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Harrison FE, May JM

FIGURE 3 In summary, this evidence suggests that the origin of excess ROS production is the result of (1) defective mitochondria (due to the abnormal and reduced distribution of cardiolipins) with high intermembrane electrical potential and (2) reduced mitophagy process (due to high expression and activity of P53 protein)

While this study primarily examined the fluctuations of GST in plasma, upcoming research could investigate its expression and activity in both the brain and neuronal cells to attain a deeper insight into the true function of GST within the nervous system

CMS posts the update on its ICD-10 codes page, and the guidelines live on the CDC's ICD-10-CM files page