We show that H2O2 increases acetylcholinesterase (AChE) expression via transcriptional activation through c-Jun N-terminal kinase (JNK), since the JNK inhibitor SP600125, but not the extracellular signal-regulated kinase (ERK) pathway inhibitor PD98059 or p38 kinase inhibitor SB203580, attenuated H2O2-induced AChE expression and its promoter activity. Overexpression of hemagglutinin (HA)-JNK increases H2O2-induced AChE expression and its promoter activity, whereas the dominant negative mutant form of JNK suppressed H2O2-induced AChE expression and promoter activity. Mutation analysis indicates that the major response elements for JNK in the AChE promoter are the AP1-like element (TGAGTCT) site, located within the -1565/-1569 region of the AChE promoter, and the ATF2 element (CCACGTCA), within the -2185/-2177 region. The AP1-like element binds to the transcription factors, c-jun and ATF2, while the ATF2 element binds mainly ATF2. Taken together, our results strongly suggest that H2O2 induces AChE expression via the JNK/AP1/ ATF2 signaling pathway.

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We developed a 35kV/90MVA Superconducting Fault Current Limiter (SFCL) and installed it in a transmission network at Puji substation of China Southern Power Grid at the end of 2007. A 72 hour period of trial operation was conducted before the SFCL was commissioned into the grid. This device demonstrated having very low impedance in normal power transmission and no adverse effect on the power network. To fully examine its current limiting capacity, current limiting tests were conducted under artificially imposed short-circuit conditions on July 20, 2009. A series of five different tests, including a fail safe test, were carried out. The experimental results are in good agreement with design expectations. The device's current limiting capacity has been convincingly demonstrated. In this paper, we report some details of these tests and the resultant data.