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Several treatments emerged as potential therapeutic modalities with the ability to spare loss of cord tissue and promote recovery of locomotor function, and to alleviate the development of neuropathic pain

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Studies in the MRL/lpr lupus-prone mouse model have demonstrated that gut dysbiosis can induce intestinal oxidative stress, compromise the gut barrier (evidenced by reduced ZO-2 and elevated fecal albumin and IgA), promote bacterial translocation, and exacerbate systemic inflammation and autoimmune responses [37]