Publications
227 results found
Waung JA, Bassett JHD, Williams GR, 2012, Thyroid hormone metabolism in skeletal development and adult bone maintenance, TRENDS IN ENDOCRINOLOGY AND METABOLISM, Vol: 23, Pages: 155-162, ISSN: 1043-2760
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- Citations: 63
Bassett JHD, van der Spek A, Gogakos A, et al., 2012, Quantitative X-ray Imaging of Rodent Bone by Faxitron, BONE RESEARCH PROTOCOLS, SECOND EDITION, Vol: 816, Pages: 499-506, ISSN: 1064-3745
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- Citations: 25
Cheung MS, Gogakos A, Bassett JHD, et al., 2011, Thyroid Disease and Osteoporosis, Oxford Textbook of Endocrinology and Diabetes, Editors: Wass, Stewart, Publisher: Oxford University Press, USA, Pages: 712-720, ISBN: 9780199235292
Vanderpump MPJ, Lazarus JH, Smyth PP, et al., 2011, Iodine status of UK schoolgirls: a cross-sectional survey., Lancet, Vol: 377, Pages: 2007-2012
BACKGROUND: Iodine deficiency is the most common cause of preventable mental impairment worldwide. It is defined by WHO as mild if the population median urinary iodine excretion is 50-99 μg/L, moderate if 20-49 μg/L, and severe if less than 20 μg/L. No contemporary data are available for the UK, which has no programme of food or salt iodination. We aimed to assess the current iodine status of the UK population. METHODS: In this cross-sectional survey, we systematically assessed iodine status in schoolgirls aged 14-15 years attending secondary school in nine UK centres. Urinary iodine concentrations and tap water iodine concentrations were measured in June-July, 2009, and November-December, 2009. Ethnic origin, postcode, and a validated diet questionnaire assessing sources of iodine were recorded. FINDINGS: 810 participants provided 737 urine samples. Data for dietary habits and iodine status were available for 664 participants. Median urinary iodine excretion was 80·1 μg/L (IQR 56·9-109·0). Urinary iodine measurements indicative of mild iodine deficiency were present in 51% (n=379) of participants, moderate deficiency in 16% (n=120), and severe deficiency in 1% (n=8). Prevalence of iodine deficiency was highest in Belfast (85%, n=135). Tap water iodine concentrations were low or undetectable and were not positively associated with urinary iodine concentrations. Multivariable general linear model analysis confirmed independent associations between low urinary iodine excretion and sampling in summer (p<0·0001), UK geographical location (p<0·0001), low intake of milk (p=0·03), and high intake of eggs (p=0·02). INTERPRETATION: Our findings suggest that the UK is iodine deficient. Since developing fetuses are the most susceptible to adverse effects of iodine deficiency and even mild perturbations of maternal and fetal thyroid function have an effect on neurodevelopment, these findings are of potential maj
Williams GR, Bassett JHD, 2011, Local control of thyroid hormone action: role of type 2 deiodinase, JOURNAL OF ENDOCRINOLOGY, Vol: 209, Pages: 261-272, ISSN: 0022-0795
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- Citations: 88
Williams GR, 2011, Extrathyroidal expression of TSH receptor, ANNALES D ENDOCRINOLOGIE, Vol: 72, Pages: 68-73, ISSN: 0003-4266
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- Citations: 82
Hu M, Bassett JHD, Danks L, et al., 2011, Activated Invariant NKT Cells Regulate Osteoclast Development and Function, JOURNAL OF IMMUNOLOGY, Vol: 186, Pages: 2910-2917, ISSN: 0022-1767
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- Citations: 32
Combs CE, Nicholls JJ, Bassett JHD, et al., 2011, Thyroid hormones and bone development, Minerva Endocrinologica, Vol: 36, Pages: 71-85
Vanleene M, Saldanha Z, Cloyd KL, et al., 2011, Transplantation of human fetal blood stem cells in the osteogenesis imperfecta mouse leads to improvement in multiscale tissue properties., Blood, Vol: 117, Pages: 1053-1060
Osteogenesis imperfecta (OI or brittle bone disease) is a disorder of connective tissues caused by mutations in the collagen genes. We previously showed that intrauterine transplantation of human blood fetal stem/stromal cells in OI mice (oim) resulted in a significant reduction of bone fracture. This work examines the cellular mechanisms and mechanical bone modifications underlying these therapeutic effects, particularly examining the direct effects of donor collagen expression on bone material properties. In this study, we found an 84% reduction in femoral fractures in transplanted oim mice. Fetal blood stem/stromal cells engrafted in bones, differentiated into mature osteoblasts, expressed osteocalcin, and produced COL1a2 protein, which is absent in oim mice. The presence of normal collagen decreased hydroxyproline content in bones, altered the apatite crystal structure, increased the bone matrix stiffness, and reduced bone brittleness. In conclusion, expression of normal collagen from mature osteoblast of donor origin significantly decreased bone brittleness by improving the mechanical integrity of the bone at the molecular, tissue, and whole bone levels.
Esapa C, Hough T, Testori S, et al., 2011, A mouse model for spondyloepiphyseal dysplasia congenita with secondary osteoarthritis due to a Col2a1 mutation, Journal of Bone and Mineral Research
Progeny of mice treated with the mutagen N-ethyl-N-nitrosourea (ENU) revealed a mouse, designated Longpockets (Lpk), with short humeri, abnormal vertebrae, and disorganized growth plates, features consistent with spondyloepiphyseal dysplasia congenita (SEDC). The Lpk phenotype was inherited as an autosomal dominant trait.Lpk/+ mice were viable and fertile and Lpk/Lpk mice died perinatally. Lpk was mapped to chromosome 15 and mutational analysis of likely candidates from the interval revealed a Col2a1 missense Ser1386Pro mutation. Transient transfection of wild type and Ser1386Pro mutant Col2a1 c-Myc constructs in COS-7 cells and CH8 chondrocytes demonstrated abnormal processing and endoplasmic reticulum retention of the mutant protein. Histology revealed growth plate disorganization in 14 day old Lpk/+ mice and embryonic cartilage from Lpk/+ and Lpk/Lpk mice had reduced safranin-O and type-II collagen staining in the extracellular matrix. The wild type and Lpk/+ embryos had vertical columns of proliferating chondrocytes, whereas those in Lpk/Lpk mice were perpendicular to the direction of bone growth. Electron microscopy of cartilage from 18.5 dpc wild type, Lpk/+ and Lpk/Lpk embryos revealed fewer and less elaborate collagen fibrils in the mutants, with enlarged vacuoles in the endoplasmic reticulum which contained amorphous inclusions. Micro-CT scans of 12 week old Lpk/+ mice revealed them to have decreased bone mineral density, and total bone volume, with erosions and osteophytes at the joints. Thus, an ENU mouse model with a Ser1386Pro mutation of the Col2a1 C-propeptide domain that results in abnormal collagen processing and phenotypic features consistent with SEDC and secondary osteoarthritis has been established. © 2011 American Society for Bone and Mineral Research.
Gogakos AI, Bassett JHD, Williams GR, 2010, Thyroid and bone, ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, Vol: 503, Pages: 129-136, ISSN: 0003-9861
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- Citations: 101
Master A, Wojcicka A, Piekielko-Witkowska A, et al., 2010, Untranslated regions of thyroid hormone receptor beta 1 mRNA are impaired in human clear cell renal cell carcinoma, BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, Vol: 1802, Pages: 995-1005, ISSN: 0925-4439
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- Citations: 33
Murphy E, Glueer CC, Reid DM, et al., 2010, Thyroid Function within the Upper Normal Range Is Associated with Reduced Bone Mineral Density and an Increased Risk of Nonvertebral Fractures in Healthy Euthyroid Postmenopausal Women, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, Vol: 95, Pages: 3173-3181, ISSN: 0021-972X
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- Citations: 136
Bassett JHD, Boyde A, Howell PGT, et al., 2010, Optimal bone strength and mineralization requires the type 2 iodothyronine deiodinase in osteoblasts, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 107, Pages: 7604-7609, ISSN: 0027-8424
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- Citations: 110
Williams GR, 2009, Actions of thyroid hormones in bone, ENDOKRYNOLOGIA POLSKA, Vol: 60, Pages: 380-388, ISSN: 0423-104X
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- Citations: 35
Tan TMM, Caputo C, Medici F, et al., 2009, MELAS syndrome, diabetes and thyroid disease: the role of mitochondrial oxidative stress, CLINICAL ENDOCRINOLOGY, Vol: 70, Pages: 340-341, ISSN: 0300-0664
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- Citations: 8
Williams GR, 2009, Does serum TSH level have thyroid hormone independent effects on bone turnover?, NATURE CLINICAL PRACTICE ENDOCRINOLOGY & METABOLISM, Vol: 5, Pages: 10-11, ISSN: 1745-8366
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- Citations: 7
Han TS, Williams GR, Vanderpump MPJ, 2009, Benzofuran derivatives and the thyroid., Clin Endocrinol (Oxf), Vol: 70, Pages: 2-13
Amiodarone and dronedarone are two clinically important benzofuran derivatives. Amiodarone has been used widely for treating resistant tachyarrhythmias in the past three decades. However amiodarone and its main metabolically active metabolite desethylamiodarone can adversely affect many organs, including the thyroid gland. Amiodarone-induced thyroid disorders are common and often present as a management challenge for endocrinologists. The pathogenesis of amiodarone-induced thyroid dysfunction is complex but the inherent effects of the drug itself as well as its high iodine content appear to play a central role. The non-iodinated dronedarone also exhibits anti-arrhythmic properties but appears to be less toxic to the thyroid. This review describes the biochemistry of benzofuran derivatives, including their pharmacology and the physiology necessary for understanding the cellular mechanisms involved in their actions. The known effects of these compounds on thyroid action are described. Recommendations for management of amiodarone-induced hypothyroidism and thyrotoxicosis are suggested. Dronedarone appears to be an alternative but less-effective anti-arrhythmic agent and it does not have adverse effects on thyroid function. It may have a future role as an alternative agent in patients being considered for amiodarone therapy especially those at high risk of developing thyroid dysfunction but not in severe heart failure.
Han TS, Williams GR, Vanderpump MPJ, 2009, Benzofuran derivatives and the thyroid, CLINICAL ENDOCRINOLOGY, Vol: 70, Pages: 2-13, ISSN: 0300-0664
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- Citations: 39
Hameed S, Dhillo WS, Patterson M, et al., 2009, The central regulation of food intake and energy expenditure by thyroid hormones, Hot Thyroidology, Vol: www.hotthyroidology.com/editorial_pdf.hameed_HT08_09.pdf
Brassill MJ, Williams GR, 2009, Advances in our understanding of hyperthyroidism-associated bone loss, European Endocrinology, Vol: 4, Pages: 103-106
Brassill MJ, Williams GR, 2009, Advances in our understanding of hyperthyroidism-associated bone loss, US Endocrinology, Vol: 4, Pages: 114-117
Gogakos AI, Cheung MS, Bassett JHD, et al., 2009, Bone signalling pathways and treatment of osteoporosis, Expert Reviews in Endocrinology and Metabolism, Vol: 4, Pages: 639-650
Hameed S, Dhillo WS, Patterson M, et al., 2009, The Central Regulation of Food Intake and Energy Expenditure by Thyroid Hormones, Hot Thyroidology (www.hotthyroidology.com
For more than a century the essential role of thyroid hormones in the regulation of energy homeostasis has been recognised. In the past, these effects were attributed to thyroid hormone action in the periphery, however in more recent years the important effects of thyroid hormones in the central nervous system (CNS) have also been described, and there is now a substantial body of evidence from genetic and molecular biology studies delineating the CNS pathways through which thyroid hormones influence food intake and energy expenditure. Nutritional signals and neurotransmitters conveying information about the metabolic milieu converge on the hypothalamus effecting changes in neuronal activity culminating in alterations in food intake and metabolic rate. These effects are mediated in part by changes in thyrotropin releasing hormone expression, local CNS thyroid hormone levels, the hypothalamo-pituitary-thyroid axis and the sympathetic nervous system. The characterisation of these pathways will not only improve our understanding of thyroid physiology, but may also translate into targeted pharmaceutical treatments for obesity the archetypal outcome of an imbalance between food intake and energy expenditure. Given the increasing worldwide prevalence of obesity, this would clearly bring significant public health benefits.
Bassett JHD, Williams GR, 2008, The skeletal phenotypes of TRα and TRβ mutant mice, JOURNAL OF MOLECULAR ENDOCRINOLOGY, Vol: 42, Pages: 269-282, ISSN: 0952-5041
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- Citations: 62
Hu M, Basssett JHD, Danks L, et al., 2008, Invariant NKT Cells Regulate Osteoclast Development and Function Under Homeostatic and during Conditions of Immune Activation, 50th Annual Meeting of the American-Society-of-Hematology, Publisher: AMER SOC HEMATOLOGY, Pages: 46-46, ISSN: 0006-4971
Bassett JHD, Williams GR, 2008, Critical role of the hypothalamic-pituitary-thyroid axis in bone, BONE, Vol: 43, Pages: 418-426, ISSN: 8756-3282
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- Citations: 97
Williams AJ, Robson H, Kester MHA, et al., 2008, Iodothyronine deiodinase enzyme activities in bone, BONE, Vol: 43, Pages: 126-134, ISSN: 8756-3282
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- Citations: 67
Williams GR, 2008, Neurodevelopmental and neurophysiological actions of thyroid hormone, JOURNAL OF NEUROENDOCRINOLOGY, Vol: 20, Pages: 784-794, ISSN: 0953-8194
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- Citations: 350
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