摘要：We welcome Sch.llnberger and Kaiser's com-ments on our review (Little et al. 2012). The biology of radiation-associated athero sclerosis has been extensively reviewed (Advisory Group on Ionising Radiation 2010; Little et al. 2010). As we stated in our paper, there are "biological data suggesting that many inflammatory end points potentially relevant to circulatory disease may be differentially regulated below and above about 0.5 Gy," which is why we studied low-to-moderate exposures (Little et al. 2012). Mitchel et al. (2011) and R.del et al. (2012) support a possible biphasic dose response, as do many other data (Advisory Group on Ionising Radiation 2010; Little et al. 2010).
