| ¿µ¹® | protein | ÇÑ±Û | ´Ü¹éÁú |
|---|---|---|---|
| ¼³¸í | ź¼Ò, ¼ö¼Ò, »ê¼Ò, Áú¼Ò, ȲÀ» ÇÔÀ¯Çϰí ÀÖ´Â À¯±âÈÇÕ¹°·Î, ¸ðµç ¼¼Æ÷ÀÇ ¿øÇüÁúÀ» ÀÌ·ç°í ÀÖ´Â ±âº» ±¸¼º¹°ÁúÀÌ´Ù. ´Ü¹éÁúÀº ±× ´ÜÀ§ÀÎ ¾Æ¹Ì³ë»êµéÀÌ ÆéƼµå°áÇÕ¿¡ ÀÇÇØ °áÇյǾî ÀÖÀ¸¸ç, º¸Åë 20°³ÀÇ ¾Æ¹Ì³ë»êµéÀÌ ´Ù¸¥ ¼ø¼¿Í Á¶¼ºÀ» °¡Áö°í ¹è¿µÇ¾î, µ¶Æ¯ÇÑ ÇϳªÀÇ ´Ü¹éÁúÀ» Çü¼ºÇÏ°Ô µÈ´Ù. |
||
| IAP | immunosuppressive acidic protein; inosinic acid pyrophosphorylase; Institute of Animal Physiology; i... |
|---|---|
| MAP | malignant atrophic papulosis; mandibular angle plane; maturation-activated protein; maximal aerobic ... |
| MBP | major basic protein; maltose-binding protein; management by policy; mannose-binding protein; mean bl... |
| RP | radial pulse; radiopharmaceutical; rapid processing [of film]; Raynaud phenomenon; reactive protein;... |
| ICA | 1) Islet Cell Antibody 2) Internal Carotid Artery |
| IAP | Islet activating protein |
|---|---|
| IAPP | Islet amyloid polypeptide |
| ICA | Islet Cell-Cytoplasmic Antibodies |
| ICA | Islet cell |
| ICA | Islet cell antibodies |
| 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 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) |
|---|---|
| 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) |
| 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) |
| 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 | 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 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 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) |
| 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) |
| acetoacetyl-acyl carrier protein synthase | <enzyme> E coli enzyme, that catalyses condensation of malonyl-acyl carrier protein plus acetyl-acyl carrier protein; not inhibited by cerulenin Registry number: EC 2.3.1.- Synonym: acetoacetyl-acp synthase (26 Jun 1999) |
| acid soluble spore protein | <molecular biology> A DNA binding protein in the spores of some bacteria, thought to stabilise the DNA in an A configuration, so protecting it from cleavage by enzymes or UV light. (18 Nov 1997) |
| acute-phase protein | <haematology> These plasma proteins (in addition to fibrinogen) increase 25% or more in response to inflammation and injury are under direct control of interleukin-6 (IL-6) (hepatocyte-stimulating factor). Other proteins which increase are ceruloplasmin, C3 and C4 which increase 50% or more; alpha-1 acid glycoprotein, alpha-1 antitrypsin, haptoglobin and fibrinogen (the major determinant of viscosity 1 ) which increase two- to fourfold; C-reactive protein (CRP) and serum amyloid A which increase several hundred-fold. Despite long-held clinical opinion to the contrary, available data indicate that neither ESR nor measurement of specific acute-phase reactants are useful in excluding underlying infection or inflammation regardless of the pretest probability. These proteins are secreted into the blood in increased or decreased quantities by hepatocytes in response to trauma, inflammation, or disease. They can serve as inhibitors or mediators of the inflammatory processes. Certain acute-phase proteins have been used to diagnose and follow the course of diseases or as tumour markers. See also: amyloid, c-reactive protein, erythrocyte sedimentation rate, viscosity. (25 Jun 1999) |
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¿© |
|---|