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The parallel comparison of radiographs taken in four time intervals (callus surface, microphotodensitometry of the bone defect) and quantitative histomorphometry revealed that bone marrow injected locally into the bone defect and TRIS-BPC157 applied intramuscularly (particularly in a daily dose of 10 g/kg b.w

Both oxidative damage to cells and reduced antioxidant capacity contribute to this disease

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These data suggest that high glucose levels promoted the proliferation of activated hPSCs through the TGF signalling pathway, and GSH has the potential to attenuate the activation phenotype of hPSCs