In tro duc tion: We hypot he si zed that pa tien ts wi th stab le an gi na ha ve in crea sed plas ma le ve ls of mR NA from ge nes res pon sib le for at he ros cle ro tic plaque de ve lop me nt and des ta bi li sa tion, i.e. from dea th-as so cia ted pro tein ki na se (DAP K1) and mo no cyte che mo tac tic pro tei n-1 (CCL2). Ma te ria ls and met ho ds: Nuc leic aci ds we re iso la ted from plas ma of pa tien ts wi th sta bi le an gi na and heal thy sub jec ts as con tro ls. mR NAs we re tran scri bed to cDNAs, quan ti fi ed by rea l-ti me PCR and stan dar di zed to the amou nt of a re fe ren ce ge ne. Rea gen ts for PCR quan ti fi ca tion are dec la red to be mR NA spe ci fi c, but in our te st con di tio ns DNA was fou nd to in ter fe re in bo th as says. Re sul ts: Pa tien ts had 5.1-times hig her plas ma le vel of DAP K1 nuc leic aci ds (mR NA and DNA) than con tro ls (P < 0.001) and the hig he st le ve ls we re as so cia ted wi th the pre sen ce of dia be tes. Howe ver, plas ma le ve ls of CCL2 ten ded to be lower than in con tro ls, and in sta ti n-trea ted pa tien ts the decre me nt reac hed sig ni fi cance (-66.3%; P = 0.041).
Con clu sion:The es ti ma ted le ve ls are expli cab le in ter ms of cur re nt knowled ge. Fur ther stu dies wi th spe ci fi c as says for mR NA PCR quan ti fi ca tion are rea so nab le to ac ce ss whet her this ap proa ch off e rs no n-in va si ve in vi vo as ses sme nt and mo ni to ri ng of ge ne expres sion pro fi le in at he ros cle ro tic vas cu lar be ds.
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