The Mount Sinai Bone Program, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA

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James Iqbal The Mount Sinai Bone Program, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA

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Li Sun The Mount Sinai Bone Program, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA

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Clifford J Rosen Maine Medical Center Research Institute, Scarborough, Maine, USA

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Tony Yuen The Mount Sinai Bone Program, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA

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). This is the likely basis of ACTH action in preventing glucocorticoid-induced osteonecrosis, as assessed in a rabbit model ( Zaidi et al . 2010 ). Figure 1 Endocrine control of bone remodeling. Bone formation is regulated by signals from

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