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  • ¿µ¹®
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  • competitive inhibitor
    °æÀï¾ïÁ¦Á¦
  • complement inhibitor
    º¸Ã¼¾ïÁ¦Á¦, µµ¿òü¾ïÁ¦Á¦
  • carbonic anhydrase inhibitor
    ź»êÅ»¼öÈ¿¼Ò¾ïÁ¦Á¦
  • converting enzyme inhibitor
    Àüȯȿ¼Ò¾ïÁ¦Á¦
  • corrosion inhibitor
    ºÎ½Ä¾ïÁ¦Á¦
  • enzyme inhibitor
    È¿¼Ò¾ïÁ¦Á¦
  • inhibitor
    1. ¾ïÁ¦Á¦ 2. ¾ïÁ¦ÀÎÀÚ
  • mitotic inhibitor
    À¯»çºÐ¿­¾ïÁ¦Á¦
  • metabolic inhibitor
    ´ë»ç¾ïÁ¦Á¦
  • oocyte maturation inhibitor
    ³­ÀÚ¼º¼÷¾ïÁ¦ÀÎÀÚ
  • polymerization inhibitor
    ÁßÇÕ¾ïÁ¦Á¦
  • protease inhibitor
    ´Ü¹éÁúºÐÇØÈ¿¼Ò¾ïÁ¦Á¦
  • particle-enhanced turbidimetric inhibitor
    ÀÔÀÚÁõ´ëȥʾïÁ¦Á¦
  • specific inhibitor
    ƯÀ̾ïÁ¦Á¦
  • specific serotonin reuptake inhibitor
    ƯÀ̼¼·ÎÅä´ÑÀçÈí¼ö¾ïÁ¦Á¦
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  • coagulation factor inhibitor
    ÀÀ°íÀÎÀÚ¾ïÁ¦Á¦
  • competitive inhibitor
    °æÀï¾ïÁ¦Á¦
  • complement inhibitor
    º¸Ã¼¾ïÁ¦Á¦, µµ¿òü¾ïÁ¦Á¦
  • converting enzyme inhibitor
    Àüȯȿ¼Ò¾ïÁ¦Á¦
  • corrosion inhibitor
    ºÎ½Ä¾ïÁ¦Á¦
  • enzyme inhibitor
    È¿¼Ò¾ïÁ¦Á¦
  • inhibitor
    ¾ïÁ¦Á¦
  • inhibitor substance
    ¾ïÁ¦¹°Áú
  • metabolic inhibitor
    ´ë»ç¾ïÁ¦Á¦
  • mitotic inhibitor
    Çٺп­¾ïÁ¦Á¦
  • oocyte maturation inhibitor
    ³­ÀÚ¼º¼÷¾ïÁ¦ÀÎÀÚ
  • particle-enhanced turbidimetric inhibitor
    ÀÔÀÚÁõ´ëȥʾïÁ¦Á¦
  • polymerization inhibitor
    ÁßÇÕ¾ïÁ¦Á¦
  • protease inhibitor
    ´Ü¹éºÐÇØÈ¿¼Ò¾ïÁ¦Á¦
  • specific inhibitor
    ƯÀ̾ïÁ¦Á¦
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  • ¿µ¹®
    ÇѱÛ
  • heat of activation
    Ȱ¼ºÈ­¿­(üÀàõûýæð)
  • photochemical activation
    ±¤È°¼ºÈ­(Ë´Ì· ËÛÌ´).
  • polyclonal B cell activation
    B¼¼Æ÷ ´Ù(¼ö)Ŭ·ÐȰ¼º, B¼¼Æ÷ ¿©·¯¹«¸®È°¼º
  • polyclonal activation
    ´Ù(¼ö)Ŭ·ÐȰ¼º, ¿©·¯¹«¸®È°¼º
  • ACEI : angiotensin converting enzyme inhibitor
    ¾ÈÁö¿ÀÅÙ½ÅÀüȯȿ¼Ò¾ïÁ¦Á¦(ï®ü½ý£áÈåäð¤ð¥).
  • CAI=£¾carbonic anhydrase inhibitor
    ź»êÅ»¼öÈ¿¼ÒÀúÇØ¾à, ź»êÅ»¼öÈ¿¼ÒÀúÇØ¹°Áú.
  • Inhibitor substance
    ¾ïÁ¦¹°Áú(åäð¤Úªòõ)
  • MAO inhibitor
    ¸ð³ë¾Æ¹Î»êÈ­È¿¼Ò ¾ïÁ¦Á¦.
  • MAO inhibitor
    ¸ð³ë¾Æ¹Î »êÈ­È¿¼Ò ÀúÇØÁ¦.
  • MAO inhibitor(MAOI)
    ´Ü°¡¾Æ¹Î»êÈ­È¿¼Ò¾ïÁ¦Á¦
  • RIMA, see reversible inhibitor of MAO-A
    °¡¿ªÀû ´Ü°¡¾Æ¹Î-A »êÈ­È¿¼Ò¾ïÁ¦Á¦
  • acetylcholinesterase inhibitor
    ¾Æ¼¼Æ®Äݸ°¿¡½ºÅÍ·¹À̽º<¿¡½ºÅ×¶óÁ¦> ¾ïÁ¦Á¦.
  • activated protein C inhibitor
    Ȱ¼ºÈ­´Ü¹éÁú C ¾ïÁ¦Á¦
  • angiotensin converting enzyme inhibitor
    ¾ÈÁö¿ÀÅٽŠÀüȯȿ¼Ò ¾ïÁ¦¹°Áú<¾à>.
  • anti-inhibitor coagulation complex
    Ç×¾ïÁ¦Á¦ÀÀ°í°áÇÕü
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    ÇѱÛ
  • activation, polyclonal B cell
    ´Ù¼¼Æ÷±º B¼¼Æ÷Ȱ¼º, ¿©·¯¹«¸® B¼¼Æ÷Ȱ¼º
  • c3, activation
    C3, Ȱ¼º (¡­üÀàõ)
  • complement activation
    º¸Ã¼È°¼ºÀÛ¿ë(¡­üÀàõíÂéÄ), º¸Ã¼È°¼ºÈ­.
  • complement activation
    º¸Ã¼È°¼ºÀÛ¿ë
  • energy of activation
    Ȱ¼ºÈ­¿¡³ÊÁö.
  • heat of activation
    Ȱ¼ºÈ­¿­(üÀàõûýæð)
  • islet-activation factor
    ¶û°Ô¸£Çѽº»ù Ȱ¼ºÀÎÀÚ, ¹éÀÏÇØ±Õµ¶¼Ò
  • macrophage,activation of
    Ȱ¼ºÈ­(üÀàõûù)
  • neutron activation analysis
    Áß¼ºÀÚ¹æ»çÈ­ºÐ¼®(~Û¯ÞÒûùÝÂà°).
  • photochemical activation
    ±¤È°¼ºÈ­(Ë´Ì· ËÛÌ´).
  • polyclonal B cell activation
    B¼¼Æ÷ ´Ù(¼ö)Ŭ·ÐȰ¼º, B¼¼Æ÷ ¿©·¯¹«¸®È°¼º
  • polyclonal activation
    ´Ù(¼ö)Ŭ·ÐȰ¼º, ¿©·¯¹«¸®È°¼º
  • sleep activation
    ¼ö¸éºÎȰ(¹ý)(¡­Ý¥üÀÛö) ³úÆÄ(Òà÷î)ÀÇ .
  • thermal activation
    ¿­È°¼ºÈ­¹ÝÀÀ(æðüÀàõûù Úãëë).
  • tissue plasminogen activation
    Á¶Á÷ ÇöóÁî¹Ì°Õ Ȱ¼º
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  • reciprocal activation
    »óº¸ Ȱ¼ºÈ­(ßÓÜÍüÀàõûù)
  • upstream activation sites
    À­ÂÊ È°¼ºÈ­(üÀàõûù)ÀÚ¸®
  • active site-directed irreversible inhibitor
    Ȱ¼º(üÀàõ)ÀÚ¸®ÁöÇâÀû ºÒ°¡¿ªÀúÇØÁ¦(ò¦ú¾îÜÝÕʦæ½îÁúªð¥)
  • Bowman-Birk inhibitor
    "º¸¿ì¸¸-¹÷Å© ÀúÇØÀÚ(îÁúªí­), º¸¿ì¸¸-¹÷Å© ÀúÇØÁ¦(îÁúªð¥)"
  • competitive inhibitor
    °æÇÕÀúÇØÁ¦(ÌæùêîÁúªð¥)
  • enzyme-inhibitor complex
    È¿¼Ò-ÀúÇØÁ¦ º¹ÇÕü (ý£áÈîÁúªð¥ÜÜùêô÷)
  • heme-controlled inhibitor
    Èû-Á¦¾î(ð¤åÙ) ÀúÇØÁ¦(îÁúªð¥)
  • inhibitor
    ÀúÇØÁ¦(îÁúªð¥)
  • inhibitor constant
    ÀúÇØÁ¦»ó¼ö(îÁúªð¥ßÈâ¦)
  • irreversible inhibitor
    ºñ°¡¿ª ÀúÇØÁ¦(ުʦæ½îÁúªð¥)
  • Kunitz inhibitor
    Äï´ÏÃ÷ ÀúÇØÁ¦(îÁúªð­)
  • mixed-type inhibitor
    È¥ÇÕÇü ÀúÇØÁ¦(ûèùêúþîÁúªð¥)
  • noncompetitive inhibitor
    ºñ°áÇÕ ÀúÇØÁ¦(ު̿ùêîÁúªðº)
  • ovulation inhibitor
    ¹è¶õ ÀúÇØÁ¦(ÛÉÕ°îÁúªð¥)
  • respiratory inhibitor
    È£Èí ÀúÇØÁ¦(îÁúªð¥)
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PTI pancreatic trypsin inhibitor; persistent tolerant infection; Pictorial Test of Intelligence; placent...
STI Scientific and Technical Information; serum trypsin inhibitor; soybean trypsin inhibitor; systolic t...
RAS   1) Reticular Activating(Activation) System
  2) Renal Artery Stenosis
VAT   1) Ventricular Activation Time
  2) Video-Assisted Thoracoscopy
ADR activation, depression, repetition [in bone remodeling]; adrenodoxin reductase; Adriamycin; adverse ...
KMLE ÀÚµ¿ÃßÃâ ÀÇÇоà¾î »çÀü À¯»ç °Ë»ö °á°ú : 5 ÆäÀÌÁö: 2
PI Plasmin inhibition
PAP Plasmin-alpha2-antiplasmin complex
PAP Plasmin-antiplasmin complexes
PL plasmin
PAP plasmin-alpha 2 antiplasmin
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    ¼³¸í
  • coagulation factor inhibitor
    ÀÀ°í ÀÎÀÚ ¾ïÁ¦Á¦
  • collagenase inhibitor
    Äݶó°Ô³ªÁ¦ ¾ïÁ¦ ¹°Áú
  • cyclooxygenase inhibitor
    »çÀÌŬ·Î¿Á½ÃÁö³×ÀÌÁî ¾ïÁ¦Àç
  • dopa decarboxylase inhibitor
    µµÆÄ µ¥Ä«¸£º¹½Ç·¹À̽º ¾ïÁ¦ÀÚ
  • lipoxygenase inhibitor
    ¸®ÆÜ½ÃÁö³×À̽º ¾ïÁ¦Á¦
  • metabolic inhibitor
    ´ë»ç ÀúÇØÁ¦, ´ë»ç ¾ïÁ¦Á¦
  • polymerization inhibitor
    ÁßÇÕ ±ÝÁöÁ¦
    ÁßÇÕ ¹ÝÀÀÀ» ¹æÇØÇϱ⵵ Çϰí, ÁßÁöÇÒ ¼ö ÀÖ´Â ¹°Áú.
  • virus hemagglutination inhibitor
    ¹ÙÀÌ·¯½º ÀûÇ÷±¸ ÀÀÁý¹ÝÀÀ ¾ïÁ¦ ÀÎÀÚ
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neutrophil activation The process in which the neutrophil is stimulated by diverse substances, resulting in degranulation and/or generation of reactive oxygen products, and culminating in the destruction of invading pathogens. The stimulatory substances, including opsonised particles, immune complexes, and chemotactic factors, bind to specific cell-surface receptors on the neutrophil.
(12 Dec 1998)
EEG activation The low voltage, fast pattern of attentive wakefulness.
(05 Mar 2000)
trans-activation (genetics) Increased rate of gene expression directed by either viral or cellular proteins. These regulatory factors (diffusible gene products) act in trans -- that is, act on homologous or heterologous molecules of DNA. (cis-acting factors act only on homologous molecules.)
(12 Dec 1998)
energy of activation Energy that must be added to that already possessed by a molecule or molecules in order to initiate a reaction; usually expressed in the Arrhenius equation relating a rate constant to absolute temperature.
(05 Mar 2000)
enzyme activation Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1) activation by ions (activators); 2) activation by cofactors (coenzymes); and 3) conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
(12 Dec 1998)
juxtacrine activation Activation of target cells by membrane anchored growth factors, also used for activation of leucocytes by PAF bound to endothelial cell surface.
(18 Nov 1997)
feedback activation The activation of an enzyme by an end product of a biochemical pathway in which that enzyme plays a part. For example, the activation of factors VIII and V by thrombin during blood clotting.
(05 Mar 2000)
feed-forward activation The activation of an enzyme by a precursor of the substrate of that enzyme.
(05 Mar 2000)
upstream activation site A DNA sequence that regulates transcription like an enhancer but does notwork if its located downstream from a promoter.
(09 Oct 1997)
low-activation materials <radiobiology> In fission reactors, one is forced to deal with the radioactive byproducts of the fission process, but in fusion reactors one generally has a choice of what materials to expose to neutrons produced by the fusion process. A major problem for fusion reactors is developing materials (such as for the reactor vacuum vessel structure) which can be exposed to high levels of neutron bombardment without becoming permanently radioactive. Candidate structural materials which have relatively low induced radiactivation (generally relative to stainless steel) are known as low-activation materials, these include titanium, vanadium, and silicon-carbide.
(09 Oct 1997)
lymphocyte activation <haematology> The change in morphology and behaviour of lymphocytes exposed to a mitogen or to an antigen to which they have been primed. The result is the production of lymphoblasts, cells that are actively engaged in protein synthesis and that divide to form effector populations. Should not be confused with transformation of the type associated with oncogenic viruses and activation is therefore perhaps a better term.
(18 Nov 1997)
a1-trypsin inhibitor A glycoprotein that is the major protease inhibitor of human serum, is synthesised in the liver, and is genetically polymorphic due to the presence of over 20 alleles; individuals appropriately homozygous are deficient in a1-trypsin and are predisposed to pulmonary emphysema and juvenile hepatic cirrhosis because of alterations in the amino acid and sialic acid components of the glycoprotein. A1-Antitrypsin also inhibits thrombin.
Synonym: a1-trypsin inhibitor, human a1-proteinase inhibitor.
(05 Mar 2000)
ACE inhibitor <pharmacology> A group of antihypertensive medications that work by inhibiting an enzyme (angiotensin-converting enzyme) that is important in the regulation of blood pressure.
Studies have also indicated that it may help prevent or slow the progression of kidney disease in patients with diabetes.
Examples include: captopril, ramipril, enalapril, losartan potassium, bepridil and lisinopril.
(12 Mar 1998)
aldose reductase inhibitor <pharmacology> A class of drugs being studied as a way to prevent eye and nerve damage in people with diabetes.
Aldose reductase is an enzyme that is normally present in the eye and in many other parts of the body. It helps change glucose (sugar) into a sugar alcohol called sorbitol. Too much sorbitol trapped in eye and nerve cells can damage these cells, leading to retinopathy and neuropathy.
Drugs that prevent or slow (inhibit) the action of aldose reductase are being studied as a way to prevent or delay these complications of diabetes.
(09 Oct 1997)
angiotensin-converting enzyme inhibitor <pharmacology> A class of drugs used in the treatment of hypertension and heart failure.
They exert their haemodynamic effect mainly by inhibiting the renin-angiotensin system and produce a reduction of peripheral arterial resistance. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility.
(14 Aug 2000)
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