These findings suggest that central nervous inflammation may act as a direct potential driver of PEM symptom development, converting peripheral immune and metabolic dysfunction signals into neurofunctional impairments
doi: 10.1007/s10147-009-0935-y 27 KurmanRJShihI-M
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Western blot - Concentrated medium and pellet samples were thawed in ice, and pellet resuspensions were briefly sonicated (High intensity ultrasonic processor VC100100 W, Sonics & Materials Inc., Newtown, CT, USA)
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We propose that impaired mitochondrial biology can be repaired and recalibrated by activating mitohormesis, which is optimally achieved using strategies that facilitate a balanced oscillation between mitochondrial stressor and recovery phases