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They demonstrated that pretreatment of cultured SOD1 G93A astrocytes with MitoQ was able to reduce the formation of superoxide and peroxynitrite radicals, protect motor neurons against oxidative damage and improve the ability of mitochondria to generate ATP (Cassina et al., G93A mouse model, treatment with MitoQ at the onset of disease also delayed the decline of mitochondrial function in the spinal cord, protected against motor neuron loss and astrogliosis in the spinal cord

Studien zeigen eine verbesserte Myogenese und funktionelle Erholung in Skelettmuskelverletzungsmodellen

Circulating human corticotropin-releasing factor-binding protein levels following cortisol infusions

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