Drug release rates from micro and nanoparticles were lower during the second and third “off” periods. Collectively, these studies showed the high degree of adaptability of using PLGA-magnetic particle systems as a controlled release platform for drugs like ciprofloxacin. The sustained release CIP from the PLGA micro/nanoparticles resulted in a bacterial activity reduction rate of 20.4% for PLGA microparticles and 25.8% for PLGA nanoparticles. According to these observations, the antibacterial activity of CIP encapsulated in PLGA nanoparticles was slightly better than that of the PLGA microparticles. As observed with the release studies, the microparticles had significant amounts of CIP remaining within the microspheres after several days, significantly longer than the time period of these standard antibacterial assays performed here and therefore may not reflect the actual in use performance. To test the biological activity of CIP released from PLGA particles under OMF, drug released from microparticles and nanoparticles after 4 h OMF treatment was diluted to 1mg/ml then applied to Pseudomonas aeruginosa biofilms for 24 h. The bacterial activity reduction caused by CIP released from micro- and nanoparticles were 32.5% and 33.3% respectively. These reductions in bacteria were slightly lower compared with 1mg/ml free CIP control. The slightly lower activity may be related to incomplete drug release, drug loss, or degradation during OMF. Elemental iron release from the MNP may also confound these observations and requires further investigation. Iron release may result higher antibacterial but SAR131675 purchase reports also suggest pseudomonas may also be supported by increased iron levels. From these studies it was confirmed that CIP released from the particles before and after OMF triggered release was still active. The objective of this study was to investigate the release property of CIP encapsulated PLGA magnetic micro/ nanoparticles, however in future studies formulations will be optimized and cytotoxicity will be tested. Angiogenesis is modulated by a variety of factors: angiogenic growth factors, cytokines, inflammatory leukocytes, bone marrow-derived progenitor cells, extracellular matrices, vasoactive substances and NADPH oxidase. In addition, it has been reported that macrophage infiltration early after ischemia is an important trigger for promoting ischemia-induced angiogenesis, since inflammatory cells release the angiogenic growth factor vascular endothelial growth factor. LOX-1 is a type II integral membrane glycoprotein with a short N-terminal cytoplasmic domain, a single transmembrane domain, a short ‘neck’ or stalk region and an extracellular C-type lectin-like fold. LOX-1 was first identified as an endothelial-specific scavenger receptor but was also detected on macrophages, smooth muscle cells, monocytes and platelets later. In early atherosclerotic lesions, LOX-1 levels are elevated both within the intima and in the endothelium surrounding the lesion, suggesting that LOX-1 is involved in endothelial dysfunction and the initiation and growth of atherosclerotic plaques.