The device utilizes small volumes of blood, a practically important feature to avoid iatrogenic anemia by repeated blood draws from critically ill or pediatric patients. The assay yields data in less than three hours, and requires only the sequential injection of two solutions through the same port of the device, without syringe pumps or complicated priming. The assay provides temporal information at the single-cell level, and while most of the neutrophils migrate at steady speed along distinct channels of our device, their migration speed can be measured to a degree of precision difficult to attain by standard methods. A comparison between this assay and other techniques based on traditional or microfluidic technologies, is presented in Table 2. For example, the Boyden chamber, which for decades served as the standard laboratory technique for evaluating chemotaxis, can only provide an overall measure of the chemotaxis function and cannot quantify the contribution of changes in migration speed, persistence or directionality to the eventual changes of the chemotaxis function in various context. While being easy to use, it also requires large numbers of cells, separated from several milliliters of blood, disallows direct visualization of individual cells, and cannot differentiate between chemotaxis and random cell motility. More sophisticated assays, such as the Zigmond and Dunn chambers, permit examination of individual cells motility and are frequently used in biology laboratories. However, the setup and use of these chambers are labor intensive, require expertise and do not translate easily to the bedside. Recently, microfluidic devices have higher precision of the chemoattractant gradients forming inside. These CP-690550 assays require only small number of cells, translated into the need for smaller blood samples, but their use relies on external pumps and trained operators. Considering the negligible effect of MCAT on the isolated EDL muscle, it appears that cardiac MCAT expression may have played a major role in our observation. Nevertheless, it is still possible that a synergistic effect of MCAT expression in both the heart and skeletal muscle underlies running performance improvement. Future studies are needed to further define the underlying mechanism. Excessive free radical production has been implicated in aging related mobility reduction and various muscle diseases such as Duchenne muscular dystrophy. Our results suggest that boosting mitochondrial antioxidant defense with AAV-mediated MCAT expression may help clear out excessive free radicals and reduce oxidative damages under these conditions. The remarkable safety profile of MCAT overexpression seen in this study as well as in MCAT transgenic mice further paves the way to future therapeutic application.