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The geomorphic expression of the frontal Western Foothills in central Taiwan is usually defined by a late Holocene scarp that ranges from tens to hundreds of meters in height. This scarp is the product of displacement on a near-surface 20-30Њ east-dipping thrust fault, the Chelungpu fault, which ruptured during the Chichi earthquake. The large scarp height may correspond directly to the accumulation of successive surface ruptures. The Chushan site is located on the southern part of this fault where the Chichi earthquake produced a scarp with a 1.7-m vertical offset for the total vertical separation. Based on core-boring estimates, the vertical displacement on both sides is 7 m along a 24Њ east-dipping thrust fault. The results from our paleoseismic analysis indicate that five large paleoearthquake events have caused the large offsets during the past 2 ka. The radiocarbon age constraints of the paleoearthquakes suggest a clustering of 540-790 cal yr B.P. (E2), 710-950 cal yr B.P. (E3), 1380-1700 cal yr B.P. (E4), 1710-1930 cal yr B.P. (E5), and the 1999 Chichi earthquake. Events E3 and E4 have not been reported in previous studies and we did not observe event E1 (300-430 cal yr B.P.) at the site. Based on displacement and fault segmentation from the geologic features, we argue that the two new events may have occurred along the northern part of the Chelungpu fault. The vertical slip rate is estimated to be at least 3.9 ‫ע‬ 0.2 mm/yr over the past 2 ka, which is similar to the long-term estimation through a calculation of late Pleistocene-Holocene terrace elevations on the hanging wall.

Overexpression of leucine aminopeptidase 3 (LAP3) is involved in proliferation, migration, and invasion of several tumor cells and plays a crucial role in tumor metastasis. However, the related mechanism remains unknown. In this study, we used MDA-MB-231 and MCF7 breast cancer cell lines to explore the role of LAP3 in the regulation of cancer cell migration and invasion by employing the natural LAP3 inhibitor bestatin and a lentivirus vector that overexpresses or knocks down LAP3. Bestatin inhibited tumor cell migration and invasion in a dose-dependent manner. Western blot assay showed that bestatin and knockdown of LAP3 upregulated phosphorylation of Hsp27 and downregulated expression of fascin. Phosphorylation of Akt and expression of matrix metalloproteinase-2/9 can also be downregulated. LAP3 overexpression showed the opposite results. Immunohistochemistry analysis was conducted to detect expression levels of LAP3 in breast cancer tissues. High LAP3 expression was correlated with the grade of malignancy. Findings of this study uncovered the molecular mechanism of LAP3 on breast cancer metastasis and indicated that LAP3 may act as a potential antimetastasis therapeutic target.fascin, leucine aminopeptidase 3 (LAP3), matrix metalloproteinases-2/9 (MMP-2/9), metastasis, signaling transduction J Cell Biochem. 2019;120:3611-3620.wileyonlinelibrary.com/journal/jcb

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Expression of L1 mRNA, the first step in the L1 copy-and-paste amplification cycle, is a prerequisite for L1-associated genomic instability. We used a reported stringent bioinformatics method to parse L1 mRNA transcripts and measure the level of L1 mRNA expressed in mouse and rat organs at a locus-specific resolution. This analysis determined that mRNA expression of L1 loci in rodents exhibits striking organ specificity with less than 0.8% of loci shared between organs of the same organism. This organ specificity in L1 mRNA expression is preserved in male and female mice and across age groups. We discovered notable differences in L1 mRNA expression between sexes with only 5% of expressed L1 loci shared between male and female mice. Moreover, we report that the levels of total L1 mRNA expression and the number and spectrum of expressed L1 loci fluctuate with age as independent variables, demonstrating different patterns in different organs and sexes. Overall, our comparisons between organs and sexes and across ages ranging from 2 to 22 months establish previously unforeseen dynamic changes in L1 mRNA expression in vivo. These findings establish the beginning of an atlas of endogenous L1 mRNA expression across a broad range of biological variables that will guide future studies.