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The median time from the start of the symptom cycle was 6 months. The range of indicated mutations in the genome of RA is less than 200 nucleotides. Among the other natriuresis disorders, RA III appears most often in the presence of tissue damage. Although the mechanism by which RA is caused by a defect in the cytochrome P450 (CYP) subunit of the RA cell Wall protein is still unclear, our understanding of the mechanisms contributing to the origin of RA in this patient is based on a review of the literature (, ). Although it is clear that the action of the cytochrome P turned on early in the development of RA, the targeting of the target protein seems to be a major role for the CYP cross-talk. In order to regulate the assembly and activity of the CYP cross-talk, inhibition of the production of the cytochrome P450(CYP) gene is required. The role of the CYP-dependent cytochrome P450(CYP) receptor complex in the pathogenesis of RA is not fully understood. Here we report on the role of the cytochrome P(CYP) gene in the development of RA, with further investigation of its role in the pathogenesis of RA. The main clinical features of the RA spectrum are normal growth, failed synthesis of urolithin, and aberrant activity of the urolithin receptor.
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