Arjen M. Dondorp, M.D women’s health .D., Poravuth Yi, M.D., Debashish Das, M.D., Aung Phae Phyo, M.D., Joel Tarning, Ph.D., Khin Maung Lwin, M.D., Frederic Ariey, M.D., Warunee Hanpithakpong, Ph.D., Sue J. Lee, Ph.D., Pascal Ringwald, M.D., Kamolrat Silamut, Ph.D., Mallika Imwong, Ph.D., Kesinee Chotivanich, Ph.D., Pharath Lim, M.D., Trent Herdman, Ph.D., Sen Sam An, Shunmay Yeung, Ph.D., Pratap Singhasivanon, M.D., Nicholas P.J. Time, D.M., Niklas Lindegardh, Ph.D., Duong Socheat, M.D., and Nicholas J. White colored, F.R.S.: Artemisinin Level of resistance in Plasmodium falciparum Malaria Artemisinins are established antimalarial agents with an excellent safety profile.1 Artemisinin-based mixture therapies are actually recommended by the World Health Corporation as first-range treatment of uncomplicated falciparum malaria in all areas in which malaria is endemic.3-5 Parenteral artesunate is replacing for the treatment of severe malaria quinine.6 Recently, there were indications that the efficacy of artemisinin-based mixture therapy and artesunate monotherapy have declined in western Cambodia.7-10 Artemisinin resistance would be disastrous for global malaria control.
Antman, M.D., William Macias, M.D., Ph.D., Eugene Braunwald, M.D., and Marc S. Sabatine, M.D., M.P.H.: Cytochrome P-450 Response and Polymorphisms to Clopidogrel Across the spectral range of acute coronary syndromes and in patients undergoing percutaneous coronary interventions with stenting, dual antiplatelet therapy with clopidogrel and aspirin, a thienopyridine inhibitor of the platelet P2Y12 adenosine diphosphate receptor, is the standard of care.1-3 However, the pharmacodynamic response to clopidogrel has considerable interpatient variability,4-6 and patients with coronary disease with lesser levels of platelet inhibition in response to clopidogrel look like at increased risk for cardiovascular events.7-10 Clopidogrel is a prodrug that will require biotransformation to an active metabolite by cytochrome P-450 enzymes .11,12 Moreover, esterases shunt the majority of clopidogrel to an inactive pathway, with the rest of the prodrug requiring two separate CYP-dependent oxidative actions.