The trabecular meshwork, upon examination showed signs of apparent acute inflammatory responses with accumulation of CD11b+ cells in some groups of animals, especially animals with PS particle or PNIPAM implants. Mild accumulation of CD11b+ cells in trabecular meshwork was also found in animals implanted with PLLA particles. Interestingly, no CD11b+ cells were found in the tissues isolated from animals implanted with either HA particles or BSS controls. Equally importantly, we found a good relationship between the numbers of CD11b+ cells in trabecular meshwork and the average IOP reduction in different groups of implants. These results suggest that particle implant-associated inflammatory responses in trabecular meshwork are responsible for IOP reduction and are supported by many earlier works in which inflammatory responses inside trabecular meshwork have been linked to the reduction of IOP. The results from this study have emphasized the fact that IOP should be measured as part of the evaluation of tissue compatibility of PF-4217903 956905-27-4 ocular implants, specifically in the case of nanoparticle and microparticle implants. Furthermore, the “normal” anatomical structure of retinal, corneal and iris tissue does not guarantee the safety of ocular particle implants. Rather, the histological evaluation of inflammatory responses in trabecular meshwork should be done as an indicator of ocular compatibility of intravitreous implants. Finally, further studies are needed to investigate the influence of material physical and chemical properties on IOP changes and on trabecular tissue responses. Duchenne muscular dystrophy is a progressive muscle wasting disease that affects approximately one in 3000 males. The absence of functional dystrophin restricts interaction and signal transduction between the cytoskeleton and the extracellular matrix in both skeletal muscle cells and cardiomyocytes. Advances in the treatment of respiratory failure in DMD patients has increased their life expectancy, but has resulted in many patients developing cardiomyopathy. In the dystrophic heart, cytoskeleton dysfunction can lead to cell membrane rupture, cardiomyocyte necrosis and replacement of contractile myocardium with fibrotic tissue. This increases wall stress, reduces cardiac function and can lead to heart failure. Current treatments, including ACE inhibitors and b-blockers, slow disease progression, but the disease remains incurable. The mdx mouse model of muscular dystrophy has been extensively studied and, although exhibiting a mild form of muscular dystrophy, has been useful for studying pathological mechanisms, disease progression and therapy. Novel gene, antisense oligonucleotide and cell therapies have been used to increase levels of dystrophin and restore skeletal and cardiac muscle function in the mdx mouse. Antisense oligonucleotide therapy, already tested in patients, has shown promise for increasing synthesis of functional dystrophin. Translate such important therapies to the clinic. Cardiac magnetic resonance imaging and echocardiography have been used to identify increased end systolic volumes and reduced ejection fractions in the right and left ventricles of muscular dystrophy patients.