| 영문 | male reproductive system | 한글 | 남성생식기계 |
|---|---|---|---|
| 설명 | 남성의 생식기는 여러 기관으로 구성되어 있다. 고환, 부고환, 정관, 정낭, 전립샘, 외부성기(음경) 등으로 구성되는데, 실제적으로 정자를 생성하는 곳은 단 한 곳 고환뿐이며, 나머지 기관은 이를 돕는 기능을 수행하고 있다. 정자는 고환의 정세관이란 곳에서 만들어진 뒤에 밖으로 나와 긴 여정을 시작하게 된다. 그 뒤 부고환을 지나 좀 더 성숙해 진 뒤에 정관에서 정낭의 분비물과 만나고 다시 요도로 나가게 된다. 이때 요도 뒤쪽에 위치하는 전립샘의 분비물이 합쳐지게 되고 이 정액은 외부성기를 거쳐서 밖으로 나가게 된다.  |
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| 영문 | lymphatic system | 한글 | 림프계 |
|---|---|---|---|
| 설명 | 대개 맥관계라고 하면, 혈관계와 림프관계를 합쳐서 말한다. 이중에 림프에 의해 이루어지는 하나의 계통이다. |
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| 영문 | immune system | 한글 | 면역체계 |
|---|---|---|---|
| 설명 | 세포성분 및 분자성분의 복합체계로서, 이의 일차기능은 자기(self)를 비자기(not self)로부터 구별하고 외부생물 또는 물질에 대해 방어하는 것이다. 일차적인 세포성분은 림프구와 큰포식세포이며 일차적인 분자성분은 항체와 림포카인이다. |
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| 영문 | urinary system | 한글 | 비뇨기계통 |
|---|---|---|---|
| 설명 | 비뇨기계통이라하면 콩팥으로부터 시작해서 요관, 방광, 요도에 이르는 일련의 오줌생성 및 저장, 배설기관을 일컫는다. 콩팥은 길이 약 2.5cm, 폭 약 5.1cm, 두께 약 2.5cm, 무게 약 120~160gm으로서, 내측에 콩팥문이 있어 혈관, 신경, 요관이 출입하고 있다. 콩팥은 속질과 겉질로 이루어져 있으며 수질은 10~15개의 추체(오줌을 모으는 역할)를 형성하고 겉질은 약 100만개의 콩팥단위으로 구성되어 있다. 요세관은 토리쪽뇨세관, 헨레고리, 먼쪽뇨세관, 집합관으로 형성되어 있으며, 추체와 술잔, 깔때기를 거쳐 요관으로 연결된다. 콩팥은 혈액을 여과하여 신체 신진대사의 최종산물을 오줌의 형태로 배설하며, 세포외액(extracellular fluid)의 전해질농도를 조절한다. 콩팥에서 형성된 오줌는 요관을 거쳐 방광에서 저장되고 있다가 적당한 시기가 되면 요도를 통해 외계로 배출된다. |
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| 영문 | reproductive system | 한글 | 생식기계통 |
|---|---|---|---|
| 설명 | 1.남성생식계통: 남성생식기는 정자(sperm)를 생성하는 고환과 정자의 성숙, 운반, 그리고 사정에 관여하는 부고환, 정관, 음경(penis) 등으로 이루어져 있으며, 부속기관으로 외분비샘인 정낭(seminal vesicle), 전립샘(prostate), 요도망물샘(bulbourethral gland, Cowper’s gland) 등을 갖추고 있다. 고환은 정자를 생산하는 생식샘인 동시에 남성호르몬(testosterone)을 분비하는 내분비샘이다. 고환에서 분비되는 남성호르몬은 정자생성과 생식기의 발달 및 유지에 필수적인 역할을 하므로 남성생식기능의 원천은 고환에 있다고 볼 수 있다. 2.여성생식계통: 여성생식기는 난자를 생성하는 난소와 난자를 자궁으로 운반하는 난관, 그리고 자궁과 질로 이루어져 있으며 외분비선인 바르톨린샘를 갖추고 있다. 난소는 난자를 생성하는 생식샘인 동시에 여성호르몬을 분비케하는 내분비샘이다. 월경주기 전반부에 난자를 생성시키기위해 성숙되고 있는 난포에서 분비되는 에스트로겐은 여성 2차 성징의 발달을 관장할 뿐 아니라 자궁내막을 장차 수정될 수정란이 착상하기에 알맞은 상태로 만들어준다. 난자가 분비되고 남은 황체에서 분비되는 푸로게스테론은 자궁내막을 붓도록 하면 분비액을 증가시키며 자궁근의 수축을 방해하여 임신시 임신을 지속시키는 역할을 한다. |
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| CNS-L | central nervous system leukemia |
|---|---|
| GANS | granulomatous angiitis of the nervous system |
| NS | natural science; Neosporin; nephrosclerosis; nephrotic syndrome; nervous system; neurological surger... |
| SNS | Senior Nursing Sister; Society of Neurological Surgeons; sympathetic nervous system |
| MDS | Master of Dental Surgery; maternal deprivation syndrome; medical data screening; medical data system... |
| enteric nervous system | Two ganglionated neural plexuses in the gut wall which form one of the three major divisions of the autonomic nervous system. The enteric nervous system innervates the gastrointestinal tract, the pancreas, and the gallbladder. It contains sensory neurons, interneurons, and motor neurons. Thus the circuitry can autonomously sense the tension and the chemical environment in the gut and regulate blood vessel tone, motility, secretions, and fluid transport. The system is itself governed by the central nervous system and receives both parasympathetic and sympathetic innervation. (12 Dec 1998) |
|---|---|
| inborn lysosomal disease | Inherited disorder of one or more degradative enzymes normally located in lysosomes leading to accumulation (storage) of abnormal quantities of a substance, such as a glycosaminoglycan as in Hurler's syndrome or a lipopolysaccharide as in Gaucher's disease. (05 Mar 2000) |
| UDP-N-acetylglucosamine-lysosomal-enzyme-N-acetylglucosaminephosphotransferase | <enzyme> Fibroblasts from patients with i-cell (mucolipidosis II) and pseudo-hurler polydystrophy (mucolipidosis III) are deficient in above enzyme; for n-acetylglucosamine transferred to dolichyl phosphate see EC 2.7.8.15 Registry number: EC 2.7.8.17 Synonym: udpgnac gp gnac phosphotransferase, udpgnac phosphotransferase, uridine 5'-diphosphate-n-acetylglucosamine glycoprotein n-acetylglucosaminylphosphotransferase, n-acetylglucosamine-1-phosphotransferase, n-agapt, udp-n-acetylglucosamine-lysosomal glycoprotein n-acetylglucosaminylphosphotransferase, udp-acetylglucosamine-glycoprotein n-acetylglucosamine-1-phosphotransferase (26 Jun 1999) |
| UDP-N-acetylglucosamine:lysosomal enzyme N-acetylglucosaminyl-1-phosphotransferase | <enzyme> An enzyme that participates in the posttranslational modification of a number of lysosomal proteins; a deficiency or defect in this enzyme results in two forms of mucolipidoses, I-cell disease, and pseudo-Hurler polydystrophy. (05 Mar 2000) |
| lysosomal disease | A disease due to inadequate functioning of a lysosomal enzyme; most such disease's are associated with a storage disease. (05 Mar 2000) |
| lysosomal enzyme | <biochemistry> A range of degradative enzymes, most of which operate best at acid pH. The best known marker enzymes are acid phosphatase and glucuronidase, but many others are known. (18 Nov 1997) |
| brancher glycogen storage disease | 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) |
| glycogen storage disease | <hepatology> A group of inherited metabolic disorders involving the enzymes responsible for the synthesis and degradation of glycogen. In some patients, prominent liver involvement is presented. In others, more generalised storage of glycogen occurs, sometimes with prominent cardiac involvement. Synonym: glycogenosis (12 Sep 2002) |
| glycogen storage disease type I | <disease> An autosomal recessive disease in which gene expression of glucose-6-phosphatase is absent, resulting in hypoglycaemia due to lack of glucose production. Accumulation of glycogen in liver and kidney leads to organomegaly, particularly massive hepatomegaly. Increased concentrations of lactic acid and hyperlipidemia appear in the plasma. Clinical gout often appears in early childhood. Inheritance: autosomal recessive. (12 Dec 1998) |
| glycogen storage disease type II | <disease> Glycogenosis due to alpha-1,4-glucosidase (acid maltase) deficiency. It affects muscle, heart, and other organs. (12 Dec 1998) |
| glycogen storage disease type III | <disease> An autosomal recessive metabolic disorder due to deficient expression of amylo-1,6-glucosidase (one part of the glycogen debranching enzyme system). The clinical course of the disease is similar to that of glycogen storage disease type I, but milder. Massive hepatomegaly, which is present in young children, diminishes and occasionally disappears with age. Levels of glycogen with short outer branches are elevated in muscle, liver, and erythrocytes. Six subgroups have been identified, with subgroups type IIIa and type IIIb being the most prevalent. Inheritance: autosomal recessive (12 Dec 1998) |
| glycogen storage disease type IV | <disease> An autosomal recessive metabolic disorder due to a deficiency in expression of branching enzyme (alpha-1,4-glucan-6-alpha-glucosyltransferase), resulting in an accumulation of abnormal glycogen with long outer branches. Clinical features are muscle hypotonia and cirrhosis. Death from liver disease usually occurs before age 2. Inheritance: autosomal recessive (12 Dec 1998) |
| glycogen storage disease type V | <disease> Glycogenosis due to muscle phosphorylase deficiency. Characterised by painful cramps following sustained exercise. Inheritance: autosomal recessive (12 Dec 1998) |
| glycogen storage disease type VI | <disease> A hepatic glycogen storage disease in which there is an apparent deficiency of hepatic phosphorylase activity. However, studies have not been able to distinguish between phosphorylase deficiency and phosphorylase kinase deficiency in patients with hepatic glycogenosis. (12 Dec 1998) |
| glycogen storage disease type VII | <disease> An autosomal recessive muscle glycogen storage disease in which there is deficient expression of muscle phosphofructokinase activity, resulting in increased concentrations of glucose-6-phosphate and fructose-6-phosphate and low concentrations of fructose-1,6-diphosphate in muscle tissue. Glycogen storage in muscle is increased, perhaps due to activation of glycogen synthase by accumulated glucose-6-phosphate. It has been proposed that shunting of glucose-6-phosphate and fructose-6-phosphate into the pentose phosphate pathway may result in increased synthesis of purines and pyrimidines, causing hyperuricaemia and gout. Erythrocytes from patients may show decreased phosphofructokinase activity and 2,3-diphosphoglycerate deficiency. Exercise intolerance is present and severe congenital muscular dystrophy has been reported. Inheritance: autosomal recessive (12 Dec 1998) |