These findings will be valuable for design of imaging and pre-clinical therapeutic studies, by providing more phenotypes and larger differences from baseline health in controls. Other imaging studies provide insight into mdx physiology, but most avoid the critical OSI-774 necrotic phase of the mdx disease course. Cardiac MRI shows mdx mice can exhibit heart dysfunction by one month, and decreased cardiac phosphocreatine content at 8 months. Agents can help visualize disrupted muscle integrity or detect transplanted stem cells. Metabolic profiling shows alterations in injured muscle and lysates of 3- to 6-month old mdx mice. T2 mapping has been performed in 20- to 60- week-old mdx. One case study reports a single mdx leg assayed longitudinally to 80 weeks. Dunn et al. initially showed dystrophic lesions can be detected via MRI and that crush injuries are repaired over approximately 3 weeks, consistent with our findings for naturally occurring mdx dystrophic lesions. Mathur and Vohra et al. characterized effects of exercise on mdx, finding effects of the mdx genotype and of running on muscle T2 and % affected area, with medial muscles particularly affected by running. Gene correction in mdx and limb girdle muscular dystrophy mouse models show MRI can be used to detect therapeutic improvement in muscular dystrophy. The mdx mouse provides researchers with a genetic model of the cause of DMD, and MRI is emerging as an important surrogate outcome measure for muscle damage. In the present study we have found NMR phenotypes and provide new information on the dynamic disease process in mdx mice. Although mdx is typically regarded as a very mild disease model, we find 31P spectroscopy and T2 imaging of the 6-week old mdx leg show significant differences from WT mice and could provide robust outcome measures, even with relatively few animals. These findings can improve preclinical trial design by reducing the number of animals required to detect effects, allowing for longitudinal non-invasive quantification of muscle disease, and using measures that are translatable to human clinical studies. Life-long use of immunosuppressive drugs is required to prevent rejection after renal transplantation. Nevertheless, the continuous use of immunosuppressive drugs does not preclude the development of chronic rejection, which is a major cause of long-term allograft loss. T cells play an important role in the pathogenesis of rejection via the recognition of alloantigens, resulting in T-cell activation, proliferation, and differentiation into CD8+ cytotoxic T cells and CD4+ T helper cells. Therefore, the most commonly used immunosuppressive drugs in transplantation are directed against T cells to inhibit these processes. On the other hand, regulatory T cells are able to suppress the immune response and prevent allograft rejection. The balance between memory and regulatory T cells during the course after transplantation can be used to predict renal graft rejection following the reduction of immunosuppressive therapy. Next to T cells, B cells can be involved in graft rejection. The presence of B-cell clusters in renal grafts during acute rejection or the presence of anti-HLA antibodies before transplantation is associated with poorer graft survival.