RESUMO
Recent advances in computing, rendering, and display technologies have generated increased accessibility for virtual reality (VR). VR allows the creation of dynamic, high-fidelity environments to simulate dangerous situations, test conditions, and visualize concepts. Consequently, numerous products have been developed, but many of these are limited in scope. Therefore, the National Institute for Occupational Safety and Health researchers developed a VR framework, called VR Mine, to rapidly create an underground mine for human data collection, simulation, visualization, and training. This paper describes the features of VR Mine using self-escape and proximity detection as case studies. Features include mine generation, simulated networks, proximity detection systems, and the integration and visualization of real-time ventilation models.
RESUMO
Diet and obesity, and their associated metabolic alterations, are some of the fastest-growing causes of disease and death in America. Findings from epidemiological studies correlating obesity, the sources of dietary fat and prostate cancer (PCa) are conflicting. We have previously shown that 15% of PB-ErbB-2 x pten(+/-) mice developed PCa and exhibited increased phosphorylated 4E-BP1, but not the key PI3-kinase intermediary phospho-protein, mTOR, when maintained on unrefined mouse chow. We report herein that 100% of animals fed refined, westernized AIN-93-based diets containing corn oil developed PCa by 12 months of age. Increases in visceral fat and mTO R activation in the tumors were also observed. Furthermore, nuclear cyclin E levels were significantly induced by the AIN-93-corn oil-based diets versus chow. Replacing 50% of the corn oil with menhaden oil, with 21% of its triglycerides being n-3 PUFA's, had no effect on tumorigenesis, fat deposition, cyclin E or mTOR. Phosphorylated BAD levels were similar in the tumors of mice in all three diets. Our data demonstrated that in the context of our preclinical model, components of crude chow, but not dietary n-3 PUFAs, protect against PCa progression. In addition, these data establish phosphorylated mTOR, nuclear cyclin E and visceral fat deposits as possible biomarkers of increased dietary risk for PCa.