Reliability-based design optimization applied to structures submitted to random fatigue loads

Structural and Multidisciplinary Optimization - The reliability-based design optimization (RBDO) aims to find the most balanced design through a compromise between cost and safety when...     

An approach for the reliability based design optimization of laminated composites

This article aims at optimizing laminated composite plates taking into account uncertainties in the structural dimensions. As laminated composites require a global optimization tool, the Particle Swarm Optimization (PSO) method is employed. A new Reliability Based Design Optimization (RBDO) methodology based on safety factors is presented and coupled with PSO. Such safety factors are derived from the Karush–Kuhn–Tucker optimality conditions of the reliability index approach and eliminate the need for reliability analysis in RBDO. The plate weight minimization is the objective function of the optimization process. The results show that the coupling of the evolutionary algorithm with the safety-factor method proposed in this article successfully performs the RBDO of laminated composite structures.     

A computationally efficient approach to swimming monofin optimization

Monofins provide swimmers with an efficient alternative to the standard pair of fins. For example, all short and long distance human swimming records have been established using monofins. Current monofin design is mostly empirical, so the objectives of this work are to analyze monofin propulsion through coupled fluid–structure simulation and to optimize its flexural stiffness distribution. The optimization process maximizes the propulsive power provided by the monofin with a constraint on the total expended power. To be able to carry out the optimization of the coupled fluid–structure system, which is numerically costly to evaluate, the following simplifications are proposed: (1) a 2-D unsteady, inviscid, and incompressible fluid flow is considered; (2) the swimmer is composed of linear articulated segments, whose kinematics is imposed and identified from experimental data; and (3) the monofin is represented by rigid bars linked by torsional springs. For various allowable swimmer powers, optimal 2-D stiffness distributions are obtained using the Globalized and Bounded Nelder–Mead algorithm. Finally, an identification procedure is described to translate the optimal 2-D stiffness distributions into 3-D thickness profiles for a given monofin planform shape.     

Characterization of the mechanical behaviour parameters of the costo-vertebral joint

Humic acid in the drinking water of blackfoot disease endemic areas in Taiwan has been implicated as one of the aetiological factors of the disease. For this report we examined the effects of humic acid on the expression of thrombomodulin (TM) cofactor activity by cultured human umbilical vein endothelial cells (HUVEC). Incubation of HUVEC with humic acid (HA) isolated from the drinking water, as a synthetic humic acid polymer (SHA) or with commercial HA, resulted in a dose-dependent reduction of cell surface thrombomodulin activity. Characterization of the mechanism by which humic acid reduced the protein C activation indicated that inhibition was not caused by production or release of a protein C inhibitor. Kinetic analysis showed that binding affinities of TM to thrombin and of TM-thrombin complex to protein C was unchanged upon humic acid treatment. However, the cell surface TM activity was reduced by humic acid, which functions as an irreversible noncompetitive inhibitor of thrombin binding. Down-regulation of TM was inhibited by non-selective protein kinase C inhibitors and a selective inhibitor. These results suggest that protein kinase C is intricately involved in HA-induced TM down-regulation. Down-regulation of TM was also inhibited by free radical scavengers. All these changes occurred in the absence of significant cytotoxic effect. In conclusion, our results suggest that HA induces down-regulation of TM by directly increasing permeability of the cell membrane, thus causing elevation in [Ca2+]i. This species functions as a second messenger to activate protein kinase C, and/or Ca-dependent enzymes eventually inducing down-regulation of TM. Attenuation of vascular endothelial cell TM cofactor activity by humic acid may play a role in the humic acid-induced thrombotic vascular disorders of blackfoot disease.