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| ¿µ¹® | receptor | ÇÑ±Û | ¼ö¿ëü |
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| ¼³¸í | ¼¼Æ÷Áú³» ¶Ç´Â ¼¼Æ÷Ç¥¸é¿¡ Á¸ÀçÇÏ´Â ºÐÀÚ±¸Á¶·Î¼ ƯÀ̹°Áú°ú ¼±ÅÃÀûÀ¸·Î °áÇÕÇÏ¸ç °áÇÕ¿¡ ÀÇÇØ ƯÀÌÇÑ »ý¸®Àû ÀÛ¿ëÀ» ³ªÅ¸³½´Ù. ÆéƼµåÈ£¸£¸ó, ½Å°æÀü´Þ¹°Áú, Ç׿ø, º¸Ã¼, ¸é¿ª±Û·ÎºÒ¸°¿¡ ´ëÇÑ ¼¼Æ÷Ç¥¸é ¼ö¿ëü¿Í ½ºÅ×·ÎÀ̵忡 ´ëÇÑ ¼¼Æ÷Áú³» ¼ö¿ëü°¡ ÀÖ´Ù. |
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| DR | degeneration reaction; delivery room; deoxyribose; diabetic retinopathy; diagnostic radiology; digit... |
|---|---|
| ER | efficiency ratio; epigastric region; ejection rate; electroresection; emergency room; endoplasmic re... |
| RAR | rapidly adapting receptor; rat insulin receptor; retinoic acid receptor; right arm reclining; right ... |
| DBH | Dopamine-Beta(¥â)-Hydroxylase |
| DA | dark adaptation; dark agouti [rat]; daunomycin; degenerative arthritis; delayed action; Dental Assis... |
| D1R | D1 dopamine receptor |
|---|---|
| DRD2 | dopamine receptor |
| DRD4 | dopamine receptor D(4 |
| DA | 14C-dopamine |
| DA | 3)H]-dopamine |
striate body neurosis
| receptors, dopamine | Cell-surface proteins that bind dopamine with high affinity and trigger intracellular changes influencing the behaviour of cells. (12 Dec 1998) |
|---|---|
| receptors, dopamine d1 | A class of dopamine receptors identified by their binding profiles for synthetic ligands, their molecular biology, and, perhaps, by their mode of action. (12 Dec 1998) |
| receptors, dopamine d2 | A class of dopamine receptors identified by their binding profiles for synthetic ligands, their molecular biology, and, perhaps, their mode of action. (12 Dec 1998) |
| dopamine | <drug> A catecholamine neurotransmitter and hormone (153 D), formed by decarboxylation of dehydroxyphenylalanine (dopa). A precursor of adrenaline and noradrenaline. Pharmacologic action: 1. Precursor of norepinephrine 2. Stimulates dopaminergic, alpha and beta-1 adrenergic receptors: 3. Dopaminergic (1-2 mcg/kg per min): cerebral, renal, and mesenteric vasodilation increase urine output 4. Mixed alpha and beta-1 (2-10 mcg/kg per min): increases cardiac ouput with moderate increase systemic vascular resistance 5. Predominantly alpha (>20 mcg/kg per min): increases systemic vascular resistance Uses: 1. Treat hypotension associated with bradycardia 2. Stimulate cardiac output and urine output Dose: 1. Start infusion at 1-5 mcg/kg per min and titrate to effect. 2. Use the lowest dose that provides the desired hemodynamic improvement. 3. Do not exceed 20 mcg/kg per min. Potential complications: 1. May increase pulmonary pressure and worsen pulmonary congestion. 2. May increase myocardial work without improving coronary blood flow, exacerbating myocardial ischemia 3. Stimulates heart rate and may cause supraventricular or ventricular arrhythmias (15 Mar 2000) |
| dopamine agents | Any drugs that are used for their effects on dopamine receptors, on the life cycle of dopamine, or on the survival of dopaminergic neurons. (12 Dec 1998) |
| dopamine agonists | Drugs that bind to and activate dopamine receptors. (12 Dec 1998) |
| dopamine antagonists | Drugs that bind to but do not activate dopamine receptors, thereby blocking the actions of dopamine or exogenous agonists. Many drugs used in the treatment of psychotic disorders (antipsychotic agents) are dopamine antagonists, although their therapeutic effects may be due to long-term adjustments of the brain rather than to the acute effects of blocking dopamine receptors. Dopamine antagonists have been used for several other clinical purposes including as antiemetics, in the treatment of tourette syndrome, and for hiccup. (12 Dec 1998) |
| dopamine beta-hydroxylase | <enzyme> Chemical name: 3,4-Dihydroxyphenethylamine, ascorbate:oxygen oxidoreductase (beta-hydroxylating) Registry number: EC 1.14.17.1 (12 Dec 1998) |
| dopamine beta-monooxygenase | A copper-containing enzyme catalyzing oxidation of ascorbate and 3,4-dihydroxyphenylethylamine simultaneously by O2 to yield norepinephrine, dehydroascorbate, and water; a crucial step in catecholamine metabolism. Synonym: dopamine beta-hydroxylase. (05 Mar 2000) |
| dopamine hydrochloride | A biogenic amine and neural transmitter substance, used as a vasopressor agent for treatment of shock. (05 Mar 2000) |
| dopamine uptake inhibitors | Drugs that block the transport of dopamine into axon terminals or into storage vesicles within terminals. most of the adrenergic uptake inhibitors also inhibit dopamine uptake. (12 Dec 1998) |
| 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) |
| ANP receptor | <molecular biology> Family of 3 receptors for atrial natriuretic peptide. ANP A and ANP B have intracellular guanylate cyclase and protein kinase like domains. ANP C, shares the extracellular ligand binding and transmembrane domains, but lacks the functional intracellular domains and is not thought to be involved in signal transduction. (18 Nov 1997) |
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