The results obtained from the simulations confirmed that the microchannels have the potential to be used as a drug delivery system depending on desired flow rates and drug concentrations. The proposed device can produce a constant delivery rate, which is favorable to the treatment of eye disease. Diffusion rates can be

customized to obtain effective levels by varying height, width, and length of microchannels. The overall fabricated device is shown in Figure 10. Currently, the functionality of the device is being explored and will be Inhibitors,research,lifescience,medical tested in future. Figure 10 PDMS-fabricated drug delivery device concept. 4. Conclusions A microdevice concept for ocular drug delivery is proposed Inhibitors,research,lifescience,medical in this paper. The design involves development of an implantable device with micro-/nanochannels with top and bottom covers. Six different channel configurations were developed and analyzed for their diffusion characteristics. Based on the results obtained, channel design of osmotic I and II satisfied the diffusion rates required for ocular drug delivery. In addition to design simulations, the top and bottom covers were fabricated from PDMS through Inhibitors,research,lifescience,medical replica-molding techniques. The microchannels along with top and bottom

covers were all integrated into the device. Currently, the device is being tested for its functionality and diffusion characteristics. However, there are significant challenges related to achieving reliable and sustainable integration, bonding, diffusion of the drug into channels, and controllability. The test evaluation will be performed measuring the

change in pH of a neutral solution using a strong Purmorphamine in vitro citric acid; it can be diffused out through the device. These challenges are being addressed and will be presented in our future work. Acknowledgments The Inhibitors,research,lifescience,medical authors thank Joshua Starliper and Dr. Hu Yang for their discussions and help during this study. Funding is provided Inhibitors,research,lifescience,medical by NSF-ECCS-1058067.

Infantile neuronal ceroid lipofuscinosis (INCL) is a severe neurodegenerative disorder of childhood characterized by selective death of cortical neurons [1]. Treatment is focused mainly to relieve the symptoms, such as sleep difficulties and epilepsy, but the average lifespan of an INCL child is Montelukast Sodium still only 10 years. INCL is caused by recessive mutations in the CLN1 gene encoding palmitoyl-protein thioesterase (PPT1) [2]. Normal PPT1 activity is essential for the development and survival of cortical and cerebellar neurons in human and mouse [3–5]. IGF-1 concentration in cerebrospinal fluid is lower in patients with INCL [3] suggesting that decreased levels of IGF-1 in brain may accelerate neurodegenerative disorders. To consistently study pathogenesis and treatment of INCL and other types of neuronal ceroid lipofuscinoses (NCLs), different mouse models have been established (CLN1, CLN2, CLN3, CLN5) and also naturally occurring NCL mouse models exist (CLN8/mnd; CLN6/nclf) [6].