| 영문 | hormone | 한글 | 호르몬 |
|---|---|---|---|
| 설명 | 호르몬이란 특정한 내분비선에서 생성, 저장되어 있다가, 관류하는 혈액 중으로 분비된 다음 혈액에 실려 멀리 떨어져 있는 표적세포(호르몬이 작용을 나타내는 세포)에 이르러 그곳에서 특정한 기능을 발휘하는 물질을 말한다. 내분비샘이 아니더라도 어느 세포나 세포군에서 세포외액 중으로 분비된 다음 다른 세포에 가서 세포의 기능을 변동시키는 물질의 일부도 호르몬의 범주에 포함시키고 있으며 이들을 특별히 국소호르몬이라 부른다(예-아세틸콜린, 아드레날린, 콜레시스토키닌 등). 이에 비해서 특정 내분비샘에서 혈중으로 분비되는 진정한 의미의 호르몬들을 일반호르몬이라고 부른다. 호르몬을 흔히 3종의 무리로 분류를 하는데 아드레날린이나 thyroxine과 같이 아미노산의 유도체로 된 호르몬들(amine derivative), 많은 아미노산을 재료로 만들어졌거나 당단백으로 된 단백호르몬(peptide hormone), 그리고 콜레스테롤을 재료로 만들어진 지방호르몬(steroid hormone) 등으로 구분되며 이들은 대체로 종류에 따라 작용메커니즘을 달리하고 있다. |
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| 영문 | luteinizing hormone(LH) | 한글 | 황체형성호르몬 |
|---|---|---|---|
| 설명 | 여성의 월경은 정해진 순서에 의해 일어나게 된다. 먼저 난포자극호르몬이 뇌에서 분비되어 여성의 난소를 자극하게 되면 난포가 자극받아 난포호르몬(에스트로젠)을 분비하게 되고 이것은 다시 되먹이기 메커니즘 의해 뇌에 작용을 하여 황체화호르몬이 뇌에서 분비되고 이것이 이른바 절정에 이르렀을 때, 난포에서 배란이 일어나게 된다. 이후 난포는 황체로 변하게 되며, 배란된 난자가 수정되지 아니하면, 황체는 황체호르몬(프로게스테론)을 분비한 뒤 퇴화되고 곧 이어 월경이 일어나게 된다. 이 일은 정상적인 대부분의 여성에서 28일을 주기로 일어나며, 대개 황체화호르몬 절정 이후 마지막은 14일로 일정하다고 한다. |
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| 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) |
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| antitrypsin deficiency | Deficiency of a1-antitrypsin, a glycoprotein of the postalbumin region of human serum. Many forms are known which may be moderate (40 to 60% of normal activity) or severe (less than 10% of normal), all autosomal dominant; the severe form is often associated with familial emphysema or hepatic cirrhosis. (05 Mar 2000) |
| arch length deficiency | The difference between the available circumference of the dental arch and that required to accommodate the succedaneous teeth in proper alignment. (05 Mar 2000) |
| arginase deficiency | <biochemistry> Arginase is the fifth enzyme of the urea cycle and catalyses the hydrolysis of arginine to ornithine and urea as the final step in the detoxification of ammonia. Deficiency of the enzyme results in hyperargininaemia and episodic hyperammonaemia, leading to moderate to severe mental retardation and spasticity. at least two isozymes of arginase exist in man. AI (the enzyme deficient in the disorder) is cytosolic and found primarily in liver and red blood cells, whereas AII is mitochondrial and found predominantly in kidney but also to a lesser extent in liver, brain, and other tissues. While AII activity appears to be induced in AI deficiency, it is only partially effective in maintaining urea cycle function. The normal in vivo function of AII is unclear. Arginase deficiency is diagnosed by observing high arginine concentrations on either qualitative or quantitative plasma or urine amino acid analysis. The diagnosis is confirmed by finding markedly decreased or absent arginase activity in an isotopic red blood cell enzymatic assay. The AI gene has been cloned, sequenced, and localised to human chromosome band 6q23. (17 Dec 1997) |
| ascorbic acid deficiency | A condition due to a dietary deficiency of ascorbic acid (vitamin c), characterised by malaise, lethargy, and weakness. As the disease progresses, joints, muscles, and subcutaneous tissues may become the sites of haemorrhage. Ascorbic acid deficiency frequently develops into scurvy in young children fed unsupplemented cow's milk exclusively during their first year. It develops also commonly in chronic alcoholism. (cecil textbook of medicine, 19th ed, p1177) (12 Dec 1998) |
| 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) |
| brancher deficiency glycogenosis | Type of glycogen storage disease, due to deficiency of amylo-1,4-1,6-transglucosidase (brancher enzyme). Synonym: brancher deficiency glycogenosis, debrancher deficiency. (05 Mar 2000) |
| calcium deficiency | A low blood calcium (hypocalcaemia) makes the nervous system highly irritable with tetany (spasms of the hands and feet, muscle cramps, abdominal cramps, overly active reflexes, etc.). Chronic calcium deficiency contributes to poor mineralization of bones, soft bones (osteomalacia) and osteoporosis; and, in children, rickets and impaired growth. Food sources of calcium include dairy foods, some leafy green vegetables such as broccoli and collards, canned salmon, clams, oysters, calcium-fortified foods, and tofu. According to the National Academy of Sciences, adequate intake of calcium is 1 gram daily for both men and women. The upper limit for calcium intake is 2.5 grams daily. (12 Dec 1998) |
| carbamoylphosphate synthetase deficiency | <biochemistry> Carbamoylphosphate synthetase is the initial enzyme of the urea cycle, catalysing the synthesis of carbamoylphosphate from ammonia, bicarbonate and ATP as the first step of ammonia detoxification. The enzyme is an intramitochondrial form called CPS I. A different isozyme found in the cytoplasm, called CPS II, is much less active and apparently not involved in the urea cycle. The deficiency state is autosomal recessive and presents in infancy with massive hyperammonaemia and neurologic deficits in survivors. Diagnosis is suggested by the blood biochemistry and confirmed by specific enzyme assay on liver or rectal biopsy. Prenatal diagnosis by molecular methods has been used successfully in informative families. Inheritance: autosomal recessive. (07 Apr 1998) |
| carbonic anhydrase II deficiency syndrome | <syndrome> An inherited deficiency of carbonic anhydrase II that results in osteopetrosis and metabolic acidosis. Synonym: osteopetrosis with renal tubular acidosis. (05 Mar 2000) |
| g-6-p-d deficiency | <biochemistry> An inherited condition that results in a deficiency in glucose-6-phosphate dehydrogenase. Particular drugs (sulphonamides) can exacerbate this problem. The result is haemolytic anaemia. (27 Sep 1997) |
| galactokinase deficiency | An inborn error of metabolism due to congenital deficiency of galactokinase, resulting in increased blood galactose concentration (galactosaemia), cataracts, hepatomegaly, and mental deficiency; autosomal recessive inheritance. Galactose epimerase deficiency and galactose-1-phosphate uridyl transferase deficiency produce much the same clinical picture. (05 Mar 2000) |
| galactokinase deficiency galactosaemia | An autosomal recessive disorder resulting in an accumulation of galactose and galactitol. (05 Mar 2000) |
| magnesium deficiency | Can occur due to inadequate intake or impaired intestinal absorption of magnesium. Low magnesium (hypomagnesaemia) is often associated with low calcium (hypocalcaemia) and low potassium (hypokalaemia). Deficiency of magnesium causes increased irritability of the nervous system with tetany (spasms of the hands and feet, muscular twitching and cramps, spasm of the larynx, etc.). According to the national academy of sciences, the recommended dietary allowances of magnesium are 420 milligrams per day for men and 320 milligrams per day for women. The upper limit of magnesium as supplements is 350 milligrams daily, in addition to the magnesium from food and water. (12 Dec 1998) |
| glucocerebrosidase deficiency | Causes Gaucher's disease (type 1), a progressive genetic disease due to an enzyme defect. The enzyme, glucocerebrosidase, is needed to break down the chemical glucocerebroside. The enzyme defect in persons with Gaucher's disease (GD) leads to the accumulation of glucocerebroside in the spleen, liver, and lymph nodes. The most common early sign is enlargement of the spleen (located in the upper left abdomen). Other signs include low red blood cell counts (anaemia), a decrease in blood clotting cells (platelets), increased pigmentation of the skin, and a yellow fatty spot on the white of the eye (a pinguecula). Severe bone involvement can lead to pain and collapse of the bone of the hips, shoulders, and spine. The GD gene is on chromosome 1. The disease is a recessive trait. Both parents carry a GD gene and transmit it for their child with the disease. The parents' risk of a child with the disease is 1 in 4 with each pregnancy. This type of Gaucher's disease (noncerebral juvenile Gaucher's disease) is most common in Ashkenazi Jews (of European origin) and is the most common genetic disease among Jews in the United States. (12 Dec 1998) |