The parameters used in this study are based on our previous work, which is able to minimize the brain tissue damage. Ultrasound pressure would have caused the microbubbles in the acoustic beam oscillation and even cavitation during sonication. These oscillation and cavitation may open vascular walls to enhance hEPO transport into brain tissues. However, the above phenomena may produce some small hemorrhages for the brain tissue in the focal zone, which might cause some damage. To achieve effective drug delivery and minimize this side-effect, we can control acoustic pressure, duty cycle, sonication time, MB dose, etc. For clinical patient treatments, FUS transducers should be combined with magnetic resonance imaging system and thus the MR imaging can be used to guide the FUS transducer to have a precision sonication and to monitor the treatment response. Recently, it has been shown the feasibility of using MRI-guided FUS with MBs to noninvasively open the localized BBB on nonhuman primates. In this preliminary study, the neuroprotective agent was used only one dose and one time. It requires further scrutiny and examination for the combination of FUS sonication with multiple treatments of neuroprotectants. MBs/FUS can transcranially and transiently open the localized BBB for the transport of macromolecular drug into the desired brain region. In this study, we utilized this modality for the localized delivery of neuroprotective agent into the infarcted brain of rats beyond the conventional therapeutic time window. The results of acute and chronic investigation show that this modality can provide an alternative treatment option to deliver neuroprotectants or drugs to the injured brain. Contrast-induced nephropathy remains a serious clinical problem in the use of iodinated contrast media. Increasing use of contrast media in interventional BI-D1870 501437-28-1 procedures has led to a parallel increase in the incidence of CIN, despite the use of newer and less nephrotoxic contrast agents in high-risk patients in recent years. The reported incidence of CIN varies widely across the literature. Its development has been associated with increased in-hospital and long-term morbidity and mortality, prolonged hospitalization, and long-term renal impairment. Proposed pathophysiologic mechanisms through which contrast administration may potentiate renal injury include oxidative stress, free radical damage, and endothelial dysfunction. However, the actual pathogenesis of CIN and the pathophysiologic mechanisms underlying the evolution from CIN to atherosclerosis and cardiovascular events remain to be determined. Vascular endothelium is a highly active organ that affects vascular tone, smooth muscle cell proliferation, monocyte adhesion, and platelet aggregation. Endothelial dysfunction plays a critical role in the clinical manifestations of established atherosclerotic lesions. Clinical studies have demonstrated that endothelial dysfunction is present in the early stages of renal insufficiency, and that it is associated with a greater decline in renal function.