| 영문 | insulin | 한글 | 인슐린 |
|---|---|---|---|
| 설명 | 이자 랑겔한스섬의 B세포가 합성-분비하는 호르몬 단백질, 포도당을 글리코겐으로 바꾸는 호르몬단백질로, 분자량은 5,807이다. 혈중의 당농도 상승으로 인하여 분비가 촉진된다. 근육-지방조직-간 등 표적세포의 수용체 단백질과 결합하여 정보를 세포내로 전달함으로써 혈액 중에서 당, 지질, 아미노산 대사를 조절한다. 당의 조직에 받아드리는 것을 촉진하여 혈당을 저하시킨다. 생성-분비량 저하, 조직세포의 수용체 부족은 고혈당의 원인이 된다. 또한 아미노산의 흡수와 단백질, 지방의 합성을 촉진하며 지방분해는 억제한다. 인슐린은 이자활성성분의 약품으로서 당뇨병 및 기타 질환의 치료에 사용된다. 인슐린이라는 명칭은 섬이란 뜻의 라틴어인 insula에서 연유한다. 1921년 캐나다의 의사 F.G. 밴팅과 C.H. 베스트에 의하여 처음으로 이자에서 채취되었고, 그 후 인슐린의 결정을 얻게 되었다. F. 생거에 의해서 소의 인슐린의 구조가 밝혀졌는데(1955), 이것은 단백질 중에서는 최초로 구조식이 밝혀진 것이다. 포도당으로부터 글리코겐의 생성, 포도당의 산화 및 지방으로의 전화 등을 촉진하는 작용이 있다. 따라서 인슐린의 수용액을 주사하면 혈당이 저하하므로 당뇨병의 치료에 쓰인다. 또 인슐린을 피하에 대량 주사하면 혼수에 빠지는 것을 이용하여 정신병 치료에 인슐린쇼크요법으로서 쓰인다. |
||
| 영문 | IDDM(Insulin-Dependent Diabetes Mellitus) | 한글 | 인슐린의존당뇨병 |
|---|---|---|---|
| 설명 | IDDM은 당뇨병의 치료에 반드시 인슐린이 필요한 경우를 말한다. 주로 원인이 이자에 있는 인슐린을 분비하는 세포의 파괴이며 이로 인해서 당뇨병의 치료제로 쓰이는 인슐린의 분비를 촉진하는 약물이 이 IDDM에서는 쓰일 수가 없고 오직 인슐린만이 치료제로 쓸 수가 있다. 전형적인 인슐린 의존형 당뇨병은 소아에서 흔히 발생하고 인슐린 분비세포의 파괴에 의해서 인슐린 분비능은 거의 없다. |
||
| AMA | 1) Anti-Mitochondrial Antibodies 2) American Medical Association |
|---|---|
| Anti-LKM | Antibodies to Liver-Kidney Microsome |
| FA | 1) Fatty Acid 2) Fluorescent Antibodies; 형광 항체 |
| MAbs | Monoclonal Antibodies |
| MHA-TP | Micro-Hemagglutination Assay for antibodies to Treponema Pallidum |
| IA | Insulin antibodies |
|---|---|
| AEA | A-anti-endomysium antibodies |
| ANCA | Anti-Neutrophil Cytoplasmic Antibodies |
| ACA | Anti-cardiolipin antibodies |
| ACL | Anti-cardiolipin antibodies |
IGF-II : insulin like growth factor-II의 약자. 많은 장기와 조직에 작용하여 단백 합성과 DNA, RNA의 합성을 증가시켜 세포의 수와 양을 증가
| 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) |
| antibodies, catalytic | Antibodies that can catalyze a wide variety of chemical reactions. They are characterised by high substrate specificity and share many mechanistic features with enzymes. (12 Dec 1998) |
| antibodies, fungal | Immunoglobulins induced by substances elaborated by fungi that have an antigenic activity. (12 Dec 1998) |
| antibodies, helminth | Antibodies produced by human or animal cells following clinical or experimental exposure to parasitic helminth antigens. The IgE class of immunoglobulins is usually formed and released, but IgG, IgM, and IgA may also occur. (12 Dec 1998) |
| antibodies, heterophile | Antibodies elicited in a different species from which the antigen originated. These antibodies are directed against a wide variety of interspecies-specific antigens, the best known of which are forssman, hanganutziu-deicher (h-d), and paul-bunnell (p-b). Incidence of antibodies to these antigens--i.e., the phenomenon of heterophile antibody response--is useful in the serodiagnosis, pathogenesis, and prognosis of infection and latent infectious states as well as in cancer classification. (12 Dec 1998) |
Synonyms : Antibodies, Insulin
제품명 |
판매사 |
보험코드 | 성분/함량 | 구분/보험급여 |
|---|
제품명 |
판매사 |
보험코드 | 성분/함량 | 구분/보험급여 |
|---|