Article: New congenital adrenal hyperplasia study findings recently were reported by researchers at University of Edinburgh.

"Patients with congenital adrenal hyperplasia arising from mutations of 11 beta-hydroxylase, the final enzyme in the glucocorticoid biosynthetic pathway, exhibit glucocorticoid deficiency, adrenal hyperplasia driven by unsuppressed hypothalamo-pituitary-adrenal activity, and excess mineralocorticoid activity caused by the accumulation of deoxycorticosterone. A mouse model, in which exons 3-7 of Cyp11b1 (the gene encoding 11 beta-hydroxylase) were replaced with cDNA encoding enhanced cyan fluorescent protein, was generated to investigate the underlying disease mechanisms," investigators in Scotland report (see also Congenital Adrenal Hyperplasia).

"Enhanced cyan ...

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