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Добірка наукової літератури з теми "Osteocyte autophagy"
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Статті в журналах з теми "Osteocyte autophagy"
Toscani, Denise, Carla Palumbo, Benedetta Dalla Palma, Marina Bolzoni, Marzia Ferretti, Paola Sena, Daniela Guasco, Eugenia Martella, Franco Aversa, and Nicola Giuliani. "Myeloma-Induced Osteocyte Death Was Blunted By Proteasome Inhibitors Through The Modulation Of Autophagy." Blood 122, no. 21 (November 15, 2013): 3096. http://dx.doi.org/10.1182/blood.v122.21.3096.3096.
Повний текст джерелаYao, Wei, Weiwei Dai, Jean X. Jiang, and Nancy E. Lane. "Glucocorticoids and osteocyte autophagy." Bone 54, no. 2 (June 2013): 279–84. http://dx.doi.org/10.1016/j.bone.2013.01.034.
Повний текст джерелаMannino, Federica, and Post Doc. "ODP599 Modulation of Wnt/b-catenin and Autophagy in an in vitro Model of Glucocorticoid-induced Osteoporosis." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A186. http://dx.doi.org/10.1210/jendso/bvac150.384.
Повний текст джерелаChou, Hsin-Chiao, Sung-Yen Lin, Liang-Yin Chou, Mei-Ling Ho, Shu-Chun Chuang, Tsung-Lin Cheng, Lin Kang, et al. "Ablation of Discoidin Domain Receptor 1 Provokes an Osteopenic Phenotype by Regulating Osteoblast/Osteocyte Autophagy and Apoptosis." Biomedicines 10, no. 9 (September 2, 2022): 2173. http://dx.doi.org/10.3390/biomedicines10092173.
Повний текст джерелаLuo, D., H. Ren, T. Li, K. Lian, and D. Lin. "Rapamycin reduces severity of senile osteoporosis by activating osteocyte autophagy." Osteoporosis International 27, no. 3 (September 22, 2015): 1093–101. http://dx.doi.org/10.1007/s00198-015-3325-5.
Повний текст джерелаFlorencio-Silva, Rinaldo, Gisela R. S. Sasso, Estela Sasso-Cerri, Manuel J. Simões, and Paulo S. Cerri. "Effects of estrogen status in osteocyte autophagy and its relation to osteocyte viability in alveolar process of ovariectomized rats." Biomedicine & Pharmacotherapy 98 (February 2018): 406–15. http://dx.doi.org/10.1016/j.biopha.2017.12.089.
Повний текст джерелаZhu, Liang, Jifei Chen, Jing Zhang, Changan Guo, Wenshuai Fan, Yi-ming Wang, and Zuoqin Yan. "Parathyroid Hormone (PTH) Induces Autophagy to Protect Osteocyte Cell Survival from Dexamethasone Damage." Medical Science Monitor 23 (August 21, 2017): 4034–40. http://dx.doi.org/10.12659/msm.903432.
Повний текст джерелаChen, Ke, Yue-Hua Yang, Sheng-Dan Jiang, and Lei-Sheng Jiang. "Decreased activity of osteocyte autophagy with aging may contribute to the bone loss in senile population." Histochemistry and Cell Biology 142, no. 3 (February 20, 2014): 285–95. http://dx.doi.org/10.1007/s00418-014-1194-1.
Повний текст джерелаWang, Peige, Jie Ding, Guangyue Yang, Wen Sun, Hailing Guo та Yongfang Zhao. "Study on the Mechanism of Qigu Capsule in Upregulating NF-κB/HIF-1α Pathway to Improve the Quality of Bone Callus in Mice at Different Stages of Osteoporotic Fracture Healing". Evidence-Based Complementary and Alternative Medicine 2021 (13 вересня 2021): 1–10. http://dx.doi.org/10.1155/2021/9943692.
Повний текст джерелаYang, Yuehua, Xinfeng Zheng, Bo Li, Shengdan Jiang, and Leisheng Jiang. "Increased activity of osteocyte autophagy in ovariectomized rats and its correlation with oxidative stress status and bone loss." Biochemical and Biophysical Research Communications 451, no. 1 (August 2014): 86–92. http://dx.doi.org/10.1016/j.bbrc.2014.07.069.
Повний текст джерелаДисертації з теми "Osteocyte autophagy"
Xavier, Andy. "Analyse multi-échelle de l'effet de différentes modalités de course sur différents sites anatomiques osseux." Electronic Thesis or Diss., Orléans, 2024. http://www.theses.fr/2024ORLE1058.
Повний текст джерелаThe effects of running on bone tissue depend on the intensity, type, and frequency of the mechanical loads applied. While running can be beneficial under certain conditions, it may become detrimental to bone tissue at high intensity, and there is no clear consensus on the best modality to promote osteogenesis. This thesis compares the effects of three running modalities (high-intensity interval training, continuous running, and a combination of the two) on the morphological, microarchitectural, and cellular parameters of Wistar rat bones. The results show that all modalities lead to bone adaptation, with an increase in the diaphyseal diameter of the bones. However, interval training particularly promotes cortical bone growth at the expense of trabecular bone in the ulna.Furthermore, the comparison of the effects of continuous running and interval training on the tibia shows that interval training improves osteocyte maturation and reduces their apoptosis by activating autophagy pathways, thereby stimulating bone formation. Thus, interval training could be an effective non-drug therapy against bone degeneration and represents a relevant model for studying osteocyte mechanotransduction in future research
Hurault, Lucile. "Étude in vitro de la toxicité de l’uranium sur les cellules osseuses en vue de la recherche de nouveaux agents décorporants." Thesis, Côte d'Azur, 2018. http://www.theses.fr/2018AZUR4106/document.
Повний текст джерелаNatural or accidental uranium exposure is a health care concern. Uranium is a natural metal found in the environment and is both used for civil or military applications. It is also naturally present in food and water. It exhibits both a radiological and a chemical toxicity, the latter being considered largely predominant for natural uranium. Kidneys and bones are the main targeted organs of its toxicity. The skeleton is the storage organ of uranium and can be retained there for years, causing a long-term bone loss. Bone cells, osteoclasts cells in charge of bone resorption, osteoblasts involved in matrix production and mineralization, and osteocytes, considered the major orchestrators of bone remodeling, are therefore likely to exhibit impaired functions. Furthermore, current chelation therapy treatments failed to demonstrate a true decorporating efficiency after internal uranium contaminations.The first part of this study describes molecular and cellular effects of acute and chronic uranium exposure on a murine osteocytic cell line MLO-A5. Acute exposure enhanced their autophagic process and CI50 determination shows less toxicity on osteocytes than on osteoclasts and osteoblasts. Moreover, mineralization capacity of these cells was strongly inhibited after a chronic exposure without affecting cell viability. In a second part, we determined the in vitro effects of 3,4,3-LI(1,2-HOPO), a potential decorporating agent, on osteoclasts and osteoblasts with the intend to develop methods for decorporating agent screening. This molecule shows an ability to partly restore differentiation and resorption function of exposed osteoclasts to uranium. These results constitute a step forward in the development of screening methods to evaluate the potential of new decorporating agent.Taken together, these results enhanced our knowledge of uranium toxicity mechanisms on bone cells and brought new toxicological data regarding the use of 3,4,3-LI(1,2-HOPO) in our cellular models
Hurault, Lucile. "Étude in vitro de la toxicité de l’uranium sur les cellules osseuses en vue de la recherche de nouveaux agents décorporants." Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2018. http://www.theses.fr/2018AZUR4106.
Повний текст джерелаNatural or accidental uranium exposure is a health care concern. Uranium is a natural metal found in the environment and is both used for civil or military applications. It is also naturally present in food and water. It exhibits both a radiological and a chemical toxicity, the latter being considered largely predominant for natural uranium. Kidneys and bones are the main targeted organs of its toxicity. The skeleton is the storage organ of uranium and can be retained there for years, causing a long-term bone loss. Bone cells, osteoclasts cells in charge of bone resorption, osteoblasts involved in matrix production and mineralization, and osteocytes, considered the major orchestrators of bone remodeling, are therefore likely to exhibit impaired functions. Furthermore, current chelation therapy treatments failed to demonstrate a true decorporating efficiency after internal uranium contaminations.The first part of this study describes molecular and cellular effects of acute and chronic uranium exposure on a murine osteocytic cell line MLO-A5. Acute exposure enhanced their autophagic process and CI50 determination shows less toxicity on osteocytes than on osteoclasts and osteoblasts. Moreover, mineralization capacity of these cells was strongly inhibited after a chronic exposure without affecting cell viability. In a second part, we determined the in vitro effects of 3,4,3-LI(1,2-HOPO), a potential decorporating agent, on osteoclasts and osteoblasts with the intend to develop methods for decorporating agent screening. This molecule shows an ability to partly restore differentiation and resorption function of exposed osteoclasts to uranium. These results constitute a step forward in the development of screening methods to evaluate the potential of new decorporating agent.Taken together, these results enhanced our knowledge of uranium toxicity mechanisms on bone cells and brought new toxicological data regarding the use of 3,4,3-LI(1,2-HOPO) in our cellular models
Gunaratnam, Krishanthi. "Mechanisms of lipotoxicity in bone." Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/14334.
Повний текст джерела