Yonsei University · Medicine
Professor Yumie Rhee's research lab focuses on the cellular and molecular mechanisms regulating bone remodeling and formation, with a particular emphasis on the role of parathyroid hormone (PTH) signaling in osteocytes and its impact on cortical bone geometry and mechanical properties. The lab investigates how PTH influences both modeling-based and remodeling-based bone formation, using transgenic mouse models and pharmacological interventions to dissect these pathways. Advanced imaging and deep learning techniques are also employed to improve the assessment of body composition and metabolic activity in bone and muscle tissues.
Figures are computed from collected data and may differ slightly.
The periosteal and endocortical surfaces of cortical bone dictate the geometry and overall mechanical properties of bone. Yet the cellular and molecular mechanisms that regulate activity on these surfaces are far from being understood. Parathyroid hormone (PTH) has profound effects in cortical bone, stimulating periosteal expansion and at the same time accelerating intracortical bone remodeling. We report herein that transgenic mice expressing a constitutive active PTH receptor in osteocytes (DM
This deep neural network model enabled the automatic volumetric segmentation of body composition on whole-body CT images, potentially expanding adjunctive sarcopenia assessment on PET-CT scan and volumetric assessment of metabolism in whole-body muscle and fat tissues.
In a 40-year-old man who had suffered from vague and generalized bone pains for 7 years due to oncogenic osteomalacia, the causative tumour was finally detected by Indium-111 octreotide scintigraphy. Some characteristics of the tumour associated with oncogenic osteomalacia, such as its size, growth rate, location and origin, often make the diagnosis difficult. However, the recent discovery of somatostatin receptors in mesenchymal tumours, which are the most common cause of oncogenic osteomalacia
In patients with PLO, LSBMD at 12 months increased in both the TPTD-treated and control groups. TPTD treatment and younger age were associated with greater increases in LSMBD irrespective of baseline LSBMD.
The contribution of remodeling-based bone formation coupled to osteoclast activity versus modeling-based bone formation that occurs independently of resorption, to the anabolic effect of PTH remains unclear. We addressed this question using transgenic mice with activated PTH receptor signaling in osteocytes that exhibit increased bone mass and remodeling, recognized skeletal effects of PTH elevation. Direct inhibition of bone formation was accomplished genetically by overexpressing the Wnt antag
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