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Chronic inflammation is clearly associated with an increase in the risk of cancer. Non-steroidal anti-inflammatory drugs (NSAIDs) are well documented as agents that inhibit tumor growth and with long-term use can prevent tumor development. NSAID-activated gene (NAG-1), a unique member of the TGF-beta superfamily, is highly induced by NSAIDs and numerous drugs and chemicals with anti-tumorigenic activities.

The invention is a STAT5 mutant mouse that can be used in research related to cancer, autoimmunity and infectious diseases as well as drug screening. The mouse model itself has multiple immunological defects resulting in formation of STAT5 dimers but not tetramers.

Airway diseases, such as Asthma and Chronic Obstructive Pulmonary Disease (COPD), constitute a major health burden worldwide. It is estimated, for example, that nearly 15.0% of the adult population in the US are affected with such diseases, and the economic cost burden is over $23 billion annually. Unfortunately, the current options for treatment of such diseases are quite limited, consisting only of bronchodilators and inhaled steroids. The need for a novel and more effective class of therapeutics agents is imperative.

The transfusion of regulatory T cells (Tregs) has been used in the clinic to successfully prevent graft vs. host disease and is currently being evaluated in the treatment of other autoimmune diseases, such as organ graft rejection, type 1 diabetes and multiple sclerosis. Prior to transfusion, adoptive regulatory T cell transfer requires the expansion of regulatory T cells in culture; this results in a mixed population of regulatory T cells that limits the effectiveness of the transferred cells.

Adenosine modulates many physiological processes by activating specific adenosine receptors. These adenosine receptors play a critical role in the regulation of cellular signaling and are broadly distributed throughout the body. Thus, the ability to modulate adenosine receptor-mediated signaling is an attractive therapeutic strategy for a broad range of diseases. This technology relates to a group of compounds that display high affinity and specificity for the A1 adenosine receptor subtype.

This technology provides novel antibodies and methods for diagnostics and treatment of disorders arising from dysregulation of the immune system using antibodies directed against glucocorticoid-induced tumor necrosis factor receptor family-related receptor ligand (GITRL). Also available are hybridomas producing anti-mouse GITRL monoclonal antibodies (clone 5F1).

There is no vaccine for malaria, and there is growing resistance to existing anti-malarial drugs. Sexual stage-specific antigens are of interest as vaccine candidates because disruption of these antigens would reduce the fertility and, thus, the infectivity of the parasite.

The invention pertains to derivatives of docosahexaenoylethanolamide (synaptamide or DEA) and their use in inducing neurogenesis, neurite growth, and/or synaptogenesis. As such, these DEA derivatives can be used as therapeutics for neurodegenerative diseases such as traumatic brain injury, spinal cord injury, peripheral nerve injury, stroke, multiple sclerosis, autism, Alzheimer's disease, Huntington's disease, Parkinson's disease, amyotrophic lateral sclerosis. The DEA derivatives of the invention have increased potency and hydrolysis resistance as compared to native DEA.

JC Virus causes a fatal disease in the brain called progressive multifocal leukoencephalopathy (PML) that occurs in many patients with immunocompromised conditions. The finding of JCV DNA in the patients with neurological symptoms of PML is a diagnostic criterion and is needed to confirm the diagnosis of PML to rule out other neurological conditions. Certain JC virus variants are known to have a greater association with PML. For example, "Prototype" JC virus is far more pathogenic than "Archetype" JC virus.