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In particular, mitochondrial dysfunction is a key finding in reactive oxygen species (ROS)-induced PD pathology [4,5,6,7]

The model was first fitted to the training concentrations (37.5 and 25 M doxorubicin), and then used to simulate the test concentrations (50, 12.5 and 10 M doxorubicin) as a means of blind validation, showing good accordance between the experimental and in silico outputs for all concentrations of doxorubicin

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MEFs lacking Bmal1 showed lower CI respiration, reduced SAM levels and decreased NDUFS2 methylation (Fig

doi: 10.3892/etm.2015.2908 138 ZhaiWMaZWangWSongLYiJ

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