Wing design involves many compromises, but none more important than the one between aerodynamics, represented by lift-to-drag ratio, and structural weight. Multidisciplinary design optimization is used to compare the effect of configuration changes on wing weight and lift/drag ratio for 1) cantilever, 2) strut-braced, and 3) truss-braced wing aircraft for a medium-range, transonic, 162 passenger mission. Pseudo-Pareto fronts are generated to illustrate maximum lift/drag ratio compared to minimum wing weight. Lower lift/drag ratio aircraft have a shorter, more highly swept wing, with a change in taper at 75% semispan. Higher lft/drag ratio aircraft have much greater span and maximum chord at 33% semispan. To increase lift/drag ratio, both wing-weight and takeoff gross weight penalties must be paid. However, there are high lift/drag ratio designs with low wing-weight penalty that are clearly displayed by the pseudo-Pareto front. Fuel weight minima were found in the high lift/drag ratio and low wing-weight region of the pseudo-Pareto front for the truss-braced wing with both fuselage-mounted and wing-mounted engine configurations and for the cantilever configuration. An interesting pseudo-Pareto front was observed for the wingmounted engine truss-braced wing configuration, where the pseudo-Pareto front almost became an asymptote to a lift/drag ratio of ∼45. Also, one can look across all the configurations and compare attractive designs from each to search for an overall best aircraft design.
RAS is a protein that is integral to the mitogen activating pathway (MAP) that controls cell growth and division. Mutations in RAS deregulate the pathway, which can result in cancer. When bound to the substrate GTP, RAS is activated; when bound to the substrate GDP, RAS is deactivated. The substrate bound to RAS catalyzes conformation changes in two switch regions, which coordinate the interaction RAS has with its substrate. To switch between GTP and GDP, RAS requires assistance from other proteins. GEFs activate RAS by exchanging GDP for GTP; GAPs deactivate RAS by assisting in GTP hydrolysis. The Moeller SMART Team in conjunction with MSOE Center for Biomolecular Modeling used 3‐D modeling and printing technology to pinpoint amino acids that play a crucial role in RAS GTP to GDP exchange. Our mentor, Dr. Nicolas Nassar, created RAS mutations and observed the effect they had on RAS. In these mutations, the two switch regions are restructured, which affects the MAP activity. This alters Mg2+ ion coordination and guanine nucleotide stabilization. These mutations also prevent the coordination of the catalytic water molecule responsible for the hydrolysis of GTP. In mutated RAS, GEFs are not able to exchange GDP for GTP. These mutants transform RAS to stay active longer compared to wt‐RAS. By learning about RAS GTP and GDP exchange, Dr. Nassar hopes to dock a small molecule into the binding site of cancerous RAS thus inhibiting the mitogen activating pathway.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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