1、 “: 8 3O S “(2007A178); 81 S “(Y2110379); 8m/ 9 “(2012C33106)T:325200 D Sv D * = STe:c(1972-), D = “57 F#M1y 池万章,易兴阳,周 强,林 静,池丽芬K 1 “ ) 7 F(AR)? 3 q# -1(COX-1)yC50T -2(COX-2)yG765C FM1。ZE 634 nQ?h 7 , Q 7 S , - 710?sY_=F(ADP) 3 (AA)l “ q(PAG),i TQK = M sZE_COX-1yC50T、COX-2yG765C 。T634 7 , F(AR)129 (
2、20.35%), F(ASR)28 (4.42%), (AS)477 (75.23%)。COX-1 C50TCOX-2 G765Cy#yASR+ARF#ASF1 sd9il(P0.05); 710?, 7 AAl “ q#ADPl “ qsY/80.00%#40.00%; COX-1 C50TCOX-2 G765C y ( V PAAl “ q#ADPl“ q,ytS1 sd9il(P0.05);COX-1yC50TyGCOX-2 765CMsAAl “ q - (Ms,sd9il(P0.05).The rate of AA-induced platelet aggregations amon
3、g the variants gene of Cox-1 C50Tand Cox-2G765C weresignificantlyhigher than thatwithout variants beforeand afteraspirin intake(P450109/L0.05),nV1。2.3 FCOX-1 C50TCOX-2 G765C s1 :COX-1 C50T s,634 597 (94.2%)BCCy,37 (5.8%)CT,nBTTy。COX-2 G765C s,442(69.7%)BGGy,156 (24.6%)GC,36 (5.7%)BCCy。COX-1C50TCOX-2
4、G765CyyASR+ARFASF1 s (d9il(P 0.05),nV2、V3。表1 两组入院时一般情况和危险因素比较 “ F(n=477) FF(n=157)M -( ) 69.3510.22 70.2310.51o (%) 215(45.07) 87(55.41) (%) 127(26.62) 47(29.94) (%) 325(66.04) 108(68.79) Uh (%) 66(13.85) 61(38.85)9%?(mmol/L) 4.964.76 5.011.05 (mmol/L) 1.790.91 1.800.81 9%?(mmol/L) 1.290.38 1.280.36
5、 9%?(mmol/L) 2.850.75 3.130.81l9 (109/L) 196.5117.97 195.0515.66: F1 P0.05);COX-1 50TCOX-2 765CMsAAl “ q - (Ms,sd9il(P0.05 81.39.5 79.610.6 0.050 -ADPl “ q(%) 87.612.6 88.913.9 0.05 88.411.4 87.913.5 0.050ADPl “ q(%) 50.98.4 51.99.6 0.05 51.98.7 51.29.4 0.05ADPl “ q/ q(%) 42.78.7 41.88.2 0.05 41.57.
6、6 41.88.3 0.05431 75h2013 M1213 6 3 ) SV 5 , F? 3 q5%40%,B is。F ASR? 3 q4.42%,AR? 3 q20.35%, H?C,ASRARF Uh#LDL ASF, y b#, M i、 “、 Uh# h,l)V ,lT =%,i % ,%, db5, V, HlF Q, ty P =r。Andreas69V ,、 ? Pl%,9F8 =l%W*, F? 3。yN, e、By ,|E F? 3。AR? 3, “ - b#。COXl s8y ARM1 “ - 1,7,8 ,Ts v。B“dsV 9,ARPIA1/A2ylMM1,C
7、OX-1、GPla、P2Y1、P2Y12y M1。 V PCOX , P A2(TXA2) 3h,V7r F “,Halushka10F ?C,COX-1-50CTCOX-2-765G ClM qsY8.6%21.3%,lMY rT。 7S =Z ,F AU,COX-1 C50TCOX-2 G765CyyASR+ARFASF1 s (d9il,COX-1 C50TCOX-2G765C y ( V PAAl “ q#ADPl “ q, OytS1 sd9il,4 US COX-1 C50TCOX-2G765Cy ARM1,9Y lQ。AR? 3y V ? Z , B、 lh 9、0GV,N VY
8、VCOXY , P A2(TXA2) 3h , ?EADP,、 / F 、 l “ 11 ,t ( V ? AR? 3y。 ?CS COX-1 C50TCOX-2G765Cy ARM1,?CCOX-150TCOX-2 765CMsAAl “ q - (Ms,4 UCOX-1 50TCOX-2 765CMsCOX Ms,TXA2 39,V7 Pl “9, V ? 7 ?hV?T,B。 ID1Goodman T, SharmaP, Ferro A.Thegenetics ofaspirin resistanceJ.IntJ Clin Pract,2007,61(5):826-834.2Han SW
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11、ailure Role of NO Bioavailability J.ArteriosclerThromb Vasc Biol,2005,25(5):1071-1077.7KunickiTJ, Williams SA, Nugent DJ, et al.Lack of association betweenaspirin responsiveness and seven candidate gene haplotypes in patients withsymptomatic vascular diseaseJ.Thromb Haemost,2009,101(1):123-133.8Chak
12、roun T, Addad F, Yacoub S, et al.The cyclooxygenase-1C50T poly-morphism is not associated with aspirin responsiveness status in stable coro-nary artery disease in Tunisian patients J.Genet Test Mol Biomarkers,2011,15(7-8):513-516.9Goodman T, FerroA, SharmaP.Pharmacogenetics of aspirin resistance:aco
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