| CH50 | Hemolytic Complement 50; 용혈 보체 검사법; (30)50 - (40)(66)80 Unit/mL |
|---|---|
| Gc globulin | Group-specific complement globulin |
| AC | abdominal circumference; abdominal compression; absorption coefficient; abuse case; acetate; acetylc... |
| AICF | autoimmune complement fixation |
| ASAC | acidified serum-acidified complement |
| complement membrane attack complex | The assembly of complement plasma glycoproteins c5b, c6, c7, c8, and polymeric c9 as a group on biological membranes. The complex forms transmembrane channels which displace lipid molecules and other constituents, thus disrupting the phospholipid bilayer of target cells leading to cell lysis by osmotic leakage. The formation of the membrane attack complex is the terminal step in the complement cascade. (12 Dec 1998) |
|---|---|
| complement pathway, alternative | The complement activation sequence initiated by the activation of complement factor c3, which is triggered by the interaction of microbial polysaccharides and properdin without participation of an antigen-antibody reaction. (12 Dec 1998) |
| complement pathway, classical | The sequential activation of complement, initiated by antigen-antibody complex and the binding of complement factor c1q to the fc region of the antibody. (12 Dec 1998) |
| complement system | A group of more than 20 serum proteins, some of which can be serially activated and participate in a cascade resulting in cell lysis. (05 Mar 2000) |
| complement unit | The smallest amount (highest dilution) of complement that will cause haemolysis of a unit of red blood cells in the presence of a haemolysin unit. Synonym: alexin unit. (05 Mar 2000) |
| component of complement | Any one of the nine distinct protein units (designated C1 through C9 and distributed in the a, b, and g electrophoretic partitions of normal serum) that effect the immunological activities long associated with complement. C1 is a complex of three subunits: C1q, C1r, and C1s. C1q (overbar indicates "active form") activates proenzyme C1r to C1r which activates C1s to C1s (also known as C1 esterase), which converts proenzyme C2 to C2b and produces C4b from C4. C2b combines with C4b to form "classical-complement-pathway C3/C5 convertase" (also known as C3 convertase, C5 convertase, and C42). This enzyme cleaves C3 to C3a and C3b, and C5 to yield C5a and C5b, as does "alternative-complement-pathway C3/C5 convertase" (also known as proenzyme factor B, properdin factor B, C3 proactivator, and heat-labile factor). Complement factor I (also known as C3b or C3b/C4b inactivator) inactivates C3b and C4b by a different proteolytic cleavage. Several autosomal recessive disorders have been identified in which one or more of the complement components have been deficient or completely absent. (05 Mar 2000) |
| heparin complement | The protein component of heparin in blood. (05 Mar 2000) |
| thyrotoxic complement-fixation factor | A form of thyrotoxin; an antigen found most readily in thyroid tissue from thyrotoxic individuals; known to be chemically and immunologically distinct from thyroglobulin, and fixes complement when combined with antibody related to the gamma-globulin fraction of serum. With the exception of extremely small concentrations, the antigen is rarely found in normal glands or in diseased glands that are not associated with thyrotoxicosis; it is probably an intracellular substance (possibly a constituent of the "microsomal fraction"), and does not contain iodine in significant quantity. Not related to the complement-fixation reaction occurring with serum in Hashimoto's disease, in which the antigen is thyroglobulin. (05 Mar 2000) |
| 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) |
| asialoglycoprotein receptor | A surface receptor found in hepatocytes that binds galactose-terminal glycoproteins; thus, this receptor removes those proteins from circulation and they are in turn acted upon by hepatocyte lysosomes. (05 Mar 2000) |
| auditory receptor cells | Columnar cell's in the epithelium of the organ of Corti, having hairs (stereocilia) on their apical ends. See: Corti's cells. (05 Mar 2000) |
| beta-adrenergic receptor blocking agent | A class of drugs that compete with beta-adrenergic agonists for available receptor sites; some compete for both b1 and b2 receptors (e.g., propranolol) while others are primarily either b1 (e.g., metoprolol) or b2 blockers; used in the treatment of a variety of cardiovascular diseases where beta-adrenergic blockade is desirable. Synonym: beta-adrenergic receptor blocking agent, beta-adrenoreceptor antagonist, beta-blocker. (05 Mar 2000) |