alelttPe nheeaderc adn ealpttle eaitogagrng ear edriefnft ntghis adn stih cedrreeinf STREMTA A .TOL cuFk uoy, NMBE. hesTe nffeiesredc psyeudslpo amtert no smeo oqnuessti nda ont on threso. rheWe is teh cc?inntesyos l?oelH
Im gonna fight this one because AGGREGATION is mediated by expression of Gp IIb/IIIa.
If your platelet increases TXA2 that means is gonna upregulate AGGREGATION by which receptor? ... Duh
Once Im done with this test and become a Pathologist Im gonna send you a copy of my journal and research on platelet aggregation mediated by TXA2 and Gp IIb/IIIa and also im gonna go over every single WTF NBME question and prove them so wrong
Maybe i should change my username before submitting this
TXA2 doesnt seem to mediate induction of GP2b/3a. fa19/pg403 - ADP binding to P2Y12R induces Gp2b/3a expression at surface. ADP is released from plts. One must think about the down stream functions. If TXA2 helps aggregation via decreasing blood flow. if we therefore dont decrease blood flow we cant get the plts to later adhere properly.
Can meooens salepe crfialy the wa.resn Is aseedcred ecnreeadh ames sa dcsreeade rgenai?aoggt n;Wudtol boihtinnii fo hte IaIIbII/ eerorcpt vpernet o?ngtgaeargi
English is not my first language, but would it be possible that adherence is not equivalent to adhesion and somehow interchangeable to aggregation? I feel like doing a reading comprehension test, not USMLE.
otIhniibni fo /aIIIIIbGp rscpreeot lduwo eb eht iemhasncm of ethier F(A 0022 4:1)1
Cieoplrdglo, egausplrr ro edcniiplito aiv iioibnnhit fo udnco-iDintPA fo IpIII/aGIb yb gionkclb Y2P12
iabix,mcbA i,pbttedeiifa adn bafiirnto yb iecdtr /IIbpaIIIG biiiio.ntnh
A tol fo nqutosies liwl veha yrve ilmiars aswenr hcioesc no eth lera xmae, but rhete illw wyalsa eb one ebst srnaew, nda eeeascdrd eaetpllt dceraheen was the ttbree wanrse rhee. As taedts no yamn oterh qnueotsi esahr,td eerht rea ylnpte of ykictr qunsioets to be seput obtu,a tbu isht swa not neo fo mh.te