| ¿µ¹® | white blood cell(WBC), leukocyte | ÇÑ±Û | ¹éÇ÷±¸ |
|---|---|---|---|
| ¼³¸í | Ç÷¾×³»¿¡ °ñ¼ö±¸°è¼¼Æ÷¿Í ¸²ÇÁ°è¼¼Æ÷, ´ÜÇÙ±¸°è¼¼Æ÷¸¦ ¸ðµÎ ÅëÆ²¾î ¸»ÇÑ´Ù. ¹éÇ÷±¸ÀÇ Áõ°¡°¡ ÀÖÀ¸¸é ´ë°³ °¨¿°ÀÌ Àְųª, ȤÀº Å»¼öÇö»óÀÌ ÀÖÀ½À» ÀǹÌÇÑ´Ù. ¶ÇÇÑ Áö³ªÄ£ ¹éÇ÷±¸¼öÀÇ °¨¼Ò´Â ÀÎü³» ¸é¿ª±â´ÉÀÌ ¶³¾îÁ® ÀÖÀ½À» ÀǹÌÇϸç, ´Ù¸¥ Áúº´¿¡ ÀÇÇØ ³ªÅ¸³ª´Â ÀÌÂ÷ÀûÀÎ Çö»óÀÌ ¾Æ´ÑÁö ²À Áø´ÜÀ» ¹Þ¾Æº¸¾Æ¾ß ÇÑ´Ù. |
||
| ¿µ¹® | mast cell | ÇÑ±Û | ºñ¸¸ ¼¼Æ÷ |
|---|---|---|---|
| ¼³¸í | µ¿¹°ÀÇ °áÇÕ Á¶Á÷ °¡¿îµ¥ ³Î¸® ºÐÆ÷ÇÏ´Â ¼¼Æ÷. °áÇÕÁ¶Á÷°ú Á¡¸·Á¶Á÷ ³»¿¡ Àִ ȣ¿°±â¼º »ö¼Ò·Î ÀÌ¿°»ö¼º(metachromasia)À» ³ªÅ¸³»´Â °ú¸³À» °¡Áø ¹æÃßÇüÀÇ ¼¼Æ÷¿¡ ÀÛÀº µÕ±Ù ÇÙÀ» °¡Áø´Ù. ºñ¸¸¼¼Æ÷ÀÇ Ç¥¸é¿¡´Â IgE¿¡ ´ëÇÑ ¼ö¿ëü°¡ Á¸ÀçÇϸç, ¼ö¿ëü¿¡ °áÇÕÇÑ IgE ºÐÀڵ鳢¸® ´Ù°¡ÀÇ Ç׿ø¿¡ ÀÇÇØ ¼·Î ¿¬°áµÇ¸é ºñ¸¸¼¼Æ÷ °ú¸³Å»Ãâ ¹ÝÀÀÀÌ ÀϾ, È÷½ºÅ¸¹Î, ¼¼·ÎÅä´Ñ, ÇìÆÄ¸° µîÀÇ ÈÇÐÀü´Þ ¹°ÁúÀÌ ¹æÃâµÇ¾î, Áï½ÃÇü ¾Ë·¹¸£±â ¹ÝÀÀ µîÀÇ Áõ»óÀ» ÀÏÀ¸Å²´Ù. ÇǺÎ, À帷, Ç÷°ü ÁÖÀ§, Á¡¸· ÁÖº¯¿¡ ÀÖ´Ù. |
||
| ¿µ¹® | cell-mediated immunity | ÇÑ±Û | ¼¼Æ÷¸Å°³¸é¿ª |
|---|---|---|---|
| ¼³¸í | ¸é¿ªÀ̶õ ½Åü¸¦ ¿ÜºÎÀÇ ¹°Áú·ÎºÎÅÍ º¸È£ÇÏ´Â ÇàÀ§¸¦ ¸»ÇÑ´Ù. ¿©±â¿¡´Â ƯÀÌÀû ¸é¿ª°ú ºñƯÀÌÀû ¸é¿ªÀÇ µÎ °¡Áö°¡ ÀÖ´Ù. ºñƯÀÌÀû ¸é¿ªÀ̶óÇÔÀº ƯÁ¤ÇÑ ¹°Áú¿¡ °ü°èÇÏ´Â ¸é¿ªÀÌ ¾Æ´Ï¶ó ƯÁ¤ ´ë»óÀÌ ¾øÀÌ ¸ðµç ¿ÜºÎ ¹°Ã¼¿¡ ÀÛ¿ëÇÒ ¼ö ÀÖ´Â ¸é¿ªÀ» ¸»ÇÑ´Ù. ¿©±â¿¡´Â ¼Òº¯ÀÇ È帧, ´«¹°ÀÇ È帧, ÇǺÎÀÇ ºñÅõ°ú¼º µîÀÇ ±â°èÀûÀÎ °Íµµ Æ÷ÇԵǰí ÇǼӿ¡ µ¹¾Æ´Ù´Ï´Â ¼¼Æ÷ Áß¿¡¼ ºñƯÀÌÀûÀ¸·Î ¿ÜºÎÀÇ ¹°ÁúÀ» Æ÷½ÄÇÏ´Â ¼¼Æ÷µé(¿¹¸¦ µé¸é Å«Æ÷½Ä¼¼Æ÷(macrophage)ÀÇ È°µ¿µµ Æ÷ÇÔÀÌ µÈ´Ù. ¼¼Æ÷¸Å°³¸é¿ªÀ̶õ ƯÀÌÇÑ ¹°ÁúÀ» °¨ÁöÇÒ ¼ö ÀÖ´Â ¼¼Æ÷¸¦ »ý¼ºÇÏ°Ô ÇÏ¿© ±×°ÍÀ¸·Î ÇÏ¿©±Ý ±× ¹°ÁúÀ» Æ÷½ÄÇÏ°Ô ÇÏ´Â °ÍÀ» ¸»ÇÑ´Ù. |
||
| MEN | Multiple Endocrine Neoplasia ; AD Trait 1. MEN Type I(= Wermer Syndro... |
|---|---|
| MC | mass casualties; mast cell; Master of Surgery [Lat. Magister Chirurgiae]; maximum concentration; Med... |
| ICA | 1) Islet Cell Antibody 2) Internal Carotid Artery |
| IC | icteric, icterus; immune complex; immunoconjugate; immunocytochemistry; immunocytotoxicity; impedanc... |
| ICA | Institute of Clinical Analysis; internal carotid artery; intracranial aneurysm; islet cell antibody |
| ICA | Islet Cell-Cytoplasmic Antibodies |
|---|---|
| ICA | Islet cell antibodies |
| ICAs | Islet cell antibodies |
| ICSA | Islet cell surface antibodies |
| ICA | Islet cell |
| islet cell antibodies | In first-degree relatives of probands with insulin-dependent diabetes mellitus the presence of high titre ICA of the IgG cytoplasmic variety (IgG -ICA) and ICA of the complement-fixing subgroup (CF-ICA) confer a relative risk of 75 for development of insulin-dependent diabetes mellitus. The presence of ICA combined with a decrease in the first-phase of insulin secretion ( less than 25 micro U/mL) is predictive with a 95% likelihood of the development of insulin-dependent diabetes mellitus within 12 months. Reproducible results among laboratories are possible with careful attention to selection of the human pancreas as substrate as well as to the use of dilutions to generate standard curves and to the conversion of results to units. The prozone phenomena described elsewhere are not common in our experience. Fifty percent of relatives with a single positive ICA test will develop insulin-dependent diabetes mellitus within 10 years, and 60-80% of relatives with both ICA and insulin autoantibodies (IAA) will develop insulin-dependent diabetes mellitus within 10 years. The predictive value for health of negative results for ICA and IAA is almost 99%. Strong, persistently positive ICA (i.e., 40 JDF U or greater), especially if accompanied by markedly decreased insulin secretion, are the best predictors of subsequent development of insulin-dependent diabetes mellitus. The 64 kD beta-cell autoantigen long thought to be an important target for ICA is not yet available from expression cloning despite efforts by several groups.13 ICA positivity correlates with rapid loss of C-peptide secretory capacity in newly diagnosed ICA-positive insulin-dependent diabetes mellitus. The predictive values of ICA for development of insulin-dependent diabetes mellitus within 10 years in first-degree relatives of patients with insulin-dependent diabetes mellitus increase from 40% at low levels of ICA to 100% at high levels, whereas the sensitivity is 88% at low levels and 31% at high levels. In general, the risk of insulin-dependent diabetes mellitus in relatives of probands increases with titre of ICA, is greater in multiplex families, and is increased in those less than 10 years of age with positive ICA. Although the prevalence of ICA in Japanese with autoimmune thyroid disease resembles that in Caucasians, the incidence of insulin-dependent diabetes mellitus in the Japanese population is only 1/30 - 1/50 that in Caucasians. Prediabetics positive for ICA and IAA have increased suppressor-inducer (CD45R) and decreased helper-inducer (CDw29) peripheral blood lymphocytes. In two randomised, prospective, placebo-controlled studies of recent-onset insulin-dependent diabetes mellitus, cyclosporine immunosuppression increased the rate of non-insulin-requiring remissions as well as beta-cell function during drug treatment. Although 12 months of cyclosporine therapy decreases titres of ICA and insulin antibodies (IA) and increases glucagon-stimulated levels of serum C-peptide, the determination of ICA and IA and HLA-DR type are of no predictive value in selecting recent- onset insulin-dependent diabetes mellitus. Patients for cyclosporine immunointervention. Genetic control of autoimmunity in insulin-dependent diabetes mellitus is reviewed. EIA for autoantibodies to a 64 kD islet-cell protein is promising for prediction of insulin-dependent diabetes mellitus, but sensitivity and specificity are still suboptimal. See also: insulin antibodies. (05 Mar 2000) |
|---|
| islet-cell-stimulating antibodies | <immunology> Autoantibodies to a putative beta-cell receptor; stimulate the release of insulin both in rodents and man; may be analogous to the thyroid stimulating antibodies that cause grave's hyperthyroidism Synonym: icsta (05 Dec 1998) |
|---|---|
| adenoma, islet cell | A benign tumour of the islets of langerhans that may occur anywhere throughout the pancreas. Such tumours may result in hyperinsulinism or zollinger-ellison syndrome. (12 Dec 1998) |
| carcinoma, islet cell | A carcinoma of the islets of langerhans. (12 Dec 1998) |
| pancreatic isleT-cell tumours | <radiology> Insulinoma (beta-cell), usually solitary, 85% benign, gastrinoma, small, slow-growing, multiple, 60% malignant, Zollinger-Ellison syndrome: mult. Intractable ulcers, VIPoma, vasoactive intestinal peptide (VIP), WDHA syndrome: watery diarrhoea, hypokalaemia, achlorhydria, Verner-Morrison syndrome, glucagonoma, hyperglycaemia, migratory necrolytic erythema APUDomas, associated with MEN-1 (12 Dec 1998) |
| islet cell | <pathology> Cells of the Islets of Langerhans within the pancreas. See: A cells, B-cells, D cells. (18 Nov 1997) |
| islet cell adenoma | <tumour> A benign neoplasm of the pancreas composed of tissue similar in structure to that of the islets of Langerhans; it may contain functioning beta cells, and may cause hypoglycaemia. See: insulinoma. Synonym: nesidioblastoma. (05 Mar 2000) |
| islet cell antigen-related protein-tyrosine phosphatase | <enzyme> Receptor-like autoantigen found in insulin-dependent diabetes; genbank l76258 Registry number: EC 3.1.3.- Synonym: iar ptp (26 Jun 1999) |
| blood islet | An aggregation of splanchnic mesodermal cells on the embryonic yolk sac, with the potentiality of forming vascular endothelium and primitive blood cells. Synonym: blood islet. (05 Mar 2000) |
| islet | A small island. (05 Mar 2000) |
| islet amyloid peptide | <hormone, protein> Peptide of 37 amino acids that selectively inhibits insulin stimulated glucose uptake in muscle. Structurally related to calcitonin gene-related peptide. (15 Oct 1997) |
| islet neogenesis-associated protein | <chemical> Constituent of ilotropin; stimulates proliferation of pancreatic ductal cells in vitro; from hamsters and humans; amino acid sequence given in first source Synonym: ingap protein, ingap gene product (05 Dec 1998) |
| islet tissue | <anatomy> Groups of cells found within the pancreas: A cells and B-cells secrete insulin and glucagon. See: D cells. (18 Nov 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) |
Á¦Ç°¸í |
ÆÇ¸Å»ç |
º¸ÇèÄÚµå | ¼ººÐ/ÇÔ·® | ±¸ºÐ/º¸Çè±Þ¿© |
|---|
Á¦Ç°¸í |
ÆÇ¸Å»ç |
º¸ÇèÄÚµå | ¼ººÐ/ÇÔ·® | ±¸ºÐ/º¸Çè±Þ¿© |
|---|