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Mechanisms underlying bone loss associated with gut inflammation
Patients with gastrointestinal diseases frequently suffer from skeletal abnormality, characterized by reduced bone mineral density, increased fracture risk, and/or joint inflammation. This pathological process is characterized by altered immune cell activity and elevated inflammatory cytokines in the bone marrow microenvironment due to disrupted gut immune response. Gastrointestinal disease is recognized as an immune malfunction driven by multiple factors, including cytokines and signaling molecules. However, the mechanism by which intestinal inflammation magnified by gut-residing actors stimulates bone loss remains to be elucidated. In this article, we discuss the main risk factors potentially contributing to intestinal disease-associated bone loss, and summarize current animal models, illustrating gut-bone axis to bridge the gap between intestinal inflammation and skeletal disease
Response to "in regard to "Tran A, Zhang J, Woods K, Yu V, Nguyen D, Gustafson G, Rosen L, Sheng K. Treatment planning comparison of IMPT, VMAT and 4Ï€ radiotherapy for prostate cases"".
In regard to our recently published paper entitled "Treatment planning comparison of IMPT, VMAT and 4Ï€ radiotherapy for prostate cases", a question was raised whether "4Ï€" was used appropriately to describe the non-coplanar planning and delivery space. In this letter, the term use is explained from both theoretical and practical perspectives. It is concluded that the self-explanatory term provides a flexible description of non-coplanar radiotherapy with beam orientation optimization. Confusions with this term can be avoided by understanding the evolving and machine/patient specific nature of 4Ï€ planning
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