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The defensin-related pseudogenes show premature stop codons, have start-codon mutations or miss different conserved amino acids

However, the invasive method and high mortality rate are two drawbacks of this model

[3] and our observations [10, 11] may soon guide the development of novel and relevant clinical studies that aim to increase the knowledge of G6PD deficiency and explore the clinical relevance of the relationship of G6PD-deficient variants with the pathophysiology of CVD

Jian-pi-yi-shen formula ameliorates oxidative stress, inflammation, and apoptosis by activating the Nrf2 signaling in 5/6 nephrectomized rats