| MHA-TP | Micro-Hemagglutination Assay for antibodies to Treponema Pallidum |
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| SMA | 1) Smooth Muscle Antibodies 2) 척수성 근위축증 3) Superior Mesent... |
| FCA | ferritin-conjugated antibodies; Freund's complete adjuvant; functional capacity assessment |
| Mabs | monoclonal antibodies |
| MAIN | medication-induced, autoimmune, infectious, and neoplastic [diseases associated with antiphospholipi... |
| fungal nail infection | The most common fungus infection of the nail is onychomycosis. Onychomycosis makes the nails look white and opaque, thickened, and brittle. Older women (perhaps because oestrogen deficiency may increase the risk of infection) and men and women with diabetes or disease of the small blood vessels (peripheral vacscular disease) are at increased risk. Artificial nails (acrylic or wraps ) increase the risk because when an artificial nail is applied, the nail surface is usually abraded with an emery board damaging it, emery boards can carry infection, and water can collect under the nail creating a moist, warm environment for fungal growth. Alternative names include tinea unguium and ringworm of the nails. (12 Dec 1998) |
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| fungal proteins | Proteins found in any species of fungus. (12 Dec 1998) |
| fungal vaccines | Suspensions of attenuated or killed fungi administered for the prevention or treatment of infectious fungal disease. (12 Dec 1998) |
| fungal vaginitis | <pathology> A local infection of the vaginal mucosa caused by Candida. (27 Sep 1997) |
| 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) |
| antibodies | Any of numerous protein molecules produced by the B-cells as a primary immune defense. (16 Dec 1997) |
| antibodies, anticardiolipin | Antiphospholipid antibodies found in association with systemic lupus erythematosus (lupus erythematosus, systemic), antiphospholipid syndrome, and in a variety of other diseases as well as in healthy individuals. The antibodies are detected by solid-phase immunoassay employing the purified phospholipid antigen cardiolipin. (12 Dec 1998) |
| antibodies, anti-idiotypic | Antibodies which react with the individual structural determinants (idiotopes) on the variable region of other antibodies. (12 Dec 1998) |
| antibodies, antineutrophil cytoplasmic | Autoantibodies directed against cytoplasmic constituents of polymorphonuclear leukocytes and/or monocytes. They are used as specific markers for wegener's granulomatosis and other diseases, though their pathophysiological role is not clear. Anca are routinely detected by indirect immunofluorescence with three different patterns: c-anca (cytoplasmic), p-anca (perinuclear), and atypical anca. (12 Dec 1998) |
| antibodies, antinuclear | See: Antinuclear antibodies. (12 Dec 1998) |
| antibodies, antiphospholipid | Autoantibodies directed against phospholipids. These antibodies are characteristically found in patients with systemic lupus erythematosus (lupus erythematosus, systemic), antiphospholipid syndrome, related autoimmune diseases, some non-autoimmune diseases, and also in healthy individuals. (12 Dec 1998) |
| antibodies, archaeal | Immunoglobulins induced by substances elaborated by archaea that have an antigenic activity. (12 Dec 1998) |
| antibodies, bacterial | Immunoglobulins induced by substances elaborated by bacteria that have an antigenic activity. (12 Dec 1998) |
| antibodies, bispecific | Antibodies, often monoclonal, in which the two antigen-binding sites are specific for separate antigenic determinants. They are artificial antibodies produced by chemical crosslinking, fusion of hybridoma cells, or by molecular genetic techniques. They function as the main mediators of targeted cellular cytotoxicity and have been shown to be efficient in the targeting of drugs, toxins, radiolabelled haptens, and effector cells to diseased tissue, primarily tumours. (12 Dec 1998) |
| antibodies, blocking | Antibodies that inhibit the reaction between antigen and other antibodies or sensitised T-lymphocytes (e.g., antibodies of the IgG class that compete with IgE antibodies for antigen, thereby blocking an allergic response). Blocking antibodies that bind tumours and prevent destruction of tumour cells by cytotoxic T-lymphocytes have also been called enhancing antibodies. (12 Dec 1998) |