Fast and reliable black start plays a key role in improving the ability of the power system to resist the risk of large-scale blackouts. For a black start with high voltage and long-distance transmission lines, it is much easier to cause phenomena such as self-excitation and power frequency/operating overvoltage, which may lead to black start failure and impact the reliability of the system's restoration. Meanwhile, the long time needed to crank up the non-black start units will impact the speed of the restoration. This paper addresses the advantages of using a thermal power unit with a fast cut back (FCB) function as a black start unit, and studies the transient process of the FCB unit during the restoration. Firstly, key problems in the power system black start process are analyzed and a practical engineering criterion of self-excitation is proposed. Secondly, the dynamic model of the FCB unit is presented. Thirdly, the field test of the FCB unit load rejection and black start is introduced, which is the first successful field test of black start with 500 kV long-distance lines in China Southern Power Grid (CSG). Finally, the transient process of this test is simulated using the PSCAD/EMTDC software, and the simulation results accord well with the field test results, which verifies the correctness of the FCB model and the self-excitation engineering criterion proposed.
OPEN ACCESSEnergies 2014, 7 2741
Rationale:Th2 polarization plays a central role in the pathogenesis of allergic diseases such as airway allergy. The underlying mechanism is not fully understood yet. X-box-binding protein-1 (XBP1) can regulate immune cell activities upon exposing stressful events. The role of XBP1 in the development of Th2 polarization has not yet been explored. Methods: Mice carrying Xbp1-deficient CD4 + T cells were employed to observe the role of XBP1 in the induction of airway allergy. A cell culture model was established to evaluate the role of XBP1 in facilitating the Th2 lineage commitment. Results: We found that Xbp1 ablation in CD4 + T cells prevented induction of Th2 polarization in the mouse airway tract. XBP1 was indispensable in the Th2 lineage commitment. XBP1 mediated the effects of 3-methyl-4-nitrophenol (MNP) on facilitating inducing antigen-specific Th2 response in the airways. Exposure to MNP induced expression of XBP1 in CD4 + T cells. RhoA facilitated the binding between XBP1 and GATA3 in CD4 + T cells. XBP1 induced GATA3 phosphorylation to promote the Il4 gene transcription. Modulation of the RhoA/XBP1 axis mitigated experimental allergic response in the mouse airways. Conclusions: A potential therapeutic target, XBP1, was identified in this study. XBP1 was required in the development of skewed Th2 response in the airways. Inhibiting XBP1 alleviated Th2 polarization-related immune inflammation in the airways. The data suggest that inhibiting XBP1 has the translation potential for the treatment of airway allergy.
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