Yumie Rhee
연세대학교 의과대학 내과학교실 · 의학
Yumie Rhee 교수의 연구실은 뼈의 구조적 및 기능적 조절 메커니즘을 규명하는 데 초점을 맞추고 있으며, 특히 파arathyroid 호르몬(PTH)이 골수막과 내피막에서의 뼈 형성과 재흡수에 미치는 영향을 유전자 조작 및 분자 생물학적 기법을 통해 연구하고 있습니다. 뼈의 기능적 기하학과 골수막/내피막 반응의 분자 기전, 그리고 PTH 수용체 신호 전달 경로의 조절 메커니즘을 중심으로 한 기초 골 대사 연구를 수행하고 있습니다. 또한, 임상적 응용을 고려한 뼈질환 진단 기술(예: 온코제닉 골연화증 진단)과 체성 구성 분석을 위한 딥러닝 기반 영상 분석 기술 개발도 함께 진행하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
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
