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Negative nitrogen balance and infection induce a breakdown of tissue protein and, hence, increase urinary excretion of riboflavin (Tucker et al., 1960)

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First, current biomarkers (such as serum GPX4) are derived from mouse controlled cortical impact (CCI) models, yet the pathological heterogeneity of human TBI far exceeds that of animal models, making these biomarkers inadequate for guiding clinical treatment

Low ChaC1 expression also promotes increased phosphorylation of NF-B p65, possibly contributing to the exacerbation of characteristic inflammation in the lungs of patients with cystic fibrosis following Pa infection (132)