Source parameters for the September 7, 1988 northeastern Kentucky earthquake have been estimated from the analysis of surface-wave amplitude spectra. The source that best fits the observed data had a seismic moment of 2.0 × 1022 dyne-cm, a mechanism with strike = 198° ± 10°, dip = 51° ± 11°, and slip = −178° ± 17°, (T) trend = 160°, plunge = 25°, (P) trend = 55°, plunge = 28°, and source depth of 4 to 7 km. Thirty-two aftershocks were recorded during 2 weeks of monitoring following the mainshock; 23 of the aftershocks were locatable and fall on a roughly NW-SE linear trend. This trend is subparallel with the NW-SE nodal plane of the mainshock. Our analysis shows the 1988 event to be different from the July 27, 1980 mb,Lg = 5.3 earthquake located 11 km to the northwest. First, the 1988 event is considerably shallower (4 to 7 km) than the 1980 event (14 to 22 km). Second, data from the 1988 event suggest the motion is on a conjugate fault and is in contrast with the 1980 event, which had right-lateral strike-slip on a southeast-dipping plane.

ß-catenin expression increased. These data presume that the cytoskeleton is loose. Further, previous studies show that the mitogen-activated protein kinase (MAPK) pathway can induce cardiac hypertrophy. Our data showed that p-p38 expression increased with the overexpression of GSN in H9c2, and the transcription factor p-GATA4 expression also increased, suggesting that the overexpression of GSN in H9c2-induced cardiac hypertrophy seemed to be regulated by the p38/GATA4 pathway. Moreover, we used both the p38 inhibitor (SB203580) and GSN siRNA to confirm our conjecture. We found that both of these factors significantly suppressed gelsolin-induced cardiac hypertrophy which through p38/GATA4 signaling pathway.Conclusions: Therefore, we predict that the gene silencing of GSN and/or the downstream blocking of GSN along the p38 pathway could be applied to ameliorate pathological cardiac hypertrophy in the future. PP.42.15 ANGIOTENSIN II-DEPENDENT DIFFERENTIAL MIRNA EXPRESSION IN RAT RENAL EPITHELIAL TUBULAR CELLS

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