injury, and PGE2 itself is also neurotoxic. In the short term, vascular permeability in response to inflammatory cell signaling leads to edema and intracranial hypertension, which further contributes to cell death. In the long term, inflammation has been linked with the development of numerous neurodegenerative diseases including amyotrophic lateral sclerosis, multiple sclerosis, Alzheimer’s Disease, and Parkinson’s Disease. The nanoprodrug contains TG-101348 chemical information a-tocopherol as an antioxidant component and stabilizing structural component. Increasing evidence suggests that vitamin E may play a promising role in the prevention and treatment of oxidative damage-related neurodegenerative diseases. However, its extreme insolubility in water poses a serious limitation to distribution in the aqueous biological environment, limiting its usefulness as a therapeutic intervention. Efforts to make a-tocopherol more water soluble by replacing the lipophilic phytyl chain with more hydrophilic moieties interfere with its antioxidant capabilities and may incur unexpected adverse biological effects. Thus, unmodified a-tocopherol was used in the formulation of the nanoprodrug as a stabilizing and size 6145492 reducing structural component, in addition to its 17526600 antioxidant benefits. Despite the hydrophobicity of Ibu2TEG and a-tocopherol alone, formation of the two into a nanoparticle generates a large surface area for hydrolytic esterase enzymes to interact and degrade prodrugs, releasing ibuprofen from the surface. Conclusion Bioluminescence imaging reveals that the novel NSAID nanoprodrug accumulates at the area of injury, possibly due to an enhanced permeability and retention effect. The nanoprodrug targets the injury with high specificity, which may NSAID Nanoprodrug for Traumatic Brain Injury potentially reduce off target effects on other organs. Behavioral testing indicates that only animals receiving the drug intravenously demonstrated a significant reduction in ambulation, whereas animals receiving the drug IP showed equivalent motor function to animals receiving PBS control. Rotorod and Barnes Maze showed no significant differences in outcome with the use of the NSAID nanoprodrug. We believe this study demonstrates the feasibility of using the NSAID nanoprodrug to target TBI. Further testing will explore off target organ toxicities, nanoprodrug half-life, and determine the minimal effective dose. Further preclinical studies may investigate the use of the nanoprodrug in a blast injury model in addition to controlled cortical impact. The novel combination of the nanoprodrug delivery strategy and NSAID therapy represents a promising therapeutic modality for the treatment of many types of TBI. ~~ ~~ Tuberculosis, owing to Mycobacterium tuberculosis infection, still remains as a major global health problem. Approximately 9 
million new cases of TB are detected each year, and close to 2 million people die from the disease. In 2008, it has been estimated that 390 000510 000 cases of multidrug-resistant tuberculosis emerged globally. In 2008, MDR-TB caused an estimated 150 000 deaths. It has also been reported that 5.4% of MDR-TB cases were found to have extensively drug-resistant tuberculosis . In addition, TB cases due to infection with totally drug-resistant strains have been reported. The emergence of drugresistant strains of M. tuberculosis has thus highlighted the need for the development of new therapeutic strategies to combat TB. Rational inhibitor design relies on me