|1.||Jiang, Guoli: 1 article (11/2015)|
|2.||Yun, Young Won: 1 article (11/2015)|
|3.||Oladele, Oso Abimbola: 1 article (11/2015)|
|4.||Lee, Beom Jun: 1 article (11/2015)|
|5.||Fan, Juexin: 1 article (11/2015)|
|6.||Wang, Shengping: 1 article (11/2015)|
|7.||Baek, In-Jeoung: 1 article (11/2015)|
|8.||Ding, Hao: 1 article (11/2015)|
|9.||Xiao, Dingfu: 1 article (11/2015)|
|10.||Yon, Jung-Min: 1 article (11/2015)|
|1.||Body Weight (Weight, Body)
05/01/1992 - "Treatment with DHT caused a dose-dependent inhibition of testicular 3 beta-hydroxysteroid dehydrogenase/delta 5-4 isomerase (3 beta-HSD) 2 h later, and this effect was apparent at the dose of 20 micrograms/100 g body weight (P less than 0.01). "
07/01/1984 - "However, no significant difference in body weight and in the weights of adrenals, uteri and ovaries and in the adrenal delta 5 3 beta-hydroxysteroid dehydrogenase (HSD) activity was found between unisexually grouped females and individually housed females. "
12/01/1999 - "Significant reduction of testicular and accessory sex organs (seminal vesicle, ventral prostate) weight, along with inhibition of testicular delta 5-3 beta-hydroxysteroid dehydrogenase (delta 5-3 beta-HSD) and 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) activity and reduction in plasma testosterone level, were observed at the doses of 2000 and 3000 micrograms/kg body weight/day. "
08/01/2002 - "Cyclophosphamide treatment at the dose of 5 mg/kg body weight/day for 28 days resulted a significant diminution in the activities of testicular delta 5, 3 beta-hydroxysteroid dehydrogenase (delta 5, 3 beta-HSD), 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) activities, plasma level of testosterone along with significant reduction in the number of germ cells at stage-VII of spermatogenesis. "
04/01/1989 - "3 beta-hydroxysteroid dehydrogenase (EC 18.104.22.168, 3 beta-HSD) and 17 beta-hydroxysteroid dehydrogenase (EC 22.214.171.124, 17 beta-HSD); cytosolic conjugation enzyme, glutathione-S-transferase (EC 126.96.36.199); and testicular as well as serum testosterone levels at the dose levels of 2.5, 5.0, 7.5 and 10 mg/kg body weight fed orally for 7 and 15 days. "
|2.||Congenital Adrenal Hyperplasia (Hyperplasia, Congenital Adrenal)
03/01/2001 - "Congenital adrenal hyperplasia owing to 3 beta-hydroxysteroid dehydrogenase deficiency."
11/01/1996 - "Classic 3 beta-hydroxysteroid dehydrogenase (3 beta HSD) deficiency congenital adrenal hyperplasia (CAH) results from a mutation in the type II 3 beta HSD gene encoding adrenal and gonadal 3 beta HSD. "
04/01/1996 - "Congenital adrenal hyperplasia due to 3 beta-hydroxysteroid dehydrogenase deficiency."
06/01/1995 - "To date the molecular basis and hormonal criteria for inherited mild late-onset 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) deficiency congenital adrenal hyperplasia (CAH) have not been defined. "
04/01/1995 - "A novel missense mutation in the type II 3 beta-hydroxysteroid dehydrogenase gene in a family with classical salt-wasting congenital adrenal hyperplasia due to 3 beta-hydroxysteroid dehydrogenase deficiency."
08/01/1990 - "Cushing syndrome, congenital adrenal hyperplasia due to 3 beta-hydroxysteroid dehydrogenase deficiency, an androgen producing adrenal tumour, and elevated plasma DHEAS due to an increased renal threshold were excluded. "
01/01/1985 - "[Effect of a 3 beta-hydroxysteroid dehydrogenase inhibitor (trilostane) on Cushing's syndrome]."
06/01/1983 - "These results suggest that trilostane does not effectively block the enzyme 3 beta-hydroxysteroid dehydrogenase delta 4,delta 5 isomerase in patients with Cushing's syndrome and that it should no longer be recommended for their treatment."
07/01/1982 - "Trilostane, a competitive inhibitor of the 3 beta-hydroxysteroid dehydrogenase enzyme system, has adrenal blocking activity and has been used to treat Cushing's syndrome and other disease. "
11/01/1978 - "It is concluded that trilostane is an effective inhibitor of 3 beta-hydroxysteroid dehydrogenase enzyme system in human adrenal gland; it inhibits biosynthesis of cortisol and it is useful in the treatment of Cushing's syndrome."
05/31/1996 - "The tumors were confined to Leydig cells using immunohistochemistry with anti-Tag antibody, specific binding of biotinylated hCG and histochemistry for 3 beta-hydroxysteroid dehydrogenase. "
11/01/1992 - "The activity of 3-beta-hydroxysteroid dehydrogenase suggested that the tumor cells were capable of androgen synthesis. "
11/15/1989 - "The tumor is hormonally active as demonstrated by proliferation of and secretions from the mammary glands in tumor-bearing animals and by the presence of delta 5-3 beta-hydroxysteroid dehydrogenase in the giant cells of the neoplasms. "
07/23/1965 - "[Deficiency of 3-beta-hydroxysteroid dehydrogenase in endocrine-active tumor of the ovary]."
02/01/1982 - "However, the 3 beta-hydroxysteroid dehydrogenase / delta 5, 4 isomerase activity was not modified by ovariectomy in the high mammary tumor strain whereas it was increased in the low mammary tumor strains. "
|5.||Adrenocortical Adenoma (Disease, Conn's)
07/01/1983 - "Enzyme histo-cytochemical staining was performed for 3 beta-hydroxysteroid dehydrogenase, alkaline phosphatase and acid phosphatase in the compact and clear cells of the adrenocortical adenomas associated with Cushing's syndrome (Cushing's adenomas). "
10/01/1992 - "Immunohistochemical analysis of steroidogenic enzymes (P-450 side-chain cleavage, 3 beta-hydroxysteroid dehydrogenase, P-450 C21-hydroxylase, P-450 17 alpha-hydroxylase and P-450 11 beta-hydroxylase) was performed on fifteen cases of small adrenocortical adenomas, which were detected incidentally in hormonally asymptomatic patients (non-functioning adrenocortical tumor), in order to study steroidogenesis in these tumors. "
05/01/1983 - "Enzyme histocytochemical staining including alkaline phosphatase, acid phosphatase, 3 beta hydroxysteroid dehydrogenase and 11 beta hydroxysteroid dehydrogenase was studied in human adrenocortical adenomas associated with primary aldosteronism. "
01/01/1994 - "To clarify the mechanism of diminished secretion of adrenal androgens in patients with adrenocortical adenoma and Cushing's syndrome and of excess secretion in patients with adrenocortical carcinoma, we investigated the enzymatic activities of cytochrome P45017 alpha, 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD), and Red as well as the content of b5 in five adenomas, three carcinomas, and two normal adrenal glands. "
|9.||Follicle Stimulating Hormone (Follitropin)
|1.||Continuous Ambulatory Peritoneal Dialysis (CAPD)