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The likely disruptions in the signaling pathways due to the mutations reported here may be considered potential causes of HFM. The lack of understanding of molecular pathologies of the solitary functioning kidney makes improving and strengthening the continuity of care between pediatric and adult nephrological patients difficult. Copy number variations (CNVs) account for a molecular cause of solitary functioning kidney, but characterization of the pathogenic genes remains challenging. In our prospective cohort study, 99 fetuses clinical
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