The Canton Tower (formerly named Guangzhou New TV Tower) of 610 m high has been instrumented with a long-term structural health monitoring (SHM) system consisting of over 700 sensors of sixteen types. Under the auspices of the Asian-Pacific Network of Centers for Research in Smart Structures Technology (ANCRiSST), an SHM benchmark problem for high-rise structures has been developed by taking the instrumented Canton Tower as a host structure. This benchmark problem aims to provide an international platform for direct comparison of various SHM-related methodologies and algorithms with the use of realworld monitoring data from a large-scale structure, and to narrow the gap that currently exists between the research and the practice of SHM. This paper first briefs the SHM system deployed on the Canton Tower, and the development of an elaborate three-dimensional (3D) full-scale finite element model (FEM) and the validation of the model using the measured modal data of the structure. In succession comes the formulation of an equivalent reduced-order FEM which is developed specifically for the benchmark study. The reducedorder FEM, which comprises 37 beam elements and a total of 185 degrees-of-freedom (DOFs), has been elaborately tuned to coincide well with the full-scale FEM in terms of both modal frequencies and mode shapes. The field measurement data (including those obtained from 20 accelerometers, one anemometer and one temperature sensor) from the Canton Tower, which are available for the benchmark study, are subsequently presented together with a description of the sensor deployment locations and the sensor specifications.

Background Previous studies have revealed the key functions of N6-methyladenosine (m6A) modification in breast cancer (BC). MALAT1 as a highly m6A modified lncRNA associated with cancer development and metastasis, but the functional relevance of m6A methyltransferase and MALAT1 in BC is still unknown. Here, our study investigated the effects of the novel m6A methyltransferase METTL3 on epithelial-mesenchymal transition (EMT) in BC via the MALAT1/miR-26b/HMGA2 axis. Methods Firstly, we collected clinical BC samples and cultured BC cells, and detected mRNA and protein levels in the human samples and human cell lines by RT-qPCR and Western blot, respectively. Then, the binding of MALAT1 and miR-26b and the targeting relationship between miR-26b and HMGA2 were examined by dual-luciferase assay. Moreover, the binding of MALAT1 and miR-26b was tested by RNA pull down and RNA immunoprecipitation (RIP) assays. Methylated-RNA immunoprecipitation (Me-RIP) was used to detect the m6A modification level of MALAT1. The interaction of METTL3 and MALAT1 was detected by photoactivatable ribonucleoside-crosslinking immunoprecipitation (PAR-CLIP). Finally, effects on invasion and migration were detected by Transwell. Results In BC, the level of miR-26b was consistently low, while the levels of METTL3, MALAT1 and HMGA2 were high. Further experiments showed that METTL3 up-regulated MALAT1 expression by modulating the m6A modification of MALAT1, and that MALAT1 could promote the expression of HMGA2 by sponging miR-26b. In BC cells, we found that silencing METTL3 could inhibit EMT and tumor cell invasion by suppressing MALAT1. Furthermore, MALAT1 mediated miR-26b to target HMGA2 and promote EMT, migration, and invasion. In summary, METTL3 promoted tumorigenesis of BC via the MALAT1/miR-26b/HMGA2 axis. Conclusions Silencing METTL3 down-regulate MALAT1 and HMGA2 by sponging miR-26b, and finally inhibit EMT, migration and invasion in BC, providing a theoretical basis for clinical treatment of BC.

No abstract