Application of global positioning systems to electrical systems synchronized phasor measurements techniques and uses
Colloquium on Developments in the Use of Global Positioning Systems (GPS) in Power Systems,Feb 8 1994; part of: IEE Colloquium (Digest)
(032):4/1-4/2CITEKEY:Phadke1994
ABSTRACT: GPS navigational satellites provide an ideal method for distributing a common timing pulse at any point in the power network. Receivers of GPS transmission can reproduce the 1 pulse-per-second at any location on earth with better than 1 μsec accuracy. Thus, if GPS receivers are built into each measuring system, phasors measured by these systems could be used as simultaneous measurements from all points of the power system, offering far more accuracy than needed for performing engineering analysis functions.
ADDRESS: Virginia Tech, Blacksburg, VA, USA
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ISSN: 0963-3308
PUBLISHER: IEE,Stevenage,Engl
CITY: London,USA
Inhibition of superoxide anion generation by YC-1 in rat neutrophils through cyclic GMP-dependent and -independent mechanisms
Biochem.Pharmacol. 63(4):577-85
CITEKEY:Wang2002
ABSTRACT: 3-(5'-Hydroxymethyl-2'-furyl)-1-benzyl indazole (YC-1), a soluble guanylyl cyclase (sGC) activator, inhibited formyl-methionyl-leucyl-phenylalanine (fMLP)-induced superoxide anion (O(2)*(-)) generation and O(2) consumption in rat neutrophils (IC(50) values of 12.7+/-3.1 and 17.7+/-6.9 microM, respectively). Inhibition of O(2)*(-) generation by YC-1 was partially reversed by the cyclic GMP-lowering agent 6-anilinoquinoline-5,8-quinone (LY83583) and by the Rp isomer of 8-(4-chlorophenylthio)guanosine-3',5'-monophosphorothioate (Rp-8-pCPT-cGMPS), a cyclic GMP-dependent protein kinase inhibitor. In cell-free systems, YC-1 failed to alter O(2)*(-) generation during dihydroxyfumaric acid autoxidation, phorbol 12-myristate 13-acetate (PMA)-activated neutrophil particulate NADPH oxidase preparation, and arachidonic acid-induced NADPH oxidase activation. YC-1 increased cellular cyclic GMP levels through the activation of sGC and the inhibition of cyclic GMP-hydrolyzing phosphodiesterase activity. The plateau phase, but not the initial spike, of fMLP-induced [Ca(2+)](i) changes was inhibited by YC-1 (IC(50) about 15 microM). fMLP- but not PMA-induced phospholipase D activation was inhibited by YC-1 (IC(50) about 28 microM). Membrane-associated ADP-ribosylation factor and Rho A in cell activation was also reduced by YC-1 at a similar concentration range. Neither cytosolic protein kinase C (PKC) activity nor PKC membrane translocation was altered by YC-1. YC-1 did not affect either fMLP-induced phosphatidylinositol 3-kinase activation or p38 mitogen-activated protein kinase phosphorylation, but slightly attenuated the phosphorylation of extracellular signal-regulated kinase. Collectively, these results indicate that the inhibition of the fMLP-induced respiratory burst by YC-1 is mediated by cyclic GMP-dependent and -independent signaling mechanisms.
ADDRESS: Department of Education and Research, Taichung Veterans General Hospital, 160 Chung Kang Road, Sec. 3, 407, ROC, Taichung, Taiwan. w1994@vghtc.gov.tw
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