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Osteoporosis: HELP
Articles by Holly Evans
Based on 4 articles published since 2010
(Why 4 articles?)

Between 2010 and 2020, H. Evans wrote the following 4 articles about Osteoporosis.
+ Citations + Abstracts
1 Article PYY is a negative regulator of bone mass and strength. 2019

Leitch, Victoria D / Brassill, Mary Jane / Rahman, Sofia / Butterfield, Natalie C / Ma, Pattara / Logan, John G / Boyde, Alan / Evans, Holly / Croucher, Peter I / Batterham, Rachel L / Williams, Graham R / Bassett, J H Duncan. ·Molecular Endocrinology Laboratory, Department of Medicine, Hammersmith Campus, Imperial College London, London W12 0NN, United Kingdom. · Centre for Obesity Research, University College London, London WC1E 6JF, United Kingdom. · Queen Mary University of London, Oral BioEngineering, Bart's and The London School of Medicine and Dentistry, London E1 4NS, United Kingdom. · Sheffield Myeloma Research Team, University of Sheffield, Sheffield S10 2RX, United Kingdom. · The Garvan Institute of Medical Research and St. Vincent's Clinical School, University of New South Wales Medicine, Sydney, New South Wales 2010, Australia. · Centre for Obesity Research, University College London, London WC1E 6JF, United Kingdom; National Institute of Health Research, University College London Hospitals Biomedical Research Centre, London Q1T 7DN, United Kingdom. · Molecular Endocrinology Laboratory, Department of Medicine, Hammersmith Campus, Imperial College London, London W12 0NN, United Kingdom. Electronic address: graham.williams@imperial.ac.uk. · Molecular Endocrinology Laboratory, Department of Medicine, Hammersmith Campus, Imperial College London, London W12 0NN, United Kingdom. Electronic address: d.bassett@imperial.ac.uk. ·Bone · Pubmed #31306808.

ABSTRACT: OBJECTIVE: Bone loss in anorexia nervosa and following bariatric surgery is associated with an elevated circulating concentration of the gastrointestinal, anorexigenic hormone, peptide YY (PYY). Selective deletion of the PYY receptor Y1R in osteoblasts or Y2R in the hypothalamus results in high bone mass, but deletion of PYY in mice has resulted in conflicting skeletal phenotypes leading to uncertainty regarding its role in the regulation of bone mass. As PYY analogs are under development for treatment of obesity, we aimed to clarify the relationship between PYY and bone mass. METHODS: The skeletal phenotype of Pyy knockout (KO) mice was investigated during growth (postnatal day P14) and adulthood (P70 and P186) using X-ray microradiography, micro-CT, back-scattered electron scanning electron microscopy (BSE-SEM), histomorphometry and biomechanical testing. RESULTS: Bones from juvenile and Pyy KO mice were longer (P < 0.001), with decreased bone mineral content (P < 0.001). Whereas, bones from adult Pyy KO mice had increased bone mineral content (P < 0.05) with increased mineralisation of both cortical (P < 0.001) and trabecular (P < 0.001) compartments. Long bones from adult Pyy KO mice were stronger (maximum load P < 0.001), with increased stiffness (P < 0.01) and toughness (P < 0.05) compared to wild-type (WT) control mice despite increased cortical vascularity and porosity (P < 0.001). The increased bone mass and strength in Pyy KO mice resulted from increases in trabecular (P < 0.01) and cortical bone formation (P < 0.05). CONCLUSIONS: These findings demonstrate that PYY acts as a negative regulator of osteoblastic bone formation, implicating increased PYY levels in the pathogenesis of bone loss during anorexia or following bariatric surgery.

2 Article An N-ethyl-N-nitrosourea induced corticotropin-releasing hormone promoter mutation provides a mouse model for endogenous glucocorticoid excess. 2014

Bentley, Liz / Esapa, Christopher T / Nesbit, M Andrew / Head, Rosie A / Evans, Holly / Lath, Darren / Scudamore, Cheryl L / Hough, Tertius A / Podrini, Christine / Hannan, Fadil M / Fraser, William D / Croucher, Peter I / Brown, Matthew A / Brown, Steve D M / Cox, Roger D / Thakker, Rajesh V. ·Mammalian Genetics Unit (L.B., C.T.E., R.A.H., S.D.M.B., R.D.C.) and Mary Lyon Centre (C.L.S., T.A.H.), Medical Research Council Harwell, Harwell Science and Innovation Campus, Oxfordshire OX11 0RD, United Kingdom · Academic Endocrine Unit (C.T.E., M.A.N., R.A.H., F.M.H., R.V.T.), Nuffield Department of Clinical Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology, and Metabolism, Churchill Hospital, Oxford OX3 7LE, United Kingdom · The Mellanby Centre for Bone Research (H.E., D.L.), Department of Human Metabolism, University of Sheffield, Sheffield S10 2RX, United Kingdom · Wellcome Trust Sanger Institute (C.P.), Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, United Kingdom · Norwich Medical School (W.D.F.), University of East Anglia, Norwich Research Park, Norwich NR4 7TJ, United Kingdom · Garvan Institute of Medical Research (P.I.C.), Musculoskeletal Medicine Division, University of New South Wales, Sydney 2010, Australia · and University of Queensland Diamantina Institute (M.A.B.), Princess Alexandra Hospital, University of Queensland, Brisbane 4102, Australia. ·Endocrinology · Pubmed #24302625.

ABSTRACT: Cushing's syndrome, which is characterized by excessive circulating glucocorticoid concentrations, may be due to ACTH-dependent or -independent causes that include anterior pituitary and adrenal cortical tumors, respectively. ACTH secretion is stimulated by CRH, and we report a mouse model for Cushing's syndrome due to an N-ethyl-N-nitrosourea (ENU) induced Crh mutation at -120 bp of the promoter region, which significantly increased luciferase reporter activity and was thus a gain-of-function mutation. Crh(-120/+) mice, when compared with wild-type littermates, had obesity, muscle wasting, thin skin, hair loss, and elevated plasma and urinary concentrations of corticosterone. In addition, Crh(-120/+) mice had hyperglycemia, hyperfructosaminemia, hyperinsulinemia, hypercholesterolemia, hypertriglyceridemia, and hyperleptinemia but normal adiponectin. Crh(-120/+) mice also had low bone mineral density, hypercalcemia, hypercalciuria, and decreased concentrations of plasma PTH and osteocalcin. Bone histomorphometry revealed Crh(-120/+) mice to have significant reductions in mineralizing surface area, mineral apposition, bone formation rates, osteoblast number, and the percentage of corticoendosteal bone covered by osteoblasts, which was accompanied by an increase in adipocytes in the bone marrow. Thus, a mouse model for Cushing's syndrome has been established, and this will help in further elucidating the pathophysiological effects of glucocorticoid excess and in evaluating treatments for corticosteroid-induced osteoporosis.

3 Article Bisphosphonates as a supplement to exercise to protect bone during long-duration spaceflight. 2013

Leblanc, A / Matsumoto, T / Jones, J / Shapiro, J / Lang, T / Shackelford, L / Smith, S M / Evans, H / Spector, E / Ploutz-Snyder, R / Sibonga, J / Keyak, J / Nakamura, T / Kohri, K / Ohshima, H. ·Universities Space Research Association, 3600 Bay Area Blvd, Houston, TX 77058, USA. leblanc@dsls.usra.edu ·Osteoporos Int · Pubmed #23334732.

ABSTRACT: INTRODUCTION: This investigation was an international collaboration between NASA and the JAXA space agencies to investigate the potential value of antiresorptive agents to mitigate the well-established bone changes associated with long-duration spaceflight. METHODS: We report the results from seven International Space Station (ISS) astronauts who spent a mean of 5.5 months on the ISS and who took an oral dose of 70 mg of alendronate weekly starting 3 weeks before flight and continuing throughout the mission. All crewmembers had available for exercise a treadmill, cycle ergometer, and a resistance exercise device. Our assessment included densitometry of multiple bone regions using X-ray absorptiometry (DXA) and quantitative computed tomography (QCT) and assays of biomarkers of bone metabolism. RESULTS: In addition to pre- and post-flight measurements, we compared our results to 18 astronauts who flew ISS missions and who exercised using an early model resistance exercise device, called the interim resistance exercise device, and to 11 ISS astronauts who exercised using the newer advanced resistance exercise device (ARED). Our findings indicate that the ARED provided significant attenuation of bone loss compared with the older device although post-flight decreases in the femur neck and hip remained. The combination of the ARED and bisphosphonate attenuated the expected decline in essentially all indices of altered bone physiology during spaceflight including: DXA-determined losses in bone mineral density of the spine, hip, and pelvis, QCT-determined compartmental losses in trabecular and cortical bone mass in the hip, calculated measures of fall and stance computed bone strength of the hip, elevated levels of bone resorption markers, and urinary excretion of calcium. CONCLUSIONS: The combination of exercise plus an antiresoptive drug may be useful for protecting bone health during long-duration spaceflight.

4 Article Rapid-throughput skeletal phenotyping of 100 knockout mice identifies 9 new genes that determine bone strength. 2012

Bassett, J H Duncan / Gogakos, Apostolos / White, Jacqueline K / Evans, Holly / Jacques, Richard M / van der Spek, Anne H / Anonymous4870733 / Ramirez-Solis, Ramiro / Ryder, Edward / Sunter, David / Boyde, Alan / Campbell, Michael J / Croucher, Peter I / Williams, Graham R. ·Molecular Endocrinology Group, Department of Medicine, Imperial College London, London, United Kingdom. ·PLoS Genet · Pubmed #22876197.

ABSTRACT: Osteoporosis is a common polygenic disease and global healthcare priority but its genetic basis remains largely unknown. We report a high-throughput multi-parameter phenotype screen to identify functionally significant skeletal phenotypes in mice generated by the Wellcome Trust Sanger Institute Mouse Genetics Project and discover novel genes that may be involved in the pathogenesis of osteoporosis. The integrated use of primary phenotype data with quantitative x-ray microradiography, micro-computed tomography, statistical approaches and biomechanical testing in 100 unselected knockout mouse strains identified nine new genetic determinants of bone mass and strength. These nine new genes include five whose deletion results in low bone mass and four whose deletion results in high bone mass. None of the nine genes have been implicated previously in skeletal disorders and detailed analysis of the biomechanical consequences of their deletion revealed a novel functional classification of bone structure and strength. The organ-specific and disease-focused strategy described in this study can be applied to any biological system or tractable polygenic disease, thus providing a general basis to define gene function in a system-specific manner. Application of the approach to diseases affecting other physiological systems will help to realize the full potential of the International Mouse Phenotyping Consortium.