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Ryoko Yamamoto Orthodontics and Craniofacial Developmental Biology, Oral Growth and Developmental Biology, Department of Molecular Genetics, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan

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Tomoko Minamizaki Orthodontics and Craniofacial Developmental Biology, Oral Growth and Developmental Biology, Department of Molecular Genetics, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan

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Yuji Yoshiko Orthodontics and Craniofacial Developmental Biology, Oral Growth and Developmental Biology, Department of Molecular Genetics, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan

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Hirotaka Yoshioka Orthodontics and Craniofacial Developmental Biology, Oral Growth and Developmental Biology, Department of Molecular Genetics, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan

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Kazuo Tanne Orthodontics and Craniofacial Developmental Biology, Oral Growth and Developmental Biology, Department of Molecular Genetics, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan

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Jane E Aubin Orthodontics and Craniofacial Developmental Biology, Oral Growth and Developmental Biology, Department of Molecular Genetics, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan

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Norihiko Maeda Orthodontics and Craniofacial Developmental Biology, Oral Growth and Developmental Biology, Department of Molecular Genetics, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8553, Japan

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-resistant rickets suggest the existence of additional phosphaturic factor(s). Recently, intensive studies of several such putative factors (e.g. matrix extracellular phosphoglycoprotein, dentin matrix protein 1 (DMP1), and fibroblast growth factor 23 (FGF23) have

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Claire L Wood Division of Functional Genetics and Development, Roslin Institute, University of Edinburgh, Edinburgh, UK
Translational and Clinical Research Institute, Newcastle University, Newcastle upon Tyne, UK

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Rob van ‘t Hof Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, UK

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Scott Dillon Division of Functional Genetics and Development, Roslin Institute, University of Edinburgh, Edinburgh, UK

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Volker Straub John Walton Muscular Dystrophy Research Centre, Newcastle University and Newcastle Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK

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

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

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Colin Farquharson Division of Functional Genetics and Development, Roslin Institute, University of Edinburgh, Edinburgh, UK

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established pharmacological intervention proven to stabilise muscle strength for a finite period of time ( Manzur et al. 2008 , Moxley et al. 2010 , Birnkrant et al. 2018 ). The side-effects of GC, however, are well recognised, with growth retardation

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Graham W Aberdeen Departments of Obstetrics, Gynecology, Reproductive Sciences and Physiology, University of Maryland School of Medicine, Baltimore, Maryland, USA

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Jeffery S Babischkin Departments of Obstetrics, Gynecology, Reproductive Sciences and Physiology, University of Maryland School of Medicine, Baltimore, Maryland, USA

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Gerald J Pepe Department of Physiological Sciences, Eastern Virginia Medical School, Norfolk, Virginia, USA

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Eugene D Albrecht Departments of Obstetrics, Gynecology, Reproductive Sciences and Physiology, University of Maryland School of Medicine, Baltimore, Maryland, USA

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growth factor (VEGF) has a well-established role in promoting angiogenesis in the adult, i.e. the formation and proliferation of capillaries ( Ferrara 1999 , Dvorak 2000 , Wagner 2011 ), and estrogen stimulates VEGF expression in many estrogen receptor

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David E Maridas Maine Medical Center Research Institute, Scarborough, Maine, USA

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Victoria E DeMambro Maine Medical Center Research Institute, Scarborough, Maine, USA

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Phuong T Le Maine Medical Center Research Institute, Scarborough, Maine, USA

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Kenichi Nagano Harvard School of Dental Medicine, Boston, Massachusetts, USA

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Roland Baron Harvard School of Dental Medicine, Boston, Massachusetts, USA

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Subburaman Mohan VA Loma Linda Healthcare System, Loma Linda, California, USA

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

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Introduction IGF signaling is a crucial pathway controlling muscle, fat and bone growth and is regulated by 6 binding proteins, IGFBP1–6. The IGF-binding proteins can enhance or inhibit IGF action locally ( Gustafsson et al . 1999 , Tahimic

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J Bryce Ortiz Barrow Neurological Institute at Phoenix Children’s Hospital, Phoenix, Arizona, USA
Department of Child Health, University of Arizona College of Medicine, Phoenix, Arizona, USA

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Sebastian Tellez Arizona State University, School of Life Sciences, Tempe, Arizona, USA

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Giri Rampal Department of Child Health, University of Arizona College of Medicine, Phoenix, Arizona, USA
Department of Biology and Biochemistry, University of Bath, Bath, United Kingdom

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Grant S Mannino Department of Integrative Physiology, University of Colorado, Boulder, Colorado, USA

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Nicole Couillard Department of Integrative Physiology, University of Colorado, Boulder, Colorado, USA

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Matias Mendez Department of Integrative Physiology, University of Colorado, Boulder, Colorado, USA

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Tabitha R F Green Department of Integrative Physiology, University of Colorado, Boulder, Colorado, USA

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Sean M Murphy Department of Integrative Physiology, University of Colorado, Boulder, Colorado, USA

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Rachel K Rowe Department of Integrative Physiology, University of Colorado, Boulder, Colorado, USA

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remains unknown. In juveniles, activation of the growth hormone (GH) axis results in linear body growth and changes in body size and composition ( Blakemore et al. 2010 ). This physical growth and increased height are linked to high levels of GH

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Shiao Y Chan School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Laura A Hancox School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Azucena Martín-Santos School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Laurence S Loubière School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Merlin N M Walter School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Ana-Maria González School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Phillip M Cox School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Ann Logan School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Christopher J McCabe School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Jayne A Franklyn School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Mark D Kilby School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK
School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Introduction Intrauterine growth restriction (IUGR) describes the failure of a fetus to attain its genetically determined growth potential, with the most common underlying etiology being uteroplacental failure associated with abnormal placental

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Valentina Pampanini Department of Women’s and Children’s Health, Pediatric Endocrinology Unit, Q2:08, Karolinska Institutet and University Hospital, Stockholm, Sweden

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Daniela Germani Department of Systems Medicine, Tor Vergata University, Rome, Italy

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Antonella Puglianiello Department of Systems Medicine, Tor Vergata University, Rome, Italy

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Jan-Bernd Stukenborg Department of Women’s and Children’s Health, Pediatric Endocrinology Unit, Q2:08, Karolinska Institutet and University Hospital, Stockholm, Sweden

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Ahmed Reda Department of Women’s and Children’s Health, Pediatric Endocrinology Unit, Q2:08, Karolinska Institutet and University Hospital, Stockholm, Sweden

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Iuliia Savchuk Department of Women’s and Children’s Health, Pediatric Endocrinology Unit, Q2:08, Karolinska Institutet and University Hospital, Stockholm, Sweden

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Kristín Rós Kjartansdóttir Department of Women’s and Children’s Health, Pediatric Endocrinology Unit, Q2:08, Karolinska Institutet and University Hospital, Stockholm, Sweden

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Stefano Cianfarani Department of Women’s and Children’s Health, Pediatric Endocrinology Unit, Q2:08, Karolinska Institutet and University Hospital, Stockholm, Sweden
Dipartimento Pediatrico Universitario Ospedaliero ‘Bambino Gesù’ Children’s Hospital – Tor Vergata University, Rome, Italy

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Olle Söder Department of Women’s and Children’s Health, Pediatric Endocrinology Unit, Q2:08, Karolinska Institutet and University Hospital, Stockholm, Sweden

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Introduction Adverse conditions during fetal life, such as low nutrient and/or oxygen supply from the placenta, can lead to intrauterine growth restriction (IUGR) and low birth weight. Besides affecting body growth, a suboptimal intrauterine

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Stuart A Lanham Bone and Joint Research Group, Centre for Human Development, Stem Cells and Regeneration, School of Medicine, University of Southampton, Southampton, UK

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Dominique Blache School of Agriculture and Environment, University of Western Australia, Crawley, Australia

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Richard O C Oreffo Bone and Joint Research Group, Centre for Human Development, Stem Cells and Regeneration, School of Medicine, University of Southampton, Southampton, UK

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Abigail L Fowden Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK

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Alison J Forhead Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK
Department of Biological and Medical Sciences, Oxford Brookes University, Oxford, UK

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Introduction Growth and development of long bones during late gestation are important for the normal functioning of the neonatal skeleton, especially in precocial species like sheep that stand and are mobile from birth. In normal and adverse

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K A Staines
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A S Pollard
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I M McGonnell
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C Farquharson Comparative Biomedical Sciences, Roslin Institute and R(D)SVS, The Royal Veterinary College, Royal College Street, London NW1 0TU, UK

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A A Pitsillides
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Introduction The transition of cartilage to bone is the basis by which all long bones form. This transition is tightly regulated to ensure both permissive foetal development through endochondral ossification and postnatal longitudinal growth at the

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Colin P Sibley Maternal and Fetal Health Research Centre, Division of Developmental Biology and Medicine, School of Medical Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK
St Mary’s Hospital, Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK

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adaptation to pregnancy, the timing of parturition, matching of supply with demand for nutrients by the fetus to enable normal growth ( Sferruzzi-Perri & Camm 2016 ) and indeed control of placental development itself. It is therefore not surprising that

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