| EPR | early progressive resistance; electron paramagnetic resonance; electronic patient record; electrophr... |
|---|---|
| IPR | insulin production rate; intraparenchymal resistance; ipratropium |
| RPPR | red cell precursor production rate |
| ACR | abnormally contracting region; absolute catabolic rate; acriflavine; adenomatosis of colon and rectu... |
| CR | calculation rate; calculus removed; calorie-restricted; cardiac rehabilitation; cardiac resuscitatio... |
| steroid diabetes | Diabetes mellitus produced by pharmacological doses of steroid hormones, particularly glucocorticoids or oestrogens; characterised by one or more of the typical manifestations of diabetes mellitus. (05 Mar 2000) |
|---|---|
| steroid fever | Fever presumably caused by elevated plasma concentrations of certain pyrogenic steroids; can be produced by administration of etiocholanolone. (05 Mar 2000) |
| steroid finger motif | Family of nuclear transcription factors, most of which are receptors for hormones of the steroid family, for example androgen, oestrogen, glucocorticoid, mineralocorticoid, progesterone, retinoic acid, ecdysone, thyroid hormone and the Drosophila transcription factors knirps, ultraspiracle and seven up. This family contains a conserved domain (the steroid finger motif) containing two C4 type zinc fingers. (18 Nov 1997) |
| steroid hormone | <endocrinology> A group of structurally related hormones, based on the cholesterol molecule. They control sex and growth characteristics, are highly lipophilic and are unique in that their receptors are in the nucleus, rather than on the plasma membrane. Examples: testosterone, oestrogen. (18 Nov 1997) |
| steroid hormones | Those hormone's possessing the steroid ring system; e.g., androgens, oestrogens, adrenocortical hormone's. (05 Mar 2000) |
| steroid hydroxylases | <enzyme> Registry number: EC 1.14.- (12 Dec 1998) |
| steroid isomerases | <enzyme> Enzymes that catalyze the transposition of double bond(s) in a steroid molecule. Registry number: EC 5.3.3.- (12 Dec 1998) |
| steroid monooxygenases | Enzymes catalyzing addition of hydroxyl groups to the steroid rings utilizing O2; differentiated into, for example, steroid 11b-monooxygenase, steroid 17a-monooxygenase, and steroid 21-monooxygenase, in accordance with the position of the catalytically introduced hydroxyl group. Synonym: steroid hydroxylases. (05 Mar 2000) |
| steroid N-acetylglucosaminyltransferase | <enzyme> Substrate steroids may be replaced by specific cpds Registry number: EC 2.4.1.- (26 Jun 1999) |
| steroid nucleus | tetracyclic steroid nucleus |
| steroid receptor | Family of nuclear transcription factors, most of which are receptors for hormones of the steroid family, for example androgen, oestrogen, glucocorticoid, mineralocorticoid, progesterone, retinoic acid, ecdysone, thyroid hormone and the Drosophila transcription factors knirps, ultraspiracle and seven up. This family contains a conserved domain (the steroid finger motif) containing two C4 type zinc fingers. (18 Nov 1997) |
| steroid sulfatase deficiency | A form of ichthyosis, due to 3-beta-hydroxysteroidsulfate sulfatase deficiency, that appears at birth or in early infancy and affects males; characterised by scaling predominantly on the neck and trunk but not on the palms and soles; histologically, there is hyperkeratosis, a granular layer in the epidermis, and normal epidermal cell turnover. Synonym: steroid sulfatase deficiency. (05 Mar 2000) |
| steroid sulfotransferase | <enzyme> Catalyses the reaction of 3'-phosphoadenylyl sulfate and a phenolic steroid to form adenosine 3',5'-bisphosphate and steroid o-sulfate; has broad specificity Registry number: EC 2.8.2.15 Synonym: phenolic steroid sulfotransferase (26 Jun 1999) |
| steroid ulcer | An ulcer, usually on the leg or foot, developing from a wound in patients undergoing long-term steroid therapy; results from the wound-healing inhibitory effects characteristic of steroids. (05 Mar 2000) |
| steroid withdrawal syndrome | <syndrome> A condition exhibited by persons who previously had been receiving large therapeutic doses of glucocorticoid hormones for long periods of time; pituitary-adrenocortical insufficiency is manifested, particularly during stress, for as long as a year or more thereafter and varying degrees of emotional disturbance may be exhibited. (05 Mar 2000) |