| ¿µ¹® | intolerance | ÇÑ±Û | ¸ø°ßµõ(Áõ) |
|---|---|---|---|
| ¼³¸í | »ó¿ë·®ÀÇ ¾à¹°À» »ç¿ëÇßÀ½¿¡µµ ºÒ±¸ÇÏ°í °ú·®ÀÇ °æ¿ì¿Í ¶È°°Àº ÁÖÀÛ¿ëÀÇ °úÀ×¹ßÇöÀ» ÇÏ´Â °æ¿ì ºÒ³»¼ºÀ̶ó°í ÇÑ´Ù. »ýü Ãø¿¡ ¾î¶°ÇÑ ÀáÀçÀû ÀåÇØ°¡ Á¸ÀçÇϰųª, ´Ù¸¥ ¾àǰÀ̳ª ±× ÷°¡¹° µî°úÀÇ »óÈ£ÀÛ¿ë¿¡ ÀÇÇØ, ±× ¾à¹°ÀÇ Èí¼ö, ´ë»ç, ¹è¼³ µî¿¡ º¯È°¡ ÀϾ, °á°úÀûÀ¸·Î ±× ¾à¹°ÀÇ Ç÷Áß³óµµÀÇ »ó½ÂÀ» ÃÊ·¡Çϱ⠶§¹®À̶ó°í »ý°¢µÈ´Ù. |
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| ¿µ¹® | congenital syphilis | ÇÑ±Û | ¼±Ãµ¸Åµ¶ |
|---|---|---|---|
| ¼³¸í | ÀӺΰ¡ ¸Åµ¶¿¡ °¨¿°µÇ¾î ÀÖÀ¸¸é ÀӽŠÈı⿡ ¸Åµ¶±ÕÀÌ Å¹ÝÀ» ÅëÇØ Ç÷Ç༺À¸·Î žƿ¡ °¨¿°(¼öÁ÷°¨¿°)µÈ °ÍÀ» ¸»ÇÏ´Ù. ´ëºÎºÐÀº À¯»ê, »ç»êÀÌ µÇÁö¸¸ Ãâ»ýÇϸé Á¦2±â ÀÌÈÄÀÇ ¹ßÁøÀ» º¸ÀδÙ. ¹ßÇö½Ã±â¿¡ µû¶ó¼ ¨ç žƸŵ¶, ¨è À¯¾Æ¸Åµ¶, ¨é ¸¸¹ß¼º ¼±Ãµ¸Åµ¶À¸·Î ºÐ·ùµÈ´Ù. ¨ç¿¡¼´Â »À¿¬°ñ¿°, °£-Áö¶ó ºñ´ë¿Í ¸Åµ¶¼º õÆ÷â, ¨è¿¡¼´Â ÆÄ·Î°¡¼º¸¶ºñ¿Í ¸Åµ¶¼º ÄÚ¿°, ¨é¿¡¼´Â ÇãÄ£½¼ ¼¼Â¡ÈÄ(ÇãÄ£½¼ Ä¡¾Æ, ¼Ó±Í¼º ³Ã», ½ÇÁú¼º °¢¸·¿°)¿¡ µû¶ó Ư¡ÀÌ ÀÖ´Ù. ±âŸ ¼öµÎÁõ, Áö´É¹ßÀ° ºÒ·® µîÀ» ÀÚÁÖ º¼ ¼ö ÀÖ´Ù. ¸Åµ¶ Ç÷û¹ÝÀÀÀº ´ëºÎºÐÀÇ °æ¿ì ¾ç¼ºÀ¸·Î ³ª¿Â´Ù. ¸Å¿ì µå¹°°Ô °£¼¼Æ÷³»¿¡¼ ¸Åµ¶±ÕÀ» ¹«¼öÈ÷ º¼ ¼ö ÀÖ´Ù. °£¼¼Æ÷ ÁÖº¯ÀÇ ¼¶À¯È¿Í ÇÔ²² ºÒ±ÔÄ¢ÇÑ ÈäÅÍ(hepar lobatum)¸¦ ¸¸µé ¼ö ÀÖ´Ù. |
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| ¿µ¹® | congenital rubella syndrome | ÇÑ±Û | ¼±ÃµÇ³ÁøÁõÈıº |
|---|---|---|---|
| ¼³¸í | ÀӽűⰣ Áß¿¡ »ê¸ð°¡ dzÁø¿¡ °É¸®¸é ÀÌ Ç³Áø ¹ÙÀÌ·¯½º´Â ŹÝÀ» ÅëÇØ¼ žƿ¡°Ô Àü´ÞµÇ¾î¼ žÆÀÇ Ç³Áø°¨¿°À» ÀÏÀ¸Å²´Ù. ÀӽŠù 3°³¿ù µ¿¾È, ƯÈ÷ ÀӽŠù´Þ¿¡ žư¡ dzÁøÀÇ °¨¿°À» ¹ÞÀ¸¸é, ½Å»ý¾Æ¿¡¼ ¼±Ãµ±âÇü, Áï ´«¿¡¼ ÃÐÁ¡À» Á¤È®È÷ ¸ÂÃß¾îÁÖ´Â ·»ÁîÀÇ ¿ªÇÒÀ» ÇÏ´Â ¼öÁ¤Ã¼ÀÇ È¥Å¹(¹é³»Àå), ½ÉÀå±âÇü, ±Í¸Ó°Å¸® ¹× ½ÉÇÑ Áö´É¹Ú¾àÀ» µ¿¹ÝÇÏ´Â ¼ÒµÎÁõ µîÀÌ ¹ß»ýÇÏ´Â ¼ö°¡ ¸¹´Ù. |
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| ¿µ¹® | congenital heart disease | ÇÑ±Û | ¼±Ãµ½ÉÀ庴 |
|---|---|---|---|
| ¼³¸í | ¼±ÃµÀûÀ¸·Î ½ÉÀåÀÇ ±¸Á¶¿¡ ÀÌ»óÀÌ ÀÖ´Â º´. |
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| CDH | 1) Chronic Daily Headache = CTH = ... |
|---|---|
| CDH | ceramide dihexoside; congenital diaphragmatic hernia; congenital dislocation of hip; congenital dysp... |
| TCBS | Thiosulfate Citrate Bile salt Sucrose agar |
| SDG | sucrose density gradient |
| SM | Master of Science; sadomasochism; self-monitoring; silicon microphysiometer; simple mastectomy; skim... |
| CMPI | Cow's Milk Protein Intolerance |
|---|---|
| HFI | Hereditary Fructose Intolerance |
| LPI | Lysinuric protein intolerance |
| OI | Orthostatic Intolerance |
| Suc | D-sucrose |
| glucose intolerance | A pathological state in which the fasting plasma glucose level is less than 140 mg per deciliter and the 30-, 60-, or 90-minute plasma glucose concentration following a glucose tolerance test exceeds 200 mg per deciliter. This condition is seen frequently in diabetes mellitus but also occurs with other diseases. (12 Dec 1998) |
|---|---|
| hereditary fructose intolerance | A metabolic error due to deficiency of hepatic fructose 1,6-bisphosphate aldolase B (which also acts on fructose 1-phosphate); the second enzyme in the specific fructose pathway; vomiting and hypoglycaemia follow ingestion of fructose; prolonged fructose ingestion in young children results in failure to thrive and in jaundice, hepatomegaly, albuminuria, aminoaciduria, and sometimes cachexia and death; autosomal recessive inheritance in most families. (05 Mar 2000) |
| intolerance | Inability to withstand, sensitivity, as to a drug. Origin: L. Tolerare = to bear (18 Nov 1997) |
| lactose intolerance | A disorder characterised by abdominal cramps and diarrhoea after the consumption of food containing lactose (for example milk, ice cream), believed to occur due to a deficiency of intestinal lactase (enzyme that breaks down lactose), may appear first in young adults who have previously tolerated milk well as infants. (27 Sep 1997) |
| fructose intolerance | An autosomal recessive fructose metabolism disorder due to deficient fructose-1-phosphate aldolase (ec 2.1.2.13) activity, resulting in accumulation of fructose-1-phosphate. The accumulated fructose-1-phosphate inhibits glycogenolysis and gluconeogenesis, causing severe hypoglycaemia following ingestion of fructose. Prolonged fructose ingestion in infants leads ultimately to hepatic failure and death. Patients develop a strong distaste for sweet food, and avoid a chronic course of the disease by remaining on a fructose- and sucrose-free diet. (12 Dec 1998) |
| lysinuric protein intolerance | An autosomal recessive disorder characterised by elevated levels of dibasic amino acids (e.g., l-lysine, l-arginine, and l-ornithine) in the urine; apparently due to a defect in dibasic amino acid transport. (05 Mar 2000) |
| sucrose | Nonreducing disaccharide, _ D glucopyranosyl _ D fructofuranose. (18 Nov 1997) |
| sucrose alpha-d-glucohydrolase | <enzyme> An enzyme hydrolyzing sucrose and maltose; in a complex with isomaltase; hence, hydrolyzes both sucrose and isomaltose; found in the intestinal mucosa; a deficiency of this enzyme results in defective digestion of sucrose and linear a1,4-glucans. Synonym: sucrase. (05 Mar 2000) |
| sucrose - fructan 6-fructosyltransferase | <enzyme> Catalyses the formation and extension of beta-2,6-linked fructans, typical of grasses; from barley, hordeum vulgare; genbank x83233 Registry number: EC 2.4.1.- Synonym: barley 6-sft (26 Jun 1999) |
| sucrose haemolysis test | Isotonic sucrose promotes binding of complement to red blood cells; in paroxysmal nocturnal haemoglobinuria a proportion of the cells is sensitive to complement-mediated lysis, and haemolysis ensues. (05 Mar 2000) |
| sucrose permease | <chemical> Sucrose-utilizing enzyme Chemical name: permease, sucrose (26 Jun 1999) |
| sucrose-phosphate synthase phosphatase | <enzyme> A type 2a phosphoprotein phosphatase Registry number: EC 3.1.3.- Synonym: sps-phosphatase (26 Jun 1999) |
| sucrose synthase | <enzyme> Sus1 gene product isolated from maise Registry number: EC 2.4.1.13 Synonym: sucrose synthetase, udp-glucose-d-fructose-2-glycosyltransferase, suc synthase 1, suc synthase1, sus1 gene product (26 Jun 1999) |
| dietary sucrose | Sucrose present in the diet. It is added to food and drinks as a sweetener. (12 Dec 1998) |
| adrenal hyperplasia, congenital | A group of inherited disorders of adrenal steroidogenesis, the physical expression of which varies with the sex of the patient, the severity of the congenital enzyme defect, and the age at which the defect makes its presence felt. The most common form, the simple virilizing form, is due to a 21-hydroxylase deficiency. There is also a salt-losing form (a more complete 21-hydroxylase deficiency), a hypertensive form (11-hydroxylase deficiency), a 17-hydroxylase deficiency form, a desmolase deficiency form, and a 3-beta-hydroxysteroid deficiency form. (12 Dec 1998) |
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