| ¿µ¹® | cardiovascular system | ÇÑ±Û | ½ÉÀåÇ÷°ü°è |
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| ¼³¸í | ½ÅüÀÇ Ç÷¾×¼øÈ¯À» ´ã´çÇÏ´Â ±â°ü. Áï ½ÉÀå°ú Ç÷°üÀ» ÅëÄªÇØ¼ À̸£´Â ¸»ÀÌ´Ù. |
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| ¿µ¹® | autonomic nervous system | ÇÑ±Û | ÀÚÀ²½Å°æ°è |
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| ¼³¸í | »ç¶÷ÀÇ ÀÇÁö¿Í °ü°è¾øÀÌ, ħÀ» È긮°Å³ª ¼Òȿ µî°ú °°Àº ½º½º·Î Á¶Á¤ÀÌ µÇ¾î ¿òÁ÷ÀÌ´Â ½Å°æ°èÀÌ¸ç ¿©±â¿¡´Â ´ÙÀ½°ú °°Àº µÎ °¡Áö°¡ ÀÖ´Ù. 1.±³°¨½Å°æ°è(sympathetic nervous system)-»ç¶÷ÀÌ À§Çè»óÅ¿¡ À̸£·¶À» °æ¿ì¿¡ ÈïºÐÀÌ µÇ´Â ÀÚÀ²½Å°æ°è. Áï ½É¹Ú¼öÀÇ Áõ°¡, ¼Òȱ⠿ÀÇ °¨¼Ò µîÀÇ ÀÏÀÌ À̰÷À» ÅëÇØ¼ ÀϾÙ. ±³°¨½Å°æÀÌ ÈïºÐµÇ¸é ±³°¨½Å°æÀÇ ¸»´Ü¿¡¼ epinephrine, norepinephrine µîÀÇ ¹°ÁúÀÌ ºÐºñµÇ°í À̰͵鿡 ÀÇÇØ¼ ¸»ÃÊÀå±â°¡ º¯È¸¦ ÀÏÀ¸Å²´Ù. ÇÏÁö¸¸ Àå±â¿¡ µû¶ó¼ epinephrineÀ̳ª norepinephrineÀÇ ¼ö¿ëü¸¦ °¡Áö°í ÀÖ¾î¼ ¿©·¯ °¡Áö ´Ù¸¥ Àå±âÀÇ ¹ÝÀÀÀ» º¼ ¼ö°¡ ÀÖ´Ù. ¼ö¿ëü´Â ´ÙÀ½°ú °°´Ù. -¾ËÆÄ¼ö¿ëü(alpha-receptor): ¸»ÃÊÇ÷°üÀÇ ¼öÃà, ±â°üÁöÀÇ ¼öÃà, µ¿°øÀÇ ±ÙÀ°ÀÇ ¼öÃà -º£Å¸1¼ö¿ëü(beta 1-receptor): ½ÉÀå¿¡ Á¸ÀçÇÏ´Â ¼ö¿ëü, ½ÉÀåÀ» »¡¸® ¶Ù°ÔÇÏ´Â ¿ªÇÒÀ» ÇÑ´Ù. -º£Å¸2¼ö¿ëü(beta 2-receptor): Ç÷°üÀÇ ÀÌ¿Ï, ±â°üÁöÀÇ ÀÌ¿Ï, Áï °¢ Àå±âµéÀº ±× Àå±â°¡ °¡Áö°í ÀÖ´Â ±³°¨½Å°æÀÇ ¼ö¿ëü¿¡ µû¶ó ±³°¨½Å°æÀÇ ÈïºÐ(±³°¨½Å°æ ¸»´Ü¿¡¼ÀÇ epinephrineÀÇ ºÐºñ)¿¡ ´ëÇÑ ¹ÝÀÀÀÌ ´Þ¶óÁø´Ù(¿¹-±³°¨½Å°æÀÌ ÈïºÐ½Ã¿¡ beta 1-¼ö¿ëü¸¦ °¡Áö°í ÀÖ´Â ½ÉÀåÀº »¡¸® ¶Ù°Ô µÈ´Ù. ±³°¨½Å°æ ÈïºÐ½Ã¿¡ µ¿°øÀÇ ±ÙÀ°ÀÌ ¼öÃàÇØ¼ µ¿°øÀÇ Å©±â°¡ Ä¿Áø´Ù) 2.ºÎ±³°¨½Å°æ°è(parasympathetic nervous system)-±³°¨½Å°æ°ú ¹Ý´ë·Î ÀÛ¿ëÇÑ´Ù. Áï »ç¶÷ÀÌ Á¹¸®°Å³ª ½¯ °æ¿ì¿¡ ÈïºÐÇÑ´Ù. ºÎ±³°¨½Å°æÀÌ ÈïºÐÇÒ ¶§¿¡´Â ½Å°æÀÇ ¸»´Ü¿¡¼ ¾Æ¼¼Ä¥Äݸ°ÀÇ ºÐºñ°¡ ÀϾ°í À̰ÍÀ¸·Î ÀÎÇØ¼ °¢ Àå±âÀÇ º¯È°¡ ÀϾÙ. |
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| ¿µ¹® | TNM staging system | ÇÑ±Û | Á¾¾çº´±âºÐ·ù°èÅë |
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| ¼³¸í | Á¾¾çÀÇ º´±â(stage)¸¦ °áÁ¤ÇÏ´Â ÇÑ ¹æ¹ý. T´Â Tumor(Á¾¾ç)¸¦ ¶æÇÏ¸ç ¿ø¹ßº´ÅÍÀÇ Å©±â, ÁÖÀ§Á¶Á÷À¸·ÎÀÇ Ä§À±Á¤µµ µî¿¡ µû¶ó T1, T2, T3, T4(¼ýÀÚ°¡ ³ôÀ» ¼ö·Ï ÁÖÀ§·Î ħÀ±ÀÌ ¸¹´Ù) µîÀ¸·Î ³ª´«´Ù. NÀº Node(¸²ÇÁÀý)¸¦ ¶æÇϸç ħ¹üµÈ ¸²ÇÁÀýÀÇ °¹¼ö, Å©±â, À§Ä¡ µî¿¡ µû¶ó N1, N2, N3 µîÀ¸·Î ³ª´«´Ù. MÀº Metastasis(ÀüÀÌ)¸¦ ¶æÇÏ¸ç ¿ø°ÝÀüÀÌÀÇ À¯¹«¿¡ µû¶ó M0, M1 µîÀ¸·Î ³ª´«´Ù. ÀÌ»óÀÇ ¹æ¹ýÀ¸·Î T, N, MÀÌ °áÁ¤µÇ¸é À̵éÀ» Á¶ÇÕÇÏ¿© ÃÖÁ¾ÀûÀÎ º´±â¸¦ °áÁ¤ÇÑ´Ù. ÀÌ·¸°Ô °áÁ¤µÈ º´±â´Â Ä¡·á ¹æÄ§ °áÁ¤°ú ¿¹ÈÄ ÆÇ´Ü¿¡ ¸Å¿ì Áß¿äÇÏ´Ù. |
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| ¿µ¹® | central nervous system(CNS) | ÇÑ±Û | ÁßÃ߽Űæ°è |
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| ¼³¸í | ½Å°æ°è´Â ÁßÃ߽Űæ°è¿Í ¸»ÃʽŰæ°è·Î ºÐ·ùÇÒ ¼ö°¡ ÀÖ´Ù. ÁßÃ߽Űæ°è¶õ ³ú¿Í ô¼ö·Î ±¸¼ºµÇ¾î ÀÖ´Â ½Å°æ°è¸¦ À̸£´Â ¸»ÀÌ´Ù. ¸»ÃʽŰæ°è¶õ ÀÌ ÀÌ¿ÜÀÇ ¸ðµç ½Å°æ°è¸¦ À̸£´Â ¸»ÀÌ´Ù. |
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| short-FRAME | short stature-facial anomalies-Rieger anomaly-midline anomalies-enamel defects [syndrome] |
|---|---|
| VACTERL | vertebral abnormalities, anal atresia, cardiac abnormalities, tracheoesophageal fistula and/or esoph... |
| VATER | vertebral defects, imperforate anus, tracheoesophageal fistula, and radial and renal dysplasia |
| ZD | zero defects; zero discharge; zinc deficiency |
| ECG | Electro-Cardio-Graphy(-Gram); ½ÉÀüµµ = EKG 1. Conducting System Structu... |
| complement cytolysis inhibitor | <protein> Vertebrate glycoprotein of uncertain function. Secreted as a 400 amino acid peptide, then cleaved to form two 200 amino acid peptides that are linked by a disulphide bridge. Synonym: complement associated protein, complement cytolysis inhibitor, glycoprotein III. (11 Jan 1998) |
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| complement factor h | <chemical> A beta-globulin that binds to complement 3b and makes ic3b (inactivated complement 3b) susceptible to cleavage by complement factor I. Complement factor h also acts as an alternative pathway complement inhibitor by interfering with the binding of properdin factor b to c3b. Chemical name: Complement factor H (12 Dec 1998) |
| complement factor I | <enzyme> Serine proteinase that acts on ic3b (inactivated complement 3b) to cleave it into c3c and c3dg with the help of a trypsin-like proteolytic enzyme. Complement factor I was formerly called kaf, c3binf, or enzyme 3b inactivator. Registry number: EC 3.4.21.45 (12 Dec 1998) |
| complement fixation | <immunology> Binding of complement as a result of its interaction with immune complexes (the classical pathway) or particular surfaces (alternative pathway). (18 Nov 1997) |
| complement-fixation reaction | <immunology> Binding of complement as a result of its interaction with immune complexes (the classical pathway) or particular surfaces (alternative pathway). (18 Nov 1997) |
| complement-fixation test | An immunological test for determining the presence of a particular antigen or antibody when one of the two is known to be present, based on the fact that complement is "fixed" in the presence of antigen and its specific antibody. See: Bordet-Gengou phenomenon. (05 Mar 2000) |
| complement fixation tests | Serologic tests based on inactivation of complement by the antigen-antibody complex (stage 1). Binding of free complement can be visualised by addition of a second antigen-antibody system such as red cells and appropriate red cell antibody (haemolysin) requiring complement for its completion (stage 2). Failure of the red cells to lyse indicates that a specific antigen-antibody reaction has taken place in stage 1. If red cells lyse, free complement is present indicating no antigen-antibody reaction occurred in stage 1. (12 Dec 1998) |
| complement-fixing antibody | Antibody that combines with and sensitises antigen leading to the activation of complement, which may result in cell lysis. Synonym: CF antibody, sensitizing substance. (05 Mar 2000) |
| complement haemolytic activity assay | Usual screening assay for complement. Dilutions of the serum to be tested are added to antibody-coated erythrocytes and the percentage of lysis is measured. The values are expressed by ch50, haemolytic complement units per milliliter, which is the dilution of serum required to lyse 50 percent of the erythrocytes in the assay. (12 Dec 1998) |
| complement inactivators | Serum proteins which act at key sites in the complement sequence to modulate or prevent the progression of the reaction. Absence of these factors leads to uncontrolled activation of the complement system with accompanying disease. (12 Dec 1998) |
| 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 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) |
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