Optimal location of FACTS devices to enhance power system security

This paper compares three heuristic methods (SA, TS and GA) applied to the optimal location of FACTS devices in a power system. The optimizations are made on three parameters: the location of the devices, their types and their sizes. The FACTS devices are located in order to enhance the system security. Five types of FACTS controllers are modeled for steady-state studies: TCSC, TCVR, TCPST, SVC and UPFC. Simulations are performed on an IEEE 118-bus power system for several numbers of devices. Results show that the three algorithms converge to similar optimal solutions. The security margin of the system may be increased with the use of FACTS devices, but some limitations are observed. The locations of the devices and their influence areas are analyze

Optimal location of multi-type FACTS devices in a power system by means of genetic algorithms

This paper presents a genetic algorithm to seek the optimal location of multi-type FACTS devices in a power system. The optimizations are performed on three parameters: the location of the devices, their types and their values. The system loadability is applied as a measure of power system performance. Four different kinds of FACTS controllers are used and modeled for steady-state studies: TCSC, TCPST, TCVR and SVC. Simulations are done on a 118-bus power system for several numbers of devices. Results show the difference of efficiency of the devices used in this context. They also show that the simultaneous use of several kinds of controllers is the most efficient solution to increase the loadability of the system. In all the cases (single- and multi-type FACTS devices), we observe a maximum number of devices beyond which this loadability cannot be improve

Aldosterone-induced serum and glucocorticoid-induced kinase 1 expression is accompanied by Nedd4-2 phosphorylation and increased Na+ transport in cortical collecting duct cells

Aldosterone plays a central role in Na+ homeostasis by controlling Na+ reabsorption in the aldosterone-sensitive distal nephron involving the epithelial Na+ channel (ENaC). Part of the effects of aldosterone is mediated by serum and glucocorticoid-induced kinase 1 (Sgk1), a Ser/Thr kinase whose expression is rapidly induced by aldosterone and that increases in heterologous expression systems ENaC cell surface abundance and activity. Previous work in Xenopus laevis oocytes suggested that Sgk1 phosphorylates specific residues (Ser212 and Ser328) on the ubiquitin-protein ligase Nedd4-2, an enzyme that directly interacts with ENaC and negatively controls channel density at the plasma membrane. It further indicated that phosphorylation of Nedd4-2 led to impairment of ENaC/Nedd4-2 interaction and consequently to more channels at the cell surface. These data suggested a novel mode of aldosterone-dependent action, yet this was not demonstrated formally in epithelial cells that physiologically express ENaC. Here it is shown, with the use of an anti-phospho-Ser328-mNedd4-2 antibody, that 2 to 6 h of aldosterone treatment induces an increase in Nedd4-2 phosphorylation, both in a mouse cortical collecting duct cell line (mpkCCDcl4) and in kidneys of adrenalectomized rats. This augmentation, which is accompanied by a raise in Sgk1 expression and transepithelial Na+ transport, is sensitive to phosphatidylinositol-3 kinase inhibition, as is Sgk1 phosphorylation and Na+ transport. Hence, these data provide evidence in cortical collecting duct cells in vitro and in vivo that Sgk1-dependent phosphorylation of Nedd4-2 is part of the aldosterone response