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38th International Symposium on Growth Hormone and Growth by H. P. F. Koppeschaar, Torsten Tuvemo, Peter Trainer, Philip

By H. P. F. Koppeschaar, Torsten Tuvemo, Peter Trainer, Philip Zeitler

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Read Online or Download 38th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: Granada, Spain, April 7-8, 2006 (Hormone Research) PDF

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Additional info for 38th International Symposium on Growth Hormone and Growth Factors in Endocrinology and Metabolism: Granada, Spain, April 7-8, 2006 (Hormone Research)

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Human trophoblast cells generally do not grow well in culture, so the original ESC colony is mechanically separated from trophoblast and any differentiating cells. The dissected colonies are cut into small pieces and grown on new feeder cell carpets and passaged as dissected pieces or in bulk culture reseeded onto mitotically inactivated feeders after light trypsinization. , STO cells) [1, 2] and human cell lines, including human embryonic Use of Embryonic Stem Cells for Endocrine Disorders fibroblasts [11], human uterine endometrium [12], human foreskin fibroblasts [13] and human adult bone marrow cells [14].

3 Kanis JA, Johnell O, Oden A, Dawson A, De Laet C, Jonsson B: Ten year probabilities of osteoporotic fractures according to BMD and diagnostic thresholds. Osteoporos Int 2001;12:989–995. 4 Birks YF, Porthouse J, Addie C, Loughney K, Saxon L, Baverstock M, Francis RM, Reid DM, Watt I, Torgerson DJ: Randomized controlled trial of hip protectors among women living in the community. Osteoporos Int 2004;15:701–706. 5 Delmas PD: Treatment of postmenopausal osteoporosis. Lancet 2002;359:2018–2026. 6 Riggs BL, Parfitt AM: Drugs used to treat osteoporosis: the critical need for a uniform nomenclature based on their action on bone remodeling.

However, in clinical practice it is possible that not all subjects benefit from treatments either because they do not fully comply with dosing instructions or because they have some coexistent disease. Treatment can be monitored by measuring bone mineral density. Bone mineral density of the spine is usually measured after 1–2 years, with an increase of more than 3–6% probably indicating a favourable response. Treatment also can be monitored using bone turnover markers. Bone resorption markers (such as N- or C-telopeptide fragments of type I collagen) are usually measured, with a decrease in the need for antiresorptive therapy of more than 30–50% probably indicating a favourable response [20].

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