artner Chemicell is conducting toxicity and other studies in support of an eventual investigational new drug application (IND) of the drug to be used in Phase II of this study. The potential market size for this product can be estimated to be in the range of several hundred million dollars, based on either the number of potential surgical users and practice sizes (i.e., 4,000 neurosurgeons, averaging 8 physicians/practice, at an expected price per system of $1 million) or the purchase price and valuations for companies with similar products (Sentinelle Medical, acquired for $85 million by Hologic, and $2 billion valuation for Intuitive Surgical).

LIPOPOLYSACCHARIDE INDUCED NEUROINFLAMMATION SELECTIVE INVOLVEMENT OF ARACHIDONIC ACID IN NEUROINFLAMMATION In a rat model of neuroinflammation, produced by a 6-day intracerebral ventricular infusion of bacterial lipopolysaccharide (LPS), we reported marked disturbances in brain arachidonic acid (AA, 20:4n-6) metabolism. In the present study, we demonstrated that parameters of brain docosahexaenoic acid (DHA, 22:6n-3) metabolism were unaffected in this model. Selective targeting of brain AA metabolism with non-steroidal antiinflammatory or other drugs should be considered for treating human brain diseases associated with neuroinflammation (Rosenberger et al., 2010). ANTI-INFLAMMATORY EFFECT OF ASPIRIN ON BRAIN ARACHIDONIC ACID METABOLITES Pro-inflammatory and anti-inflammatory mediators derived from arachidonic acid (AA) modulate peripheral inflammation and its resolution. Aspirin (ASA) is a non-steroidal anti-inflammatory drug (NSAID) that switches AA metabolism from prostaglandin E (PGE) and thromboxane B (TXB) to lipoxin A (LXA) and 15-epi-LXA. It is unknown whether chronic therapeutic doses of ASA are anti-inflammatory in the brain. We hypothesized that ASA would dampen increases in brain concentrations of AA metabolites in a rat model of neuroinflammation, produced by a 6-day intracerebroventricular infusion of bacterial lipopolysaccharide (LPS). In rats infused wi