Vehicle optimal road departure prevention via model predictive control

This article addresses the problem of road departure prevention using integrated brake control. The scenario considered is when a high speed vehicle leaves the highway on a curve and enters the shoulder or another lane, due to excessive speed, or where the friction of the road drops due to adverse weather conditions. In such a scenario, the vehicle speed is too high for the available tyre-road friction and road departure is inevitable; however, its effect can be minimized with an optimal braking strategy. To achieve online implementation, the task is formulated as a receding horizon optimization problem and solved in a linear model predictive control (MPC) framework. In this formulation, a nonlinear tire model is adopted in order to work properly at the friction limits. The optimization results are close to those obtained previously using a particle model optimization, PPR, coupled to a control algorithm, MHA, specifically designed to operate at the vehicle friction limits. This shows the MPC formulation may equally be effective for vehicle control at the friction limits. The major difference here, compared to the earlier PPR/MHA control formulation, is that the proposed MPC strategy directly generates an optimal brake sequence, while PPR provides an optimal reference first, then MHA responds to the reference to give closed-loop actuator control. The presented MPC approach has the potential to be used in futur

Chapter 10: Tools for modeling, simulation, control, and verification of piecewise affine systems

A review of available software for modeling, simulation, control, identification and verification for piecewise affine system

The glutamate signalling in islet of Langerhans: molecular mechanisms of modulation

Increasing evidence suggests that the excitatory neurotransmitter L-glutamate functions as a modulator in the islet of Langerhans, an endocrine organ involved in blood glucose homeostasis. It is release by \u3b1-cells and, by acting on specific receptors, it modulates hormone secretion and \u3b2-cell mass. Its extracellular concentration is mainly controlled by the glutamate transporter GLT1 which is expressed on the plasma membrane of \u3b2-cells (Di Cairano et al, JBC 2011; 286: 14007). Aim of the proposed research was to verify the impact of acute and chronic changes in glucose concentrations on GLT1 localization/function and glutamate signalling in the islet. We found that acute exposure of human and clonal \u3b2-cells to high glucose concentrations (15 mM glucose) inhibited the GLT1 transport activity measured by [3H]D-glutamate uptake, in a dose-dependent manner. Furthermore, total internal reflection microscopy experiments performed on \u3b2-cells transfected with a GFP-GLT1 tagged transporter demonstrated that glucose stimulation decreased the surface stability of GLT1 and increased its endocytosis. Chronic exposure of human and clonal \u3b2-cells to high glucose concentrations caused the GLT1 relocalization in degradative compartments and significantly reduced its total expression. Interestingly, a similar intracellular GLT1 staining was detected in human islets from type 2 diabetic donors (n=8) but not from healthy controls (n=5). Understanding the molecular mechanisms that control glutamate release and signalling in islet of Langerhans may be important to control glucose homeostasis in health and disease