| 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 production rate | The total quantity of a given steroid formed in the body, usually expressed as milligrams per day; represents the sum of the glandular secretion of the steroid and extraglandular formation of it from various steroid precursors. (05 Mar 2000) |
| steroid secretory rate | The rate of glandular secretion of a given steroid, usually expressed as milligrams per day; does not include any amount of the steroid that might be formed extraglandularly. (05 Mar 2000) |
| 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) |
| 17-ketogenic steroid assay test | A colourimetric test, based on the Zimmermann reaction, which indicates metabolites or adrenal and testicular steroids excreted as 17-ketones in the urine; increased values are most striking in adrenocortical tumours, decreased values in Addison's disease or in panhypopituitarism. Synonym: ketogenic corticoids test. (05 Mar 2000) |
| 3 beta-hydroxy-delta 5-C(27)-steroid dehydrogenase | <enzyme> Second enzyme in the sequence that converts cholesterol to bile acids; deficiency leads to chronic liver disease in childhood Registry number: EC 1.1.1.- Synonym: 7 alpha-hydroxycholesterol 3 beta-dehydrogenase, 7-hydroxycholesterol 3-dehydrogenase, 3 beta-hydroxy-delta(5)-c(27)-steroid oxidoreductase, 5-cholestene-3beta,7alpha-diol oxidase (26 Jun 1999) |
| 3-oxo-5 beta-steroid delta 4-dehydrogenase | <enzyme> Do not confuse with EC 1.3.1.23 (cholestenone 5 beta-reductase) which is also steroid 5 beta-reductase in chemline; do not use for enzyme using NADP-see EC 1.3.1.23 and EC 1.3.1.3 Chemical name: 3-oxo-5 beta-steroid delta(4)dehydrogenase Registry number: EC 1.3.99.6 Synonym: steroid 5 beta-reductase, testosterone 5 beta-reductase, 4-ene-5 beta-reductase, delta(4)-3-ketosteroid-5 beta-(acceptor)-reductase, testosterone 5beta-reductase, delta(4)-5beta-reductase, cytosolic 4-ene-reductase (26 Jun 1999) |
| acetylcholine receptor antibodies | <neurology, investigation> A test used to measure the amount of antibodies to acetylcholine receptors on nerve endings. This is a diagnostic test for myasthenia gravis. A normal value is no antibodies in the bloodstream. Acetylcholine receptor (AChR) binding autoantibodies (i.e. Antibodies reactive with several epitopes other than the binding site for acetylcholine or alpha-bungarotoxin) are present in approximately 88% of patients with generalised myasthenia gravis, 70% of ocular myasthenia and in approximately 80% of myasthenia gravis in remission. Although serum concentrations of AChR binding autoantibodies do not in general correlate well with severity of weakness, there is typical decrease in concentration as weakness improves with immunosuppressive therapy. AChR blocking autoantibodies (i.e., antibodies reactive with the AChR binding site) are present in about 50% of patients with myasthenia gravis, 30% with ocular myasthenia gravis and 20% of myasthenia gravis in remission, AChR blocking autoantibodies are the only AChR autoantibodies present in about 1% of myasthenia gravis. AChR modulating autoantibodies (i.e., autoantibodies which cross-link AChRs and cause their removal from muscle membrane surfaces) are present in more than 90% of myasthenia gravis and occasionally are the only AchR autoantibodies detectable in mild, recent onset or ocular-restricted myasthenia gravis. Results for AChR modulating autoantibodies can be transiently false-positive due to curare-like drugs used during general anesthesia. AChR autoantibodies of one or more types are found in at least 80% of ocular myasthenia gravis. Although generally absent in neurological conditions other than myasthenia gravis(and consequently unlikely to cause confusion in neurodiagnosis), false-positive results for AChR autoantibodies occasionally occur in primary biliary cirrhosis, tardive dyskinesia, autoimmune thyroiditis, the elderly, amyotrophic lateral sclerosis patients treated with cobra venom and patients with thymoma in the absence of myasthenia gravis. Approximately 1% of patients with rheumatoid arthritis treated with D-penicillamine develop AChR autoantibodies and myasthenia gravis, both of which disappear when the drug is discontinued. Babies born to ~10% of myasthenia gravis mothers have a transient neonatal form of myasthenia gravis that responds well to anticholinesterase therapy and usually remits within 1 month as maternal IgG disappears. (29 Dec 1997) |
| amino acid receptor | <biochemistry> Ligand gated ion channels with specific receptors for amino acid transmitters. An extended protein superfamily that also includes subunits of the nicotinic acetylcholine receptor. (18 Nov 1997) |
| AMPA receptor | <cell biology> Glutamate operated ion channel. See: excitatory amino acid receptor channels. (05 Feb 1998) |