| ¿µ¹® | iron deficiency anemia | ÇÑ±Û | ö°áÇ̺óÇ÷ |
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| ¿µ¹® | infectious disease | ÇÑ±Û | °¨¿°º´ |
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| ¼³¸í | ¹ÙÀÌ·¯½º·ÎºÎÅÍ ±â»ýÃæ Å©±â±îÁöÀÇ »ý¹°À» ¿øÀÎÀ¸·Î ÇÏ´Â º´. ¿øÀÎÀº Á¢ÃËÀü¿°¼ºÀ̸ç, º´¿ø¿¡¼ °¨¿°µÇ´Â °æ¿ìµµ ÀÖ´Ù. °¨¿°À» ¿øÀαտ¡ µû¶ó ºÐ·ùÇÏ¸é ¹ÙÀÌ·¯½º, ¼¼±Õ, Ŭ¶ó¹Ìµð¾Æ, ¸®ÄÏÂ÷, ¹ÌÄÚ¹ÚÅ׸®¿ò, °õÆÎÀÌ, ¿øÃæ, À±Ãæ, ¿ÜºÎ±â»ýÃæ °¨¿°À¸·Î ³ª´ ¼ö ÀÖ´Ù. |
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| ¿µ¹® | hypertensive heart disease | ÇÑ±Û | °íÇ÷¾Ð½ÉÀ庴 |
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| ¼³¸í | °íÇ÷¾Ð¿¡ ÀÇÇØ¼ »ý±â´Â ½ÉÀ庴. °íÇ÷¾Ð½ÉÀ庴À̶ó´Â Áø´ÜÀ» ºÙÀ̱â À§Çؼ´Â ÃÖ¼ÒÇÑ ´ÙÀ½°ú °°Àº Á¶°ÇÀÌ ºÎÇյǾî¾ß Çϴµ¥, ù° ½ÉÀåÇ÷°ü°è¿¡ ½ÉÀ庴À» À¯¹ßÇÒ ¼ö ÀÖÀ» ¸¸ÇÑ ´Ù¸¥ º´º¯ÀÌ ¾øÀÌ ÁÂ½É½Ç ºñ´ë°¡ ÀÖ¾î¾ß Çϸç, µÑ° °íÇ÷¾ÐÀ» ¾Î¾Ò´Ù´Â º´·ÂÀÌ ÀÖ¾î¾ß ÇÑ´Ù. ÁÖ·Î °íÇ÷¾Ð¿¡ ÀÇÇÑ ½ÉÀ庴Àº Ãʱ⿡´Â Á½ɽÇÀÌ ºñÈĶó´Â °ÍÀ¸·Î Ư¡µÇ¾îÁø´Ù. Áï Ç÷¾ÐÀÌ ³ôÀ¸¹Ç·Î Ç÷¾×À» ¼øÈ¯½Ã۱â À§Çؼ´Â ±×¸¸Å ½ÉÀåÀÇ Ç÷¾×À» º¸³»´Â ÈûÀÌ ÁÁ¾Æ¾ß ÇÑ´Ù. ±× ÈûÀ» ¾ò±âÀ§Çؼ´Â ½É±ÙÀÇ ºñÈİ¡ ÇÊ¿ä·Î ÇÏ¿© ÁÂ½É½Ç ±ÙÀ°ÀÇ ºñÈİ¡ »ý±ä´Ù. ±×¸®°í °íÇ÷¾ÐÀÌ Áö¼ÓÀÌ µÉ °æ¿ì¿¡´Â °á±¹ ½ÉÀåÀÌ Á¦ ±¸½ÇÀ» ÇÏÁö ¸øÇÏ°í ÆßÇÁ·Î¼ÀÇ ±â´ÉÀ» ÀÒ¾î¹ö¸®°Ô µÇ¾î ½ÉÀå±â´É»ó½Ç¿¡ ºüÁö°Ô µÈ´Ù. |
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| ¿µ¹® | pelvic inflammatory disease | ÇÑ±Û | °ñ¹Ý¿°Áúȯ |
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| ¼³¸í | °ñ¹ÝÁÖÀ§ÀÇ Àå±â¿¡ ¹ß»ýÇÏ´Â ¿°ÁõÀ» ¸»ÇÔ. ÁÖ·Î ¿©¼º¿¡¼ ¹ß»ýÇÏ¸ç ¿øÀÎÀº ÀÓ±Õ(gonococcus)°ú ºñÀÓ±Õ¿¡ ÀÇÇÑ °¨¿°(non-gonorrheal infection)¿¡ ÀÇÇÑ´Ù. Áõ»óÀº Ãʱ⿡´Â ÁúºÐºñ¹°, ÇϺ¹ºÎµ¿Åë, ¿©¼ºÀÇ »ý½Ä±âºÎÀ§¿¡ ¹ß»ýÇÏ´Â ¾ÐÅë, ¿ù°æÅë, ¿ù°æ·®ÀÇ Áõ°¡ µîÀÌ´Ù. ÀÏÂï Ä¡·áÇØ¾ß Çϸç, °è¼ÓÀûÀ¸·Î º´ÀÌ Áö¼Ó½Ã ¿©¼ºÀÇ ºÒÀÓÀÇ ¿øÀÎÀÌ µÈ´Ù. ÈÄÁø±¹¿¡¼´Â °¡Àå ¸¹Àº ¿©¼ººÒÀÓÀÇ ¿øÀÎÀ̱⵵ ÇÔ. Ä¡·á´Â Ç×»ýÁ¦ÀÇ Åõ¿©ÀÌ´Ù. |
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| ¿µ¹® | Graves' disease | ÇÑ±Û | ±×·¹À̺꽺º´ |
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| ¼³¸í | °©»ó»ùÀÇ ºñ´ë¿Í °©»ó»ùÈ£¸£¸óÀÇ °ú´ÙºÐºñ°¡ Ư¡ÀÎ º´ÀÌ´Ù. ÀÌ º´Àº ÁÖ·Î 25~50¼¼¿¡ È£¹ßÇϰí ÁÖ·Î ¿©ÀÚ¿¡°Ô¼ ¸¹ÀÌ »ý±ä´Ù. °©»ó»ù È£¸£¸óÀº ÀúÀåµÇ¾î ÀÖ´Â ¿¡³ÊÁö¸¦ ¼Ò¸ðÇÏ¿© ½ÅüÀÇ ´ë»çÀ²À» ³ôÀ̴ ȣ¸£¸óÀ̹ǷΠÀÔ¸ÀÀÌ ÁÁÀº µ¥µµ ºÒ±¸ÇÏ°í °è¼ÓÀûÀΠüÁßÀÇ °¨¼Ò, ±×¸®°í ÃàÀûµÈ ¿¡³ÊÁö¸¦ ¼Ò¸ðÇÏ¿© ¿»ý¸¹ÀÌ ÇÏ¿©¼ ´õÀ§¸¦ Âü±â Èûµé¾îÇÏ°í ¸¸¼º ¼è¾à°¨À̳ª ±Ù·ÂÀÇ ¾àȸ¦ º¸ÀÏ ¼ö°¡ ÀÖ´Ù. ±×¸®°í ´«¿¡ Ư¡ÀûÀÎ Áõ»óÀÌ ³ªÅ¸³ª´Âµ¥ ´«²¨Ç®ÀÌ ºñÁ¤»óÀûÀ¸·Î À§·Î ¿Ã¶ó°¡ ÀÖ°í, ´«ÀÌ ¾Æ·¡ÀÇ ¹°°ÇÀ» ÁÖ½ÃÇÒ °æ¿ì¿¡ ´«²¨Ç®ÀÌ Á¤»óÀûÀ¸·Î´Â óÁ®¾ß ÇÏÁö¸¸ °©»ó»ù È£¸£¸óÀÌ °úµµÇÏ°Ô ³ª¿Ã °æ¿ì¿¡´Â ´«²¨Ç®ÀÌ Ã³ÁöÁö ¾Ê´Â´Ù. ¶Ç ´«¾ËÀÌ ¾ÕÂÊÀ¸·Î µ¹ÃâÇÏ´Â ¾È±¸µ¹ÃâÀ» º¼ ¼ö°¡ ÀÖ´Ù. ¶Ç ÇǺΰ¡ ¾ÆÁÖ ºÎµå·´°í ¹°±â°¡ ¸¹¾Æ¼ ÃàÃàÇÏ´Ù. ±×¸®°í Ư¡ÀûÀ¸·Î ÇÏÁöÀÇ ¾ÕÂÊ¿¡ ÇǺΰ¡ µÎ²¨¿öÁ® ±¹¼ÒÀû À¶±â¸¦ ÀÌ·ç´Â °ÍÀÌ Àִµ¥ À̰ÍÀº ÀÌ º´ÀÇ Æ¯Â¡ÀûÀÎ º´ÅÍÀÌ´Ù. |
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| MD | Doctor of Medicine [Lat. Medicinae Doctor]; magnesium deficiency; main duct; maintenance dose; major... |
|---|---|
| CD | cadaver donor; canine distemper; canine dose; carbohydrate dehydratase; carbon dioxide; cardiac dise... |
| HD | Haab-Dimmer [syndrome]; Hajna-Damon [broth]; Hansen disease; hearing distance; heart disease; helix ... |
| MCD | magnetic circular dichroism; mast-cell degranulation; mean cell diameter; mean of consecutive differ... |
| DDD | AV universal [pacemaker]; defined daily dose; degenerative disc disease; dehydroxydinaphthyl disulfi... |
| GUS | Beta-glucuronidase |
|---|---|
| beta G | Beta-glucuronidase |
| beta-Glu | Beta-glucuronidase |
| GUS | Promoter-beta-glucuronidase |
| BG | beta glucuronidase |
Kugelberg-Welander disease ±Ù À§ÃàÁõÀÇ À¯Àü¼º ¿¬¼ÒÇüÀ¸·Î¼ º¸Åë »ó¿°»öü¼º ¿¼º ÇüÁú·Î À¯ÀüµÈ´Ù. ô¼ö Àü°¢ÀÇ º´º¯ÀÌ ±× ¿øÀÎÀÌ´Ù.
kukuruku ¿øÀÎ ºÒ¸íÀ̸ç, ³ªÀÌÁö¸®¾Æ¿¡¼ º¼ ¼ö ÀÖ´Â ÁúȯÀ¸·Î, ¿
| beta-d-glucuronidase deficiency | A rare deficiency of beta-d-glucuronidase; an autosomal recessive disorder with several allelic forms, characterised by abnormal mucopolysaccharide metabolism leading to progressive mental deterioration, splenic and hepatic enlargement, and dysostosis multiplex. Synonym: mucopolysaccharidase. (05 Mar 2000) |
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| alpha-(4-O-methyl)-D-glucuronidase | <enzyme> Removes 4-o-methyl-glucopyranosyl uronic acid residues from the 2-position of fungal cell wall xylans Registry number: EC 3.2.1.- Synonym: 4-o-methyl-glucuronidase (26 Jun 1999) |
| beta-d-glucuronidase | <enzyme> An enzyme catalyzing the hydrolysis of various beta-d-glucuronides, liberating free d-glucuronic acid and an alcohol; a deficiency of this enzyme is associated with Sly syndrome. Synonym: glusulase, glycuronidase. (05 Mar 2000) |
| glucuronidase | <enzyme> Chemical name: beta-D-Glucuronoside glucuronosohydrolase Registry number: EC 3.2.1.31 (12 Dec 1998) |
| glycyrrhizin beta-D-glucuronidase | <enzyme> From eubacterium sp. Found in human intestinal flora; hydrolyzes glycyrrhizin to glycyrrhetic acid Registry number: EC 3.2.1.- Synonym: gbd-glucuronidase (26 Jun 1999) |
| antibody deficiency disease | <syndrome> Any of a group of disorders associated with a defective antibody production due to defects in the B-type lymphocyte system or in T-type lymphocytes; chief manifestation is an increased susceptibility to infection by various microorganisms. See: agammaglobulinaemia, hypogammaglobulinaemia, immunodeficiency. Synonym: antibody deficiency disease. (05 Mar 2000) |
| deficiency disease | Any disease resulting from undernutrition or an inadequacy of calories, proteins, essential amino acids, fatty acids, vitamins, or trace minerals. (05 Mar 2000) |
| thrombotic disease due to protein c deficiency | Protein C is a protein in plasma that enters into the cascade of biochemical events leading to the formation of a clot. Deficiency of protein c results in thrombotic (clotting) disease and excess platelets with recurrent thrombophlebitis (inflammation of the vein that occurs when a clot forms). The clot can break loose and travel through the blood stream (thromboembolism) to the lungs causing a pulmonary embolism, brain causing a stroke (cerebrovascular accident), heart causing an early heart attack, skin causing what in the newborn is called neonatal purpura fulminans, the adrenal gland causing haemorrhage with abdominal pain, abnormally low blood pressure (hypotension), and salt loss. Protein c deficiency is due to possession of one gene (heterozygosity) in chromosome band 2q13-14. The possession of two such genes (homozygosity) is usually lethal. (12 Dec 1998) |
| abdominal muscle deficiency syndrome | <syndrome> Congenital absence (partial or complete) of abdominal muscles, in which the outline of the intestines is visible through the protruding abdominal wall; in males, genitourinary anomalies (urinary tract dilation and cryptorchidism) are also found; genetics unclear. (05 Mar 2000) |
| adult lactase deficiency | Onset of lactase deficiency, with resulting milk intolerance and malabsorption, in adulthood. Inherited forms may not be manifested until adulthood; any process that damages the intestinal lining cells can cause lactase deficiency in adults. (05 Mar 2000) |
| alpha-1 antitrypsin deficiency | <chest medicine> Deficiency of the protease inhibitor alpha-1 antitrypsin, leads primarily to degradation of elastin of the alveolar walls, as well as other structural proteins of a variety of tissues. The lack of this protein leads to damage of various organs, but mainly to the lung and liver. symptoms may become apparent at a very early age or in adulthood, manifesting either as shortness of breath or liver related symptoms (jaundice, fatigue, fluid in the abdomen, mental changes, or gastrointestinal bleeding). There are several options for treatment of the lung disease, including replacement of the missing protein. Treatment of the liver disease is a well-timed liver transplant (12 Dec 1998) |
| alpha-1-proteinase deficiency | Absence of a serum proteinase inhibitor that may cause nodular non-suppurative panniculitis. (05 Mar 2000) |
| alpha-antitrypsin deficiency | <enzyme> A specific enzyme (alpha 1 antitrypsinase) that when absent genetically can result in panacinar emphysema (lung disease) and liver disease. There is no specific treatment for this condition other than supportive care for the liver and lung complications. Medications such as alpha-1proteinase inhibitor is given regularly to these patients. Incidence: approximately 1 in 10,000. (02 Jan 1998) |
| anaemia, iron deficiency | Deficiency of iron results in anaemia because iron is necessary to make haemoglobin, the key molecule in red blood cells responsible for the transport of oxygen. In iron deficiency anaemia, the red cells are unusally small (microcytic) and pale (hypochromic). Characteristic features of iron deficiency anaemia in children include failure to thrive (grow) and increased infections. The treatment of iron deficiency anaemia, whether it be in children or adults, is with iron and iron-containing foods. Food sources of iron include meat, poultry, eggs, vegetables and cereals (especially those fortified with iron). According to the National Academy of Sciences, the Recommended Dietary Allowances of iron are 15 milligrams per day for women and 10 milligrams per day for men. Anaemia characterised by low or absent iron stores, low serum iron concentration, elevated free erythrocyte porphorin, low transferrin saturation, elevated transferrin, low serum ferritin, low haemoglobin concentration or haematocrit, and hypochromic microcytic red blood cells. Symptoms may include pallor, angular stomatitis and other oral lesions, gastrointestinal complaints, retinal haemorrhages and exudates, and thinning and brittleness of the nails. Among the causes of iron-deficiency anaemia are inadequate iron intake, impaired iron absorption, increased blood loss and increased requirements such as infancy, pregnancy, and lactation. (12 Dec 1998) |
| antibody deficiency syndrome | <syndrome> Any of a group of disorders associated with a defective antibody production due to defects in the B-type lymphocyte system or in T-type lymphocytes; chief manifestation is an increased susceptibility to infection by various microorganisms. See: agammaglobulinaemia, hypogammaglobulinaemia, immunodeficiency. Synonym: antibody deficiency disease. (05 Mar 2000) |
| Glucuronidase deficiency disease |
Mucopolysaccharidosis VII.
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