I found this article extremely interesting while I was writing my paper. This article focused on the differences between clotting factors of African Americans and European-descent American. The article driven their research on how it can improve medications and even lead to personalized medication in the future for heart related problems.
African Americans have a greater chance of incidence of heart attacks then White patients and lower survival rates, with is 21/2 times lower then whites. This difference has lead researchers to study the differences between African American that can contribute to higher incidence of heart disease. Despite the traditional differences such as socioeconomic status, diet, and environment, researchers at Thomas Jefferson University found that African American have an more potent blood clotting factor then Caucasians. In the experiment, Bray et.Al. took blood samples from 154 subjects( 70 blacks and 84 whites) and tested the blood clotting affinity. They found that that Blacks blood clots faster because of the clotting agent PAR4. PAR4 bind more thrombin, a blood platelet activator, faster then other agents in Whites. Another gene called PCTP, which mediates platelet activation of the PAR4 was another difference between clot formation of blacks and whites. PCTP was expressed higher in black then in whites.
This new research present new way of thinking about prescriptions. Many blood thinners work by targeting the PAR gene family to prevent blood clotting. However in Blacks that have PAR4 genes are unaffected by drugs currently on the market. In class we have often talked about individualized treatments an I think that this article is strong evidence that support the idea of individualized medicine in the future.
Leonard C Edelstein, Lukas M Simon, Raúl Teruel Montoya, Michael Holinstat, Edward S Chen, Angela Bergeron, Xianguo Kong, Srikanth Nagalla, Narla Mohandas, David E Cohen, Jing-fei Dong, Chad Shaw, Paul F Bray. Racial differences in human platelet PAR4 reactivity reflect expression of PCTP and miR-376c. Nature Medicine, 2013; DOI: 10.1038/nm.3385