Modelization and analysis of the electric arc in low voltage circuit breakers

246 p.

Gain Scheduling Control of an Islanded Microgrid Voltage

The aim of this research study has been to design a gain scheduling (GS) digital controller in order to control the voltage of an islanded microgrid in the presence of fast varying loads (FVLs), and to compare it to a robust controller. The inverter which feeds the microgrid is connected to it through an inductance-capacitor-inductance (LCL) filter. The oscillatory and nonlinear behaviour of the plant is analyzed in the whole operating zone. Afterwards, the design of the controllers which contain two loops in cascade are described. The first loop concerns the current control, while the second is linked to the voltage regulation. Two controllers, one defined as Robust and another one as GS controller, are designed for the two loops, emphasizing in their robustness and their ability to damp the oscillatory plant behaviour. To finish, some simulations are carried out to study and compare the two kinds of controllers in different operating points. The results show that both controllers damp the oscillatory behaviour of the plant in closed loop (CL), and that the GS controller ensures a better rejection of current disturbances from FVLs.

CGP37157, an inhibitor of the mitochondrial Na+/Ca2+ exchanger, protects neurons from excitotoxicity by blocking voltage-gated Ca2+ channels

Inhibition of the mitochondrial Na+/Ca2+ exchanger (NCLX) by CGP37157 is protective in models of neuronal injury that involve disruption of intracellular Ca2+ homeostasis. However, the Ca2+ signaling pathways and stores underlying neuroprotection by that inhibitor are not well defined. In the present study, we analyzed how intracellular Ca2+ levels are modulated by CGP37157 (10 mu M) during NMDA insults in primary cultures of rat cortical neurons. We initially assessed the presence of NCLX in mitochondria of cultured neurons by immunolabeling, and subsequently, we analyzed the effects of CGP37157 on neuronal Ca2+ homeostasis using cameleon-based mitochondrial Ca2+ and cytosolic Ca2+ ([Ca2+](i)) live imaging. We observed that NCLX-driven mitochondrial Ca2+ exchange occurs in cortical neurons under basal conditions as CGP37157 induced a decrease in [Ca-2](i) concomitant with a Ca2+ accumulation inside the mitochondria. In turn, CGP37157 also inhibited mitochondrial Ca2+ efflux after the stimulation of acetylcholine receptors. In contrast, CGP37157 strongly prevented depolarization-induced [Ca2+](i) increase by blocking voltage-gated Ca2+ channels (VGCCs), whereas it did not induce depletion of ER Ca2+ stores. Moreover, mitochondrial Ca2+ overload was reduced as a consequence of diminished Ca2+ entry through VGCCs. The decrease in cytosolic and mitochondrial Ca2+ overload by CGP37157 resulted in a reduction of excitotoxic mitochondrial damage, characterized here by a reduction in mitochondrial membrane depolarization, oxidative stress and calpain activation. In summary, our results provide evidence that during excitotoxicity CGP37157 modulates cytosolic and mitochondrial Ca2+ dynamics that leads to attenuation of NMDA-induced mitochondrial dysfunction and neuronal cell death by blocking VGCCs.