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Figure 3 below summarizes these processes, highlighting the interplay between bacterial infection, immune mediators (e.g., TNF-, IL-6, transforming growth factor-beta [TGF-], IL-10), and cellular actors (e.g., neutrophils, M1/M2 macrophages, fibroblasts, keratinocytes, endothelial cells) during wound healing [43, 48]
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Johns Hopkins declined to confirm the number, calling it a personnel issue
In musculoskeletal models, BPC-157 has consistently outperformed controls in healing timeframes for tendon transection, muscle crush injury, and bone defect models