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Further animal studies are needed in SCI models to determine if the overexpression of ubiquitin or Uch-L1 can lead to resistance to neural injury or promote neuroregeneration or neuroplasticity with benefits to functional recovery

Crit Rev Toxicol 1999;29(3):283-330

Importantly, deletion of NOX2 and NOX1 significantly delays disease progression and prolongs survival in SOD1 G93A mice (Bruijn et al., 2005

For a patient with severe dysautonomia or a broken cellular energy metabolism, the physical act of digesting a heavy meal can actually trigger a symptom crash or post-exertional malaise (PEM)

Protein concentrations were determined using bovine serum albumin (BSA) as the standard

& Staruschenko, A