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I'll use it well.

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These have been shown in models of muscle injury, tendon degeneration, and experimental colitis

[24] That observation is quietly profound for this articles theme: even in intact human physiology, local IGF-1 signaling can carry much of the growth load while circulating, protein-bound IGF-1 is dramatically reduced, which is exactly the local matters logic that made the MGF splice variant interesting in the first place

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