| ¿µ¹® | protein | ÇÑ±Û | ´Ü¹éÁú |
|---|---|---|---|
| ¼³¸í | ź¼Ò, ¼ö¼Ò, »ê¼Ò, Áú¼Ò, ȲÀ» ÇÔÀ¯Çϰí ÀÖ´Â À¯±âÈÇÕ¹°·Î, ¸ðµç ¼¼Æ÷ÀÇ ¿øÇüÁúÀ» ÀÌ·ç°í ÀÖ´Â ±âº» ±¸¼º¹°ÁúÀÌ´Ù. ´Ü¹éÁúÀº ±× ´ÜÀ§ÀÎ ¾Æ¹Ì³ë»êµéÀÌ ÆéƼµå°áÇÕ¿¡ ÀÇÇØ °áÇյǾî ÀÖÀ¸¸ç, º¸Åë 20°³ÀÇ ¾Æ¹Ì³ë»êµéÀÌ ´Ù¸¥ ¼ø¼¿Í Á¶¼ºÀ» °¡Áö°í ¹è¿µÇ¾î, µ¶Æ¯ÇÑ ÇϳªÀÇ ´Ü¹éÁúÀ» Çü¼ºÇÏ°Ô µÈ´Ù. |
||
| ¿µ¹® | testicular feminization syndrome | ÇÑ±Û | °íȯ¿©¼ºÈÁõÈıº |
|---|---|---|---|
| ¼³¸í | ÀÌÂ÷¼ºÀåÀ» Æ÷ÇÔÇÏ¿©, ¿Ü¼º±âÀÇ ¹ßÀ°Àº ¿©¼ºÀÌÁö¸¸ °íȯÀÌ Á¸ÀçÇϰí, Àڱðú ÀڱðüÀÌ °áÇ̵Ǿî ÀÖ´Â ³²¼º °ÅÁþ³²³àÇѸöÁõÀÇ ±Ø´ÜÀû ÇüÅÂÀÌ´Ù. À̰ÍÀº Å×½ºÅ佺Å×·ÐÀÇ ÀÛ¿ë¿¡ ´ëÇÑ ¸»´Ü±â°üÀÇ ÀúÇ׿¡ ±âÀÎÇÑ´Ù. |
||
| ¿µ¹® | irritable bowel syndrome | ÇÑ±Û | °ú¹Î¼º´ëÀåÁõÈıº |
|---|---|---|---|
| ¼³¸í | ¹èº¯Àå¾Ö, º¹Åë, º¹ºÎÆØ¸¸ µîÀÇ Áõ»óÀÌ ÀÖÀ¸³ª ±âÁúÀûÀÎ º´º¯ÀÌ ¾øÀ½ÀÌ È®ÀÎµÈ ¿¹¸¦ ÃѸÁ¶óÇÑ ÀÓ»ó ÁõÈıºÀÌ´Ù. °¡Àå ÈçÇÑ ¼Òȱâ ÁúȯÀ̸ç(Àü¼Òȱâ ȯÀÚÀÇ 70~80%) °¡Àå ÈçÇÑ Áúº´(Àüü Àα¸ÀÇ ¾à 20%)ÀÌ´Ù. ¿©¼ºÀÌ ³²¼º¿¡ ºñÇØ 2¹è Á¤µµ ¸¹ÀÌ ¹ß»ýÇϸç 30´ë ¹× 40´ë¿¡¼ È£¹ßÇÏ°í ¼±Áø °ø¾÷±¹¿¡¼ ¸¹ÀÌ ¹ß»ýÇÑ´Ù. Áø´ÜÀ» À§Çؼ´Â º´·Â ûÃë°¡ °¡Àå Áß¿äÇÏ°í °¢Á¾ °Ë»ç·Î¼ ±âÁúº´À» Á¦¿ÜÇØ¾ß ÇÑ´Ù. Ä¡·á·Î´Â ¾ÈÁ¤¿ä¹ý(Á¤½Å°úÀû ¸é´ã ¹× ½É¸®¿ä¹ý, ½Å°æ¾ÈÁ¤Á¦), ½Ä»ç¿ä¹ý(°í¼¶À¯Áú À½½Ä ¼·Ãë, Àڱؼº À½½Ä ÇÇÇϱâ), ¾à¹° ¿ä¹ý(âÀÚ°æ·Ã ÁøÁ¤Á¦, º¯ºñ ¿ÏÈÁ¦, Áö»çÁ¦) µîÀ» »ç¿ëÇÑ´Ù. |
||
| ¿µ¹® | withdrawal syndrome | ÇÑ±Û | ±Ý´ÜÁõÈı٠|
|---|---|---|---|
| ¼³¸í | ¾ËÄÚ¿Ã, ¸¶¾à, ¹ÙºñÅõ¸£»ê°è ÃÖ¸é¾à µîÀÇ ¾à¹°À» Àå±â°£ º¹¿ëÇÏ¿© ¾à¹°ÀÌ ¾øÀÌ´Â °ßµô ¼ö ¾ø°ÔµÈ µÚ, ±× ¾à¹°À» ÁßÁöÇÑ °æ¿ì¿¡ ³ªÅ¸³ª´Â, °íÅëÀÌ ¼ö¹ÝµÇ´Â ½ÅüÀû Áõ»óÀ» ¸»ÇÑ´Ù. ¿¬¼Ó º¹¿ëÀÇ ±â°£¿¡ µû¶ó Áõ»óÀÌ ¹«°Å¿öÁø´Ù. Åë»óÀûÀ¸·Î ±¸Åä, ¼³»ç, Ç÷¾Ð»ó½Â, ºü¸¥¸Æ, ¶¡³², È¥¼ö µîÀÇ Áõ»óÀÌ ³ªÅ¸³´Ù. |
||
| ¿µ¹® | organic brain syndrome | ÇÑ±Û | ±âÁúÀû ³úÁõÈıº |
|---|---|---|---|
| ¼³¸í | ³úÀÇ ±âÁúÀûÀÎ(organic-:ÀÌ ¸»Àº ±â´ÉÀûÀÎ(functional)¿¡ ¹ÝÇÏ´Â ¸»·Î½á) ¸ðµç °Ë»ç¸¦ ½ÃÇàÇÏ¸é ¾î¶² ÀÌ»óÀ» ¹ß°ßÇÒ ¼ö ÀÖ´Ù´Â ¶æÀÌ´Ù. ¹Ù²Ù¾î ¸»Çϸé, ±â´ÉÀûÀÎ ÀÌ»ó¿¡ ÀÇÇÑ ³úÁõÈıºÀº ¾î¶°ÇÑ °Ë»ç·Îµµ ÀÌ»óÀ» ¹ß°ßÇÒ ¼ö ¾øÀ¸³ª ºÐ¸íÈ÷ ȯÀÚ¿¡°Ô ÀÌ»óÁõ»óÀÌ ³ªÅ¸³µÀ» ¶§ À̸¦ ¹¾î¼ ¸»ÇÑ´Ù. ÀÌ»ó¿¡ ÀÇÇØ ½Å°æÇÐÀûÀÎ ÀÌ»óÀ» ³ªÅ¸³»´Â ÀÏ·ÃÀÇ º´ÀûÇö»óÀ» ¸ðµÎ ÅëÆ²¾î ¸»ÇÑ´Ù. ÀÌ º´Àº ÈçÈ÷ º¸¾Æ ¸¶Ä¡ Á¤½Åº´È¯ÀÚó·³ ¸»À» Ⱦ¼³¼ö¼³Çϰí, ¾Ë¾ÆµéÀ» ¼ö ¾ø´Â ¸»À» Çϸç, ¶§·Î´Â ´Ù¸¥ »ç¶÷¿¡°Ô °ø°ÝÀûÀÎ ¼ºÇâÀ» ³ªÅ¸³»±âµµ ÇÑ´Ù. ±×¸®°í ´Ù¸¥ »ç¶÷°ú µµÀúÈ÷ ±³·ù¸¦ ÇÒ ¼ö ¾ø´Â Á¤¼¸¦ ³ªÅ¸³»±âµµ ÇÑ´Ù. ±×·¯³ª, ÀÌ º´ÀÌ ´Ù¸¥ Á¤½Åº´°ú ±¸º°µÇ´Â Ư¡ÀûÀÎ Áõ»óÀº ¸ÕÀú, ÀǽÄÀÇ È¥Å¹ÀÌ µ¿¹ÝµÇ´Â °æ¿ì°¡ ¸¹°í, ¶ÇÇÑ ±× Áõ»óÀÇ Á¤µµ°¡ º¯ÇÑ´Ù´Â °ÍÀÌ´Ù. Áï, ¾ÆÄ§¿¡´Â Á¤»óÀûÀÎ ÇൿÀ» ÇÏ´Ù°¡ ¿ÀÈİ¡ µÇ¸é, ÀǽÄÀÌ Èå·ÁÁö¸é¼ ¸»À» Ⱦ¼³¼ö¼³ÇÑ´Ù¸é, ÀÌ´Â ±âÁú¼º³úÁõÈıºÀÏ °¡´É¼ºÀÌ ³ô´Ù. |
||
| LNP | large neuronal polypeptide |
|---|---|
| NCL | neuronal ceroid-lipofuscinosis; nucleolin |
| SCN1A | sodium channel, neuronal alpha-subunit type 1 |
| MS | Maffuci syndrome; maladjustment score; mandibular series; Marfan syndrome; Marie-Strumpell [syndrome... |
| PPS | Personal Preference Scale; physician, patient and society [course]; polyvalent pneumococcal polysacc... |
| NAIP | Neuronal Apoptosis Inhibitor Protein |
|---|---|
| DND | Delayed neuronal death |
| INCL | Infantile neuronal ceroid lipofuscinosis |
| IND | Intestinal Neuronal Dysplasia |
| JNCL | Juvenile neuronal ceroid lipofuscinosis |
| adrenergic neuronal blocking agent | A drug that prevents the release of norepinephrine from sympathetic nerve terminals; it does not inhibit the responses of the adrenergic receptors to circulating epinephrine, norepinephrine, and other adrenergic amines. (05 Mar 2000) |
|---|---|
| cell adhesion molecules, neuronal | Surface ligands that mediate cell-to-cell adhesion and function in the assembly and interconnection of the vertebrate nervous system. These molecules promote cell adhesion via a homophilic mechanism. These are not to be confused with ncam (neural cell adhesion molecule), now known to be expressed in a variety of tissues and cell types in addition to nervous tissue. (12 Dec 1998) |
| primary neuronal degeneration | <disease> A progressive, neurodegenerative disease characterised by loss of function and death of nerve cells in several areas of the brain leading to loss of cognitive function such as memory and language. The cause of nerve cell death is unknown but the cells are recognised by the appearance of unusual helical protein filaments in the nerve cells (neurofibrillary tangles) and by degeneration in cortical regions of brain, especially frontal and temporal lobes. Alzheimer's disease is the most common cause of dementia. (22 May 1997) |
| neuronal | <anatomy> Pertaining to a neuron or neurons (= conducting cells of the nervous system). (18 Nov 1997) |
| neuronal ceroid-lipofuscinosis | A heritable lipidosis with cytoplasmic inclusions staining for ceroid and lipofuscin. Clinically the patient has progressive dementia, retinal degeneration, seizures, and myoclonic jerks. It was formerly thought to be related to tay-sachs disease but the biochemical defect is as yet undetermined. Named according to age of onset: jansky-bielschowsky disease, 2-4 years; batten-spielmeyer-vogt disease, 5-11 years; and kufs disease, adult. (12 Dec 1998) |
| neuronal differentiation | Acquisition during development of specific biochemical, physiological and morphological properties by nerve cells. (18 Nov 1997) |
| neuronal guidance | <cell biology> General term for mechanisms that ensure correct projections by nerve cells in developing and regenerating nervous systems. Implies accurate navigation by growth cones, the highly motile tips of growing neuronal processes. See: growth cone collapse. (12 Mar 1998) |
| neuronal hyperplasia | Increased numbers of ganglion cells with myenteric plexus hyperplasia and increased acetylcholinesterase activity in nerves of the mucosa and submucosa. Clinically, neuronal hyperplasia mimics Hirschprung's disease. Similar findings are seen in patients with multiple endocrine neoplasia syndrome, type IIB, and in neurofibromatosis. Synonym: hyperganglionosis, neuronal intestinal dysplasia. (05 Mar 2000) |
| neuronal intestinal dysplasia | Increased numbers of ganglion cells with myenteric plexus hyperplasia and increased acetylcholinesterase activity in nerves of the mucosa and submucosa. Clinically, neuronal hyperplasia mimics Hirschprung's disease. Similar findings are seen in patients with multiple endocrine neoplasia syndrome, type IIB, and in neurofibromatosis. Synonym: hyperganglionosis, neuronal intestinal dysplasia. (05 Mar 2000) |
| neuronal plasticity | Ability of nerve cells to change their properties for example by sprouting new processes, making new synapses or altering the strength of existing synapses. See: long-term potentiation. (18 Nov 1997) |
| neuronal polarity | Distribution of specific functions to discrete cellular domains: for example axons and dendrites that have different molecular composition, morphology and ultrastructure and perform different functions. (18 Nov 1997) |
| infantile neuronal degeneration | <neurology, paediatrics> Degenerative disorder of infants with widespread neuronal loss in thalamus, cerebellum, pons, and spinal cord, resembling infantile muscular atrophy. (05 Mar 2000) |
| acetoacetyl-acyl carrier protein synthase | <enzyme> E coli enzyme, that catalyses condensation of malonyl-acyl carrier protein plus acetyl-acyl carrier protein; not inhibited by cerulenin Registry number: EC 2.3.1.- Synonym: acetoacetyl-acp synthase (26 Jun 1999) |
| acid soluble spore protein | <molecular biology> A DNA binding protein in the spores of some bacteria, thought to stabilise the DNA in an A configuration, so protecting it from cleavage by enzymes or UV light. (18 Nov 1997) |
| acute-phase protein | <haematology> These plasma proteins (in addition to fibrinogen) increase 25% or more in response to inflammation and injury are under direct control of interleukin-6 (IL-6) (hepatocyte-stimulating factor). Other proteins which increase are ceruloplasmin, C3 and C4 which increase 50% or more; alpha-1 acid glycoprotein, alpha-1 antitrypsin, haptoglobin and fibrinogen (the major determinant of viscosity 1 ) which increase two- to fourfold; C-reactive protein (CRP) and serum amyloid A which increase several hundred-fold. Despite long-held clinical opinion to the contrary, available data indicate that neither ESR nor measurement of specific acute-phase reactants are useful in excluding underlying infection or inflammation regardless of the pretest probability. These proteins are secreted into the blood in increased or decreased quantities by hepatocytes in response to trauma, inflammation, or disease. They can serve as inhibitors or mediators of the inflammatory processes. Certain acute-phase proteins have been used to diagnose and follow the course of diseases or as tumour markers. See also: amyloid, c-reactive protein, erythrocyte sedimentation rate, viscosity. (25 Jun 1999) |
Synonyms : N-WASP Wiskott-Aldrich Syndrome Protein, WASL Wiskott-Aldrich Syndrome Protein, Wiskott-Aldrich Syndrome Gene-Like Protein, N WASP Protein, N WASP Wiskott Aldrich Syndrome Protein, Neuronal Wiskott Aldrich Syndrome Protein
Á¦Ç°¸í |
ÆÇ¸Å»ç |
º¸ÇèÄÚµå | ¼ººÐ/ÇÔ·® | ±¸ºÐ/º¸Çè±Þ¿© |
|---|
Á¦Ç°¸í |
ÆÇ¸Å»ç |
º¸ÇèÄÚµå | ¼ººÐ/ÇÔ·® | ±¸ºÐ/º¸Çè±Þ¿© |
|---|