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3) ¸ÞÅ䯮·º¼¼ÀÌÆ® : ºñ½ºÅ×·ÎÀ̵强 ¼Ò¿°ÁøÅëÁ¦(NSAIDs) ¹× »ì¸®½Ç»ê°úÀÇ º´¿ëÅõ¿©·Î ½Å¼¼´¢°ü¿¡¼ ¸ÞÅ䯮·º¼¼ÀÌÆ®ÀÇ ¹è¼³ÀÌ Áö¿¬µÇ¾î Ä¡¸íÀûÀÎ ¸ÞÅ䯮·º¼¼ÀÌÆ®ÀÇ Ç÷¾×ÇÐÀû µ¶¼ºÀÌ Áõ°¡µÉ ¼ö ÀÖÀ¸¹Ç·Î °í¿ë·®ÀÇ ¸ÞÅ䯮·º¼¼ÀÌÆ®(15mg/ÁÖ ÀÌ»ó)´Â ¾Æ½ºÇǸ°°ú º´¿ëÅõ¿©ÇÏÁö ¾ÊÀ¸¸ç º´¿ëÅõ¿©ÇÏ´Â °æ¿ì¿¡´Â Àú¿ë·®ÀÇ ¸ÞÅ䯮·º¼¼ÀÌÆ®¿Í ½ÅÁßÈ÷ Åõ¿©ÇÏ¿©¾ß ÇÑ´Ù.
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5) À̺ÎÇÁ·ÎÆæ, ³ªÇÁ·Ï¼¾ µî ÀϺΠºñ½ºÅ×·ÎÀ̵强 ¼Ò¿°ÁøÅëÁ¦(NSAIDs) : ÀÌ ¾à°ú º´¿ëÅõ¿©½Ã ¾Æ½ºÇǸ°¿¡ ÀÇÇÑ ºñ°¡¿ªÀû Ç÷¼ÒÆÇ ÀÀÁý¾ïÁ¦ ÀÛ¿ëÀÌ °¨¼ÒµÉ ¼ö ÀÖ´Ù. ÀÌ »óÈ£ÀÛ¿ëÀÇ ÀÓ»óÀû °ü·Ã¼ºÀº ¾Ë·ÁÁöÁö ¾Ê¾Ò´Ù. ½ÉÇ÷°ü°è Áúȯ¿¡ ´ëÇÑ À§ÇèÀÌ Áõ°¡µÈ ȯÀÚ¿¡°Ô ÀÌ ¾à°ú À̺ÎÇÁ·ÎÆæ, ³ªÇÁ·Ï¼¾ µî ÀϺΠºñ½ºÅ×·ÎÀ̵强 ¼Ò¿°ÁøÅëÁ¦(NSAIDs)¿Í º´¿ëÅõ¿©½Ã ¾Æ½ºÇǸ°ÀÇ ½ÉÇ÷°ü º¸È£ È¿°ú°¡ Á¦ÇÑµÉ ¼ö ÀÖ´Ù.
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8) µð°î½Å : ÀÌ ¾à°ú º´¿ëÅõ¿©½Ã ½ÅÀå ¹è¼³ÀÌ °¨¼ÒµÇ¾î µð°î½ÅÀÇ Ç÷Àå ³óµµ°¡ Áõ°¡ÇÒ ¼ö ÀÖ´Ù.
9) Àü½Å ÀÛ¿ë ºÎ½ÅÇÇÁúÈ£¸£¸ó Á¦Á¦(¾Öµð½¼º´ ´ëü¿ä¹ý¿ë È÷µå·ÎÄÚÆ¼¼Õ Á¦¿Ü) : ÀÌ ¾à°ú º´¿ë Åõ¿©½Ã »ì¸®½Ç»ê Á¦Á¦ÀÇ Ç÷Áß ³óµµ¸¦ °¨¼Ò½ÃŲ´Ù. º´¿ë Åõ¿©½Ã À§Àå ÃâÇ÷ ¹× ±Ë¾ç ¹ß»ýÀÌ Áõ°¡ÇÒ ¼ö ÀÖ´Ù.
10) ¾ÈÁö¿ÀÅٽŠÀüȯ È¿¼Ò ¾ïÁ¦Á¦(ACE inhibitor) : ÀÌ ¾àÀÇ °í¿ë·®°ú º´¿ë Åõ¿©½Ã Ç÷°üÈ®À强 ÇÁ·Î½ºÅ¸±Û¶õµòÀÇ ¾ïÁ¦·Î ÀÎÇØ »ç±¸Ã¼ ¿©°úÀ²ÀÌ °¨¼ÒÇϰí, Ç÷¾Ð °ÇÏ È¿°ú°¡ °¨¼ÒµÈ´Ù.
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[º´¿ë±Ý±â ¹× ¿¬·É´ë±Ý±â ±Ù°ÅÁ¶È¸]
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| º¸°ü»ó ÁÖÀÇ |
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| Á¶Á¦½Ã ÁÖÀÇ |
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°ü»óµ¿¸Æ ½ºÅÙÆ® »ðÀÔ¼ú ÈÄ Ç÷ÀüÁõ°ú Àç ÇùÂø ¹æÁö¸¦ ¸ñÀûÀ¸·Î Åõ¿©ÇÏ´Â Ç×Ç÷¼ÒÆÇ 3Á¦¿ä¹ý(aspirin, clopidogrel, cilostazol)ÀÇ ÀÎÁ¤¹üÀ§
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- ¡¯05.2.17: chest painÀ» ÁÖ È£¼Ò·Î ³»¿ø (¡®05.1.31 ÀÌÈÄ 3Â÷·Ê)
nature:squeezing, duration: 5min, agg. factor: µî»ê, °è´Ü ¿À¸¦ ¶§
relieving:resting, radiating pain(+): Lt arm, resting pain(-)
-¡®05.2.18: CAG & PCI(TherapeuticIntervention)
Lt - Lt main(body) : Discrete eccentric stenosis 80%
LCXand LAD : relatively good patency
Rt- No significant luminal stenosis
Balloon angioplasty with Aqua 3.5x15mm 8atm 10" after then suboptimalresult with RS 50%. Stent insertion with Driver 4.0x15mm 14atm 10"
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- ¡¯06.3.30: ³»¿ø 20ÀÏÀü resting½Ã 1½Ã°£ °¡·®ÀÇ chest pain ÀÖ¾úÀ¸¸ç ³»¿ø 1ÁÖÀÏ Àü chest painÀÌ ¼öÂ÷·Ê ÀÖ¾úÀ¸³ª NTG¿¡ response¸¦ º¸¿´°í ³»¿ø ´çÀÏ »õº® ÀÚ´Ù°¡ chest pain ÀÖ¾îÀÔ¿øÇÔ.
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Rt-No luminal stenosis
Balloon angioplasty with Aqua 2.5x20mm 4atm 4atm 6atm 10" Stent implantationwith Cypher 2.75x33mm 8atm 14atm 10" (stent indication : suboptimal resultwith RS 60%)
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¡á Âü°í
¡Û EBH Æò°¡º¸°í¼(2008.12.4)
¡Û ´ëÇѽÉÀåÇÐȸ Àǰß
¡Û Comparison of TripleVersus Dual Antiplatelet Therapy After Drug-Eluting Stent Implantation (fromthe DECLARE-Long trial) Lee SW, Am J Cardiol. 2007 Oct 1;100(7):1103-8
¡Û Reduced 6-monthresource use and costs associated with cilostazol in patients after successfulcoronary stent implantation: Results from the Cilostazol for RESTenosis (CREST)trial Zefeng Zhang, Am Heart J 2006;152:770-6
¡Û Triple Versus Dual Antiplatelet Therapy after Coronary Stenting-Impact on stent Thrombosis
Seung-Whab Lee, J Am CollCardiol 2005;46:1833-7
¡Û Coronary stentrestenosis in patients treated with cilostazol. Douglas JS Jr, Circulation. 2005; 112:2826-2832.
¡á ½ÉÀdz»¿ë
- °ü»óµ¿¸Æ½ºÅÙÆ®»ðÀÔ¼ú ÈÄ ½ºÅÙÆ®Ç÷ÀüÁõ ¹× Àç ÇùÂø ¹æÁö¸¦ ¸ñÀûÀ¸·Î ½ÃÇàÇÏ´Â Ç×Ç÷¼ÒÆÇ 3Á¦¿ä¹ý(aspirin, clopidogrel, cilostazol)ÀÇÀû¿ë´ë»ó ¹× Åõ¿©±â°£¿¡ ´ëÇÏ¿© ³íÀÇÇÑ °á°ú, Àӻ󿬱¸¹®Çå ¹× °ü·ÃÇÐȸ ÀÇ°ß µî¿¡¼ ½ºÅÙÆ®»ðÀÔ¼ú °ü·ÃÇÑÀç ÇùÂø ¹ß»ý µîÀÌ ³ôÀº °í À§Ç豺Àº ¡®´ç´¢, Long stenting, small lesion,multi-stenting¡¯µîÀ¸·Î º¸°í ÀÖÀ¸¸ç, EBH Æò°¡º¸°í¼¿¡¼ ¡°°ü»óµ¿¸Æ½ºÅÙÆ® ½Ã¼úÈÄ »ç¿ëÇÑ ½Ç·Î½ºÅ¸Á¹À» Æ÷ÇÔÇÑ Ç×Ç÷¼ÒÆÇ 3Á¦¿ä¹ýÀº ÀÓ»óÀû À¯¿ë¼º Ãø¸é¿¡¼ ±âÁ¸ÀÇ 2Á¦¿ä¹ý°ú ºñ±³ÇÒ ¶§ ÁÖ¿ä½ÉÀå»ç°Ç(MACE) ¹× Ç¥Àûº´º¯Àç½Ã¼ú, Ç¥ÀûÇ÷°üÀç½Ã¼ú, Àç ÇùÂø·ü, Èıâ¼Õ½ÇÀÇ À§ÇèÀ» ÁÙÀ̴µ¥ ´õ ¿ì¿ùÇÑ °á°ú¡±¸¦ º¸¿´´Ù°í ÇÔ.
- µû¶ó¼, Ç×Ç÷¼ÒÆÇ 3Á¦¿ä¹ýÀ»ÀÎÁ¤ÇÏ´Â °í À§Ç豺ÀÇ Àû¿ë¹üÀ§´Â ¡°´ç´¢º´ ȯÀÚ, ÀçÇùÂø º´º¯, ´ÙÇ÷°üÇùÂø¿¡ ´ëÇÑ ½ºÅÙÆ® ½Ã¼ú(multi-stenting)¡±·Î ÇϵÇ, Åõ¿©±â°£Àº 6°³¿ù±îÁö ÀÎÁ¤Å°·Î ÇÔ.
[2009.3.2 Áø·á½É»çÆò°¡À§¿øÈ¸]
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| DUR °ü·Ã °í½Ã |
[º´¿ë¿¬·É±Ý±â ÀǾàǰ / ÀӺαݱâ ÀǾàǰ / ºñ¿ëÈ¿°úÀû ÇÔ·® ÀǾàǰ / ¾ÈÀü¼º °ü·Ã ±Þ¿©ÁßÁö ÀǾàǰ]
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| Ç׸ñ |
³»¿ë |
| DUR (ÀǾàǰ»ç¿ëÆò°¡) |
º´¿ë±Ý±â :
[ketorolac tromethamine]
[ketorolac tromethamine]
[methotrexate]
[methotrexate]
[»óÈ£ÀÛ¿ë/º´¿ë±Ý±â°Ë»ö]
¿¬·É´ë±Ý±â :
°í½ÃµÈ ¿¬·É±Ý±â ³»¿ëÀº ¾ø½À´Ï´Ù.
[¿¬·É´ë±Ý±â»ó¼¼°Ë»ö]
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| Mechanism of Action |
Aspirin¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ The analgesic, antipyretic, and anti-inflammatory effects of aspirin are due to actions by both the acetyl and the salicylate portions of the intact molecule as well as by the active salicylate metabolite. Aspirin directly and irreversibly inhibits the activity of both types of cyclo-oxygenase (COX-1 and COX-2) to decrease the formation of precursors of prostaglandins and thromboxanes from arachidonic acid. This makes aspirin different from other NSAIDS (such as diclofenac and ibuprofen) which are reversible inhibitors. Salicylate may competitively inhibit prostaglandin formation. Aspirin's antirheumatic (nonsteroidal anti-inflammatory) actions are a result of its analgesic and anti-inflammatory mechanisms; the therapeutic effects are not due to pituitary-adrenal stimulation. The platelet aggregation–inhibiting effect of aspirin specifically involves the compound's ability to act as an acetyl donor to the platelet membrane; the nonacetylated salicylates have no clinically significant effect on platelet aggregation. Aspirin affects platelet function by inhibiting the enzyme prostaglandin cyclooxygenase in platelets, thereby preventing the formation of the aggregating agent thromboxane A2. This action is irreversible; the effects persist for the life of the platelets exposed. Aspirin may also inhibit formation of the platelet aggregation inhibitor prostacyclin (prostaglandin I2) in blood vessels; however, this action is reversible.
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| Pharmacology |
Aspirin¿¡ ´ëÇÑ Pharmacology Á¤º¸ Aspirin (acetylsalicylic acid) is an analgesic, antipyretic, antirheumatic, and anti-inflammatory agent. Aspirin's mode of action as an antiinflammatory and antirheumatic agent may be due to inhibition of synthesis and release of prostaglandins. Aspirin appears to produce analgesia by virtue of both a peripheral and CNS effect. Peripherally, Aspirin acts by inhibiting the synthesis and release of prostaglandins. Acting centrally, it would appear to produce analgesia at a hypothalamic site in the brain, although the mode of action is not known. Aspirin also acts on the hypothalamus to produce antipyresis; heat dissipation is increased as a result of vasodilation and increased peripheral blood flow. Aspirin's antipyretic activity may also be related to inhibition of synthesis and release of prostaglandins.
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| Protein Binding |
Aspirin¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ High (99.5%) to albumin. Decreases as plasma salicylate concentration increases, with reduced plasma albumin concentration or renal dysfunction, and during pregnancy.
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| Half-life |
Aspirin¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ The plasma half-life is approximately 15 minutes; that for salicylate lengthens as the dose increases: doses of 300 to 650 mg have a half-life of 3.1 to 3.2 hours; with doses of 1 gram, the half-life is increased to 5 hours and with 2 grams it is increased to about 9 hours.
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| Absorption |
Aspirin¿¡ ´ëÇÑ Absorption Á¤º¸ Absorption is generally rapid and complete following oral administration but may vary according to specific salicylate used, dosage form, and other factors such as tablet dissolution rate and gastric or intraluminal pH.
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| Biotransformation |
Aspirin¿¡ ´ëÇÑ Biotransformation Á¤º¸ Aspirin is rapidly hydrolyzed primarily in the liver to salicylic acid, which is conjugated with glycine (forming salicyluric acid) and glucuronic acid and excreted largely in the urine.
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| Toxicity |
Aspirin¿¡ ´ëÇÑ Toxicity Á¤º¸ Oral, mouse: LD50 = 250 mg/kg; Oral, rabbit: LD50 = 1010 mg/kg; Oral, rat: LD50 = 200 mg/kg. Effects of overdose include: tinnitus, abdominal pain, hypokalemia, hypoglycemia, pyrexia, hyperventilation, dysrhythmia, hypotension, hallucination, renal failure, confusion, seizure, coma, and death.
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| Drug Interactions |
Aspirin¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Acetazolamide The salicylate at high dose increases the effect of the carbonic anyhydraseAcetohexamide The salicylate increases the effect of sulfonylureaMethotrexate The salicylate increases the effect and toxicity of methotrexateAnisindione The salicylate increases effect of anticoagulantBetamethasone The corticosteroid decreases the effect of salicylatesChlorpropamide The salicylate increases the effect of sulfonylureaDexamethasone The corticosteroid decreases the effect of salicylatesDichlorphenamide The salicylate at high dose increases the effect of the carbonic anyhydrase inhibitorsDicumarol The salicylate increases effect of anticoagulantValproic Acid The salicylate increases the effect of valproic acidFludrocortisone The corticosteroid decreases the effect of salicylatesGliclazide The salicylate increases the effect of sulfonylureaGlipizide The salicylate increases the effect of sulfonylureaGlisoxepide The salicylate increases the effect of sulfonylureaGlibenclamide The salicylate increases the effect of sulfonylureaTolazamide The salicylate increases the effect of sulfonylureaTolbutamide The salicylate increases the effect of sulfonylureaGriseofulvin Anticipate decrease of ASA efficiency in presence of griseofulvinHeparin Association of ASA/heparin increases risk of bleedingHydrocortisone The corticosteroid decreases the effect of salicylatesPrednisolone The corticosteroid decreases the effect of salicylatesPrednisone The corticosteroid decreases the effect of salicylatesTriamcinolone The corticosteroid decreases the effect of salicylatesWarfarin The salicylate increases the effect of anticoagulantAcenocoumarol The salicylate increases the effect of anticoagulantMethylprednisolone The corticosteroid decreases the effect of salicylatesIbuprofen Ibuprofen reduces ASA cardioprotective effectsInsulin-aspart The salicylate increases the effect of insulinInsulin-detemir The salicylate increases the effect of insulinInsulin-glargine The salicylate increases the effect of insulinInsulin-glulisine The salicylate increases the effect of insulinInsulin-lispro The salicylate increases the effect of insulinKetorolac ASA increases toxicity of ketorolacMethazolamide The salicylate at high dose increases the effect of the carbonic anhydrase inhibitorsProbenecid The salicylate decreases the uricosuric effect of probenecidSulfinpyrazone The salicylate antagonizes the uricosuric effect of sulfinpyrazoneTiclopidine Increased effect of ticlopidineCortisone acetate The corticosteroid decreases the effect of salicylatesGinkgo biloba Association of ASA/ginkgo increases risk of bleedingGlycodiazine The salicylate increases the effect of sulfonylureaInsulin The salicylate increases the effect of insulinParamethasone The corticosteroid decreases the effect of salicylates
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CYP450 Drug Interaction |
[CYP450 TableÁ÷Á¢Á¶È¸]
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| Food Interaction |
Aspirin¿¡ ´ëÇÑ Food Interaction Á¤º¸ Avoid drastic changes in dietary habit.Consult your doctor before taking large amounts of Vitamin K (Green leafy vegetables).Avoid alcohol, alcohol appears to cause a 50 to 100% increases in ASA serum levels.Take with food to reduce irritation.Take with a full glass of water.
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| Drug Target |
[Drug Target]
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| SNP Á¤º¸ |
Name:Aspirin (DB00945)
Interacting Gene/Enzyme:Leukotriene C4 Synthase (Gene symbol = LTC4S) Swissprot Q16873
SNP(s):rs730012 (C allele)
Effect:Aspirin-induced urticaria
Reference(s):Mastalerz L, Setkowicz M, Sanak M, Rybarczyk H, Szczeklik A: Familial aggregation of aspirin-induced urticaria and leukotriene C synthase allelic variant. Br J Dermatol. 2006 Feb;154(2):256-60. [PubMed]
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| Description |
Aspirin¿¡ ´ëÇÑ Description Á¤º¸ The prototypical analgesic used in the treatment of mild to moderate pain. It has anti-inflammatory and antipyretic properties and acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5)
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| Drug Category |
Aspirin¿¡ ´ëÇÑ Drug_Category Á¤º¸ Anti-Inflammatory Agents, Non-SteroidalAnticoagulantsCyclooxygenase InhibitorsFibrinolytic AgentsPlatelet Aggregation InhibitorsSalicylates
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| Smiles String Canonical |
Aspirin¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ CC(=O)OC1=CC=CC=C1C(O)=O
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| Smiles String Isomeric |
Aspirin¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ CC(=O)OC1=CC=CC=C1C(O)=O
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| InChI Identifier |
Aspirin¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C9H8O4/c1-6(10)13-8-5-3-2-4-7(8)9(11)12/h2-5H,1H3,(H,11,12)/f/h11H
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| Chemical IUPAC Name |
Aspirin¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ 2-acetyloxybenzoic acid
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| Drug-Induced Toxicity Related Proteins |
ASPIRIN ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:Vimentin Drug:aspirin Toxicity:aspirin-induced gastric mucosal microvessels injury . [¹Ù·Î°¡±â] Replated Protein:Angiopoietin-related protein Drug:aspirin Toxicity:damage to microvessels. rupture of capillary walls. necrosis of endothelial cells. damage to endothelial organelles. deposition of fibrin. adherence of platelets to damaged endothelium. [¹Ù·Î°¡±â] Replated Protein:Myeloperoxidase Drug:aspirin Toxicity:haemorrhagic erosions. [¹Ù·Î°¡±â] Replated Protein:Thromboxane A2 receptor Drug:aspirin Toxicity:thrombotic complications. [¹Ù·Î°¡±â] Replated Protein:Integrin beta-3 Drug:Aspirin Toxicity:Antiplatelet effect. [¹Ù·Î°¡±â] Replated Protein:Integrin alpha-Iib Drug:Aspirin Toxicity:Antiplatelet effect. [¹Ù·Î°¡±â] Replated Protein:Nuclear factor NF-kappa-B p105 subunit Drug:aspirin Toxicity:apoptosis in human colon cancer cells. [¹Ù·Î°¡±â]
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µå·°ÀÎÆ÷ ÀǾàÇмúÁ¤º¸´Â ½ÄǰÀǾàǰ¾ÈÀüóÀÇ Á¦Ç°Çã°¡»çÇ×, Çмú¹®Çå, Á¦¾àȸ»ç Á¦°øÁ¤º¸ µîÀ» ±Ù°Å·Î ÀÛ¼ºµÈ Âü°í Á¤º¸ÀÔ´Ï´Ù.
Á¤º¸ÀÇ Á¤È®¼ºÀ» À§ÇØ ³ë·ÂÇϰí ÀÖÀ¸³ª ÆíÁý»óÀÇ ¿À·ù, Çã°¡»çÇ× º¯°æ, Ãß°¡ÀûÀÎ Çмú¿¬±¸ ¶Ç´Â Àӻ󿬱¸ ¹ßÇ¥ µîÀ¸·Î ÀÎÇØ ¹ß»ýÇÏ´Â ¹®Á¦¿¡ ´ëÇØ µå·°ÀÎÆ÷´Â
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ÀüÈ: 02-3486-1061 ¤Ó À̸ÞÀÏ: webmaster@druginfo.co.kr
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