Jean D. Wilson

TL;DR: It has been shown that in the presence of a NADPH2-generating system prostatic nuclei convert testosterone to dihydrotestosterone, whereas prostatic cytoplasm reduces dihydotestosterone to androstandiol.

TL;DR: In the 20 years since it was established that impairment of dihydrotestosterone formation is the cause of a rare form of human intersex, a wealth of information has accumulated about the genetics, endocrinology, and variable phenotypic manifestations, culminating in the cloning of cDNAs encoding two 5 alpha-reductase genes.

TL;DR: Four substitution and two splice junction mutations were identified in the 17βHSD3 genes of five unrelated male pseudohermaphrodites that severely compromised the activity of the 17 β–HSD type 3 isozyme.

TL;DR: It was concluded that testosterone is the principal androgen formed by the fetal testis at the time of male sexual differentiation.

TL;DR: The demonstration of markedly deficient dihydrotestosterone formation in slices of perineal skin, epididymis and phallus, is compatible with the fact that dihydotestosterone is the fetal hormone responsible for male differentiation of the external genitalia, iscompatible with the idea that androgen resistance in this syndrome is different from that in other androgen-resistant states.