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Metabolic profiling of a myalgic encephalomyelitis/chronic fatigue syndrome discovery cohort reveals disturbances in fatty acid and lipid metabolism

Ultimately, it seems as though injury to the NMJ is a culmination of mutant protein aggregation at the presynaptic nerve terminal, presynaptic cholinergic dysfunction, impaired axonal transport, reduced synaptic acetylcholinesterase, and diseased muscle itself, among others [292]

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Data shown in Figure 2b evidenced that in hypertensive/MTC-treated retinas, a dramatic expression of caspase 3 occurs (lane 3)