Dynamic Identification Tests of 20th Century Historic Masonry Buildings in Japan

This paper discussed the application of health monitoring systems to 20th-century historic buildings. Natural disasters are major threats to monuments. They are often seismically vulnerable and require interventions. However, taking into account their historic and cultural values, it is appropriate to observe long-term behaviour before making a decision on intervention schemes. To this aim, health monitoring is considered an effective approach. In recent years, MEMS (micro-electromechanical systems) accelerometers have been attracting attention for their convenience and efficacy. Nonetheless, the reliability of MEMS accelerometers still needs to be examined for the monitoring of monuments as sufficient research contributions have not been made. This paper presented two case studies that were monitored by means of MEMS accelerometers. They were masonry structures positioned in seismic-prone regions in Japan. A number of earthquakes were detected by the accelerometers during one year of monitoring. To examine the accuracy of the adopted MEMS accelerometers, dynamic identification tests were conducted using high-sensitivity strain-gauge accelerometers and servo velocity meters. Based on responses obtained from the tests, numerical simulation was performed. Nonlinear static analysis was performed. The numerical simulation permitted the comparison of reliability among sensors and test types. This paper provided suggestions for the dynamic identification tests of heritage structures

NFIA differentially controls adipogenic and myogenic gene program through distinct pathways to ensure brown and beige adipocyte differentiation.

The transcription factor nuclear factor I-A (NFIA) is a regulator of brown adipocyte differentiation. Here we show that the C-terminal 17 amino acid residues of NFIA (which we call pro#3 domain) are required for the transcriptional activity of NFIA. Full-length NFIA-but not deletion mutant lacking pro#3 domain-rescued impaired expression of PPARγ, the master transcriptional regulator of adipogenesis and impaired adipocyte differentiation in NFIA-knockout cells. Mechanistically, the ability of NFIA to penetrate chromatin and bind to the crucial Pparg enhancer is mediated through pro#3 domain. However, the deletion mutant still binds to Myod1 enhancer to repress expression of MyoD, the master transcriptional regulator of myogenesis as well as proximally transcribed non-coding RNA called DRReRNA, via competition with KLF5 in terms of enhancer binding, leading to suppression of myogenic gene program. Therefore, the negative effect of NFIA on the myogenic gene program is, at least partly, independent of the positive effect on PPARγ expression and its downstream adipogenic gene program. These results uncover multiple ways of action of NFIA to ensure optimal regulation of brown and beige adipocyte differentiation

1,2,3-Triazine formation mechanism of the fairy chemical 2-azahypoxanthine in the fairy ring-forming fungus Lepista sordida

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