The Cyclone Global Navigation Satellite System (CYGNSS) is a new NASA earth science mission scheduled to be launched in 2016 that focuses on tropical cyclones (TCs) and tropical convection. The mission’s two primary objectives are the measurement of ocean surface wind speed with sufficient temporal resolution to resolve short-time-scale processes such as the rapid intensification phase of TC development and the ability of the surface measurements to penetrate through the extremely high precipitation rates typically encountered in the TC inner core. The mission’s goal is to support significant improvements in our ability to forecast TC track, intensity, and storm surge through better observations and, ultimately, better understanding of inner-core processes. CYGNSS meets its temporal sampling objective by deploying a constellation of eight satellites. Its ability to see through heavy precipitation is enabled by its operation as a bistatic radar using low-frequency GPS signals. The mission will deploy an eight-spacecraft constellation in a low-inclination (35°) circular orbit to maximize coverage and sampling in the tropics. Each CYGNSS spacecraft carries a four-channel radar receiver that measures GPS navigation signals scattered by the ocean surface. The mission will measure inner-core surface winds with high temporal resolution and spatial coverage, under all precipitating conditions, and over the full dynamic range of TC wind speeds.

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Aspirin, the pro-drug of salicylate, is associated with reduced incidence of death from cancers of the colon, lung and prostate and is commonly prescribed in combination with metformin in individuals with type 2 diabetes. Salicylate activates the AMP-activated protein kinase (AMPK) by binding at the A-769662 drug binding site on the AMPK β1-subunit, a mechanism that is distinct from metformin which disrupts the adenylate charge of the cell. A hallmark of many cancers is high rates of fatty acid synthesis and AMPK inhibits this pathway through phosphorylation of acetyl-CoA carboxylase (ACC). It is currently unknown whether targeting the AMPK-ACC-lipogenic pathway using salicylate and/or metformin may be effective for inhibiting cancer cell survival. Salicylate suppresses clonogenic survival of prostate and lung cancer cells at therapeutic concentrations achievable following the ingestion of aspirin (<1.0 mM); effects not observed in prostate (PNT1A) and lung (MRC-5) epithelial cell lines. Salicylate concentrations of 1 mM increased the phosphorylation of ACC and suppressed de novo lipogenesis and these effects were enhanced with the addition of clinical concentrations of metformin (100 μM) and eliminated in mouse embryonic fibroblasts (MEFs) deficient in AMPK β1. Supplementation of media with fatty acids and/or cholesterol reverses the suppressive effects of salicylate and metformin on cell survival indicating the inhibition of de novo lipogenesis is probably important. Pre-clinical studies evaluating the use of salicylate based drugs alone and in combination with metformin to inhibit de novo lipogenesis and the survival of prostate and lung cancers are warranted.

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