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Association Between Social Support and Bone Health Outcomes: a Systematic Review 社会支持与骨骼健康结果之间的关系:一项系统综述
IF 1.8 Q4 ENDOCRINOLOGY & METABOLISM Pub Date : 2018-08-17 DOI: 10.1007/s12018-018-9248-x
Y. Youm, Seungwon Lee, E. Baldina
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引用次数: 2
Vitamin D Status in the North African Population: a Review 北非人口维生素D状况综述
IF 1.8 Q4 ENDOCRINOLOGY & METABOLISM Pub Date : 2018-07-06 DOI: 10.1007/s12018-018-9247-y
A. El Maataoui, Z. Ouzzif
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引用次数: 1
Skeletal Effects of Thyroid Hormones 甲状腺激素对骨骼的影响
IF 1.8 Q4 ENDOCRINOLOGY & METABOLISM Pub Date : 2018-04-24 DOI: 10.1007/s12018-018-9246-z
Bence Bakos, I. Takács, P. Stern, P. Lakatos
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引用次数: 1
Testosterone and Male Osteoporosis 睾酮与男性骨质疏松症
IF 1.8 Q4 ENDOCRINOLOGY & METABOLISM Pub Date : 2018-04-12 DOI: 10.1007/s12018-018-9245-0
Dong-Eun Shin, T. Ahn, Jee-Woong Kim, Chi-Hoon Oh, SeongJu Choi
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引用次数: 1
GLUCOCORTICOID EXCESS IN BONE AND MUSCLE. 骨骼和肌肉中的糖皮质激素过量。
IF 1.8 Q4 ENDOCRINOLOGY & METABOLISM Pub Date : 2018-03-01 Epub Date: 2018-02-05 DOI: 10.1007/s12018-018-9242-3
Amy Y Sato, Munro Peacock, Teresita Bellido

Glucocorticoids (GC), produced and released by the adrenal glands, regulate numerous physiological processes in a wide range of tissues. Because of their profound immunosuppressive and anti-inflammatory actions, GC are extensively used for the treatment of immune and inflammatory conditions, the management of organ transplantation, and as a component of chemotherapy regimens for cancers. However, both pathologic endogenous elevation and long-term use of exogenous GC are associated with severe adverse effects. In particular, excess GC has devastating effects on the musculoskeletal system. GC increase bone resorption and decrease formation leading to bone loss, microarchitectural deterioration and fracture. GC also induce loss of muscle mass and strength leading to an increased incidence of falls. The combined effects on bone and muscle account for the increased fracture risk with GC. This review summarizes the advance in knowledge in the last two decades about the mechanisms of action of GC in bone and muscle and the attempts to interfere with the damaging actions of GC in these tissues with the goal of developing more effective therapeutic strategies.

糖皮质激素(GC)由肾上腺产生和释放,在广泛的组织中调节许多生理过程。由于其深刻的免疫抑制和抗炎作用,GC被广泛用于免疫和炎症的治疗,器官移植的管理,以及作为癌症化疗方案的组成部分。然而,病理性内源性升高和长期使用外源性GC都与严重的不良反应相关。特别是,过量的GC对肌肉骨骼系统有毁灭性的影响。GC增加骨吸收,减少骨形成,导致骨丢失、微结构恶化和骨折。GC还会引起肌肉质量和力量的损失,导致跌倒的发生率增加。对骨骼和肌肉的综合影响是GC增加骨折风险的原因。本文综述了近二十年来关于GC在骨和肌肉中的作用机制以及干扰GC在这些组织中的破坏作用的研究进展,以期开发出更有效的治疗策略。
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引用次数: 32
Stress and Insufficiency Fractures 应力和不全骨折
IF 1.8 Q4 ENDOCRINOLOGY & METABOLISM Pub Date : 2018-03-01 DOI: 10.1007/s12018-017-9239-3
J. Shaker
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引用次数: 1
2018—Changing Times for CRBM 2018年——CRBM的变革时代
IF 1.8 Q4 ENDOCRINOLOGY & METABOLISM Pub Date : 2018-02-07 DOI: 10.1007/s12018-018-9244-1
M. Allen
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引用次数: 1
Effects of Bazedoxifene on Bone Mineral Density and Fracture in Post-Menopausal Osteoporotic Women: a Systematic Review and Meta-Analysis 巴多昔芬对绝经后骨质疏松妇女骨密度和骨折的影响:系统评价和荟萃分析
IF 1.8 Q4 ENDOCRINOLOGY & METABOLISM Pub Date : 2018-02-05 DOI: 10.1007/s12018-018-9241-4
Malahat Khalili, A. Hosseinzadeh, Habibollah Mohammadi Kiavandani, N. Khanjani
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引用次数: 2
Myokine—Irisin—and Its Effects Linking Bone and Muscle Function 肌因子-鸢尾素及其连接骨骼和肌肉功能的作用
IF 1.8 Q4 ENDOCRINOLOGY & METABOLISM Pub Date : 2018-02-02 DOI: 10.1007/s12018-017-9240-x
G. Colaianni, G. Brunetti, S. Colucci, M. Grano
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引用次数: 3
Bone Fracture Acute Phase Response-A Unifying Theory of Fracture Repair: Clinical and Scientific Implications. 骨折急性期反应-骨折修复的统一理论:临床和科学意义。
IF 1.8 Q4 ENDOCRINOLOGY & METABOLISM Pub Date : 2018-01-01 Epub Date: 2018-12-29 DOI: 10.1007/s12018-018-9256-x
Courtney E Baker, Stephanie N Moore-Lotridge, Alexander A Hysong, Samuel L Posey, J Patton Robinette, Deke M Blum, Michael A Benvenuti, Heather A Cole, Satoru Egawa, Atsushi Okawa, Masanori Saito, Jason R McCarthy, Jeffry S Nyman, Masato Yuasa, Jonathan G Schoenecker

Bone fractures create five problems that must be resolved: bleeding, risk of infection, hypoxia, disproportionate strain, and inability to bear weight. There have been enormous advancements in our understanding of the molecular mechanisms that resolve these problems after fractures, and in best clinical practices of repairing fractures. We put forth a modern, comprehensive model of fracture repair that synthesizes the literature on the biology and biomechanics of fracture repair to address the primary problems of fractures. This updated model is a framework for both fracture management and future studies aimed at understanding and treating this complex process. This model is based upon the fracture acute phase response (APR), which encompasses the molecular mechanisms that respond to injury. The APR is divided into sequential stages of "survival" and "repair." Early in convalescence, during "survival," bleeding and infection are resolved by collaborative efforts of the hemostatic and inflammatory pathways. Later, in "repair," avascular and biomechanically insufficient bone is replaced by a variable combination of intramembranous and endochondral ossification. Progression to repair cannot occur until survival has been ensured. A disproportionate APR-either insufficient or exuberant-leads to complications of survival (hemorrhage, thrombosis, systemic inflammatory response syndrome, infection, death) and/or repair (delayed- or non-union). The type of ossification utilized for fracture repair is dependent on the relative amounts of strain and vascularity in the fracture microenvironment, but any failure along this process can disrupt or delay fracture healing and result in a similar non-union. Therefore, incomplete understanding of the principles herein can result in mismanagement of fracture care or application of hardware that interferes with fracture repair. This unifying model of fracture repair not only informs clinicians how their interventions fit within the framework of normal biological healing but also instructs investigators about the critical variables and outputs to assess during a study of fracture repair.

骨折产生了五个必须解决的问题:出血、感染风险、缺氧、不成比例的劳损和无法承重。我们对解决骨折后这些问题的分子机制的理解有了巨大的进步,在骨折修复的最佳临床实践中也有了巨大的进步。我们提出了一个现代的、综合性的骨折修复模型,该模型综合了骨折修复的生物学和生物力学方面的文献,以解决骨折的主要问题。这个更新的模型是骨折管理和未来研究的框架,旨在理解和治疗这一复杂过程。该模型基于骨折急性期反应(APR),它包含了对损伤作出反应的分子机制。APR分为连续的“生存”和“修复”阶段。在恢复期早期,在“生存期”,出血和感染是通过止血和炎症途径的共同努力来解决的。随后,在“修复”中,无血管和生物力学不足的骨被膜内和软骨内成骨的可变组合所取代。在确保存活之前,无法进行修复。不成比例的apr,无论是不足还是旺盛,都会导致生存并发症(出血、血栓形成、全身炎症反应综合征、感染、死亡)和/或修复(延迟或不愈合)。用于骨折修复的骨化类型取决于骨折微环境中应变和血管的相对量,但这一过程中的任何失败都可能破坏或延迟骨折愈合,并导致类似的不愈合。因此,对上述原则的不完全理解可能导致骨折护理管理不当或干扰骨折修复的硬件应用。这种统一的骨折修复模型不仅告诉临床医生他们的干预措施如何适应正常生物愈合的框架,而且还指导研究人员在骨折修复研究中评估关键变量和输出。
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引用次数: 53
期刊
Clinical Reviews in Bone and Mineral Metabolism
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