Simultaneous state and unknown input reconstruction using cascaded high-gain observers

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Adaptive high gain observer based output feedback predictive controller for induction motor

International audienceAn accurate estimation of both rotor and stator resistances is usually required to achieve high performance control in induction machine drive systems. In our study, an output feedback predictive controller which is adaptive with respect to these parameters uncertainties is proposed. Such design attempts to a fully decoupling in speed and flux magnitude when conjoint estimation of the state and the critical parameters is performed. Precisely, two-stage of high gain observer are used to provide on-line update of rotor and stator resistances as well as following time evolution of the rotor flux and the load torque. Then, the instantaneous estimates are exploited in a constrained predictive controller for achieving the admissible tracking objective. The little number of the synthesis parameters and the ability of the control scheme to handle input constraints constitute the two main benefits of our design. Simulation results show that the proposed controller is suitable for high dynamics performance applications

Cascade High Gain Observers Based State and Unknown Input Reconstruction

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Improved high gain observer design for a class of disturbed nonlinear systems

International audienceAbstract This paper provides a redesigned version of the Standard High Gain Observer (SHGO) to cope with the peaking phenomenon occurring during the transient periods as well as the sensitivity to high frequency measurement noise. The observer design is performed for a class of uniformly observable systems with noise free as well as noisy output measurements and the resulting observer is referred to as Non Peaking Filtered High Gain Observer (NPFHGO). The NPFHGO shares the same structure as its underlying SHGO and differs only by its corrective term which is still parameterized by a unique positive scalar up to an appropriate expression involving nested saturations. Of a fundamental interest, the power of the scalar parameter does not exceed one unlike in the case of the SHGO where this power grows from 1 to the system dimension. Moreover, it is shown that the equations of the NPFHGO become identical to those of the SHGO after a transient time horizon that can made arbitrarily small for sufficiently high values of the design parameter. A particular emphasis is put on the case of systems with noisy output measurements. It is shown how a multiple integrator of the corrupted outputs can be cascaded with the original system leading to an augmented system included in the class of systems for which the NPFHGO has been designed. The performance and main properties of the NPFHGO are highlighted and compared to those of its underlying SHGO through simulation results involving a single link robot arm system

Quantitative and Topographical Analysis of the Losses of Cone Photoreceptors and Retinal Ganglion Cells Under Taurine Depletion

PURPOSE: Taurine depletion is known to induce photoreceptor degeneration and was recently found to also trigger retinal ganglion cell (RGC) loss similar to the retinal toxicity of vigabatrin. Our objective was to study the topographical loss of RGCs and cone photoreceptors, with a distinction between the two cone types (S- and L- cones) in an animal model of induced taurine depletion. METHODS: We used the taurine transporter (Tau-T) inhibitor, guanidoethane sulfonate (GES), to induce taurine depletion at a concentration of 1% in the drinking water. Spectral-domain optical coherence tomography (SD-OCT) and electroretinograms (ERG) were performed on animals after 2 months of GES treatment administered through the drinking water. Retinas were dissected as wholemounts and immunodetection of Brn3a (RGC), S-opsin (S-cones), and L-opsin (L-cones) was performed. The number of Brn3a+ RGCs, and L- and S-opsin+ cones was automatically quantified and their retinal distribution studied using isodensity maps. RESULTS: The treatment resulted in a significant reduction in plasma taurine levels and a profound dysfunction of visual performance as shown by ERG recordings. Optical coherence tomography analysis revealed that the retina was thinner in the taurine-depleted group. S-opsin+cones were more affected (36%) than L-opsin+cones (27%) with greater cone cell loss in the dorsal area whereas RGC loss (12%) was uniformly distributed. CONCLUSIONS: This study confirms that taurine depletion causes RGC and cone loss. Electroretinograms results show that taurine depletion induces retinal dysfunction in photoreceptors and in the inner retina. It establishes a gradient of cell loss depending on the cell type from S-opsin+cones, L-opsin+cones, to RGCs. The greater cell loss in the dorsal retina and of the S-cone population may underline different cellular mechanisms of cellular degeneration and suggests that S-cones may be more sensitive to light-induced retinal toxicity enhanced by the taurine depletion