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MRC-Versus Arthritis Centre for Musculoskeletal Ageing Research, Clinical, Metabolic and Molecular Physiology, University of Nottingham, Royal Derby Hospital Centre, Derby, UK
Mitochondrial Metabolism and Ageing Laboratory, Garvan Institute of Medical Research, Sydney, New South Wales, Australia
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St Vincent’s Clinical School, UNSW Medicine, UNSW Sydney, New South Wales, Australia
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ANZAC Research Institute, University of Sydney, Sydney, New South Wales, Australia
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UTS Centenary Centre for Inflammation, University Technology Sydney, New South Wales, Australia
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UTS Centenary Centre for Inflammation, University Technology Sydney, New South Wales, Australia
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St Vincent’s Clinical School, UNSW Medicine, UNSW Sydney, New South Wales, Australia
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Introduction Vitamin D deficiency, characterised by serum 25-hydroxyvitamin D (25(OH)D) levels of < 50 nmol/L, remains prevalent across both Europe and the United States of America ( Forrest & Stuhldreher 2011 , Cashman et al. 2016
College of Medical and Dental Sciences, College of Medical and Dental Sciences, Departments of Pediatrics, Reproductive and Vascular Biology Group, Fetal Medicine Centre, Centre for Women's and Children's Health
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College of Medical and Dental Sciences, College of Medical and Dental Sciences, Departments of Pediatrics, Reproductive and Vascular Biology Group, Fetal Medicine Centre, Centre for Women's and Children's Health
College of Medical and Dental Sciences, College of Medical and Dental Sciences, Departments of Pediatrics, Reproductive and Vascular Biology Group, Fetal Medicine Centre, Centre for Women's and Children's Health
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of vitamin D at the maternal–fetal interface. Illustration of both the innate and adaptive leukocyte decidual subsets with the potential capacity for intrinsic 1,25-dihydroxyvitamin D (1,25(OH) 2 D) synthesis from 25-hydroxyvitamin D (25OHD
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Introduction The musculoskeletal benefits of vitamin D are widely known: they promote the calcification of bone matrix and increase the absorption of calcium and phosphate in the intestine. Vitamin D deficiency can cause rickets in children
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Department of Orthopaedic Surgery, Molecular Biology Institute, David Geffen School of Medicine, UCLA, 615 Charles E Young Drive South, Los Angeles, California 90095, USA
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Department of Orthopaedic Surgery, Molecular Biology Institute, David Geffen School of Medicine, UCLA, 615 Charles E Young Drive South, Los Angeles, California 90095, USA
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Introduction At the end of 2007, Time magazine listed the ‘Benefits of Vitamin D’ as one of its top ten ‘medical breakthroughs’ of the year. The reason for this they stated has been the recent remarkable increase in studies documenting new actions
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Fetal Medicine Centre, Birmingham Women’s NHS Foundation Trust, Birmingham, UK
CEDAM, Birmingham Health Partners, The University of Birmingham, Birmingham, UK
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Fetal Medicine Centre, Birmingham Women’s NHS Foundation Trust, Birmingham, UK
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Fetal Medicine Centre, Birmingham Women’s NHS Foundation Trust, Birmingham, UK
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CEDAM, Birmingham Health Partners, The University of Birmingham, Birmingham, UK
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regulation of trophoblast invasion have been well documented ( Menkhorst et al . 2016 ). The aim of the current review is to provide an overview of these early events in placental development, with particular emphasis on the potential role of vitamin D as a
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addition to smoking, physical inactivity, oxidative stress, and systemic inflammation, other factors such as vitamin D deficiency may contribute to the large variability in the prevalence and severity of skeletal muscle dysfunction in COPD ( Maltais et al
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Introduction The quality of early life environment is a powerful determinant of adult health outcomes, including brain function ( Cottrell & Seckl 2009 ). The abundant expression of vitamin D receptors within the foetal brain ( Eyles et al
Department of Animal Physiology, Faculty of Science, Radboud University Nijmegen, Toernooiveld 1 NL-6525ED, Nijmegen, The Netherlands
Division of Pediatrics, Department of Clinical and Molecular Medicine, University of Bergen, Haukeland University Hospital, N-5021, Bergen, Norway
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Department of Animal Physiology, Faculty of Science, Radboud University Nijmegen, Toernooiveld 1 NL-6525ED, Nijmegen, The Netherlands
Division of Pediatrics, Department of Clinical and Molecular Medicine, University of Bergen, Haukeland University Hospital, N-5021, Bergen, Norway
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Department of Animal Physiology, Faculty of Science, Radboud University Nijmegen, Toernooiveld 1 NL-6525ED, Nijmegen, The Netherlands
Division of Pediatrics, Department of Clinical and Molecular Medicine, University of Bergen, Haukeland University Hospital, N-5021, Bergen, Norway
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Department of Animal Physiology, Faculty of Science, Radboud University Nijmegen, Toernooiveld 1 NL-6525ED, Nijmegen, The Netherlands
Division of Pediatrics, Department of Clinical and Molecular Medicine, University of Bergen, Haukeland University Hospital, N-5021, Bergen, Norway
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Department of Animal Physiology, Faculty of Science, Radboud University Nijmegen, Toernooiveld 1 NL-6525ED, Nijmegen, The Netherlands
Division of Pediatrics, Department of Clinical and Molecular Medicine, University of Bergen, Haukeland University Hospital, N-5021, Bergen, Norway
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Department of Animal Physiology, Faculty of Science, Radboud University Nijmegen, Toernooiveld 1 NL-6525ED, Nijmegen, The Netherlands
Division of Pediatrics, Department of Clinical and Molecular Medicine, University of Bergen, Haukeland University Hospital, N-5021, Bergen, Norway
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Introduction The vitamin D endocrine system in vertebrates is a major regulator of calcium and phosphate homeostasis ( Norman et al. 2002 ). Current research focuses on the two vitamin D metabolites 24 R ,25-dihydroxyvitamin D 3
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CriBioM, Criblage Biologique Marseille, Faculté de Médecine de la Timone, Marseille, France
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CriBioM, Criblage Biologique Marseille, Faculté de Médecine de la Timone, Marseille, France
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CriBioM, Criblage Biologique Marseille, Faculté de Médecine de la Timone, Marseille, France
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CriBioM, Criblage Biologique Marseille, Faculté de Médecine de la Timone, Marseille, France
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Introduction Low levels of total circulating 25-hydroxy-vitamin D (25(OH)D) are strongly associated with obesity and more specially with increased fat mass and BMI ( Vilarrasa et al. 2007 , Earthman et al. 2012 , Landrier et al. 2016
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In 1961, Prader et al. (1961) reported on a new form of vitamin D resistant rickets, which differed from the classic hypophosphatemic type (Albright et al. 1937) by its early onset (within the first year of life), the development of severe hypocalcemia with tetany, moderate hypophosphatemia and hyperaminoaciduria both reflecting secondary hyperparathyroidism, enamel hypoplasia and the complete correction of all clinical and biochemical evidence of rickets (including stunted growth rate) with high daily doses of vitamin D. In the initial report identifying this hereditary form of pseudo-vitamin D deficiency rickets (PDDR), transmission was reported to be autosomal dominant. Later, recessive inheritance was established (Fanconi & Prader 1969). In view of the fact that to maintain health, intake of vitamin D had to be consistently in vast excess of the recommended daily allowance (400 IU), the term 'vitamin D dependency' (VDD) was proposed to describe the new syndrome (Scriver 1970).
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