RESUMEN
The purpose of this study was to improve the accuracy of the theoretical analysis of sound absorption mechanisms when a back air space is used in nonwoven fabrics. In the case of a nonwoven sheet with a back air space, it can be shown that there is a difference between the experimental results and theoretical analysis results obtained using the Miki model when the area of the nonwoven sheet is large. Therefore, in this study, the accuracy of the theoretical values was improved using the plate vibration model in conjunction with the Miki model. The experimental results showed that when the vibration of the nonwoven sheet was suppressed, the sound absorption coefficient was higher than that of the vibration-prone nonwoven sheet alone. The sound absorption coefficient at the peak frequency was increased by >0.2, especially for 3501BD. Using the support frame, the sound absorption coefficient at the peak frequencies of 3A01A and 3701B was increased to 0.99. In the theoretical analysis of a large-area, vibration-prone nonwoven fabric, in which the vibration of the nonwoven fabric was taken into account, the theoretical values were in agreement with the experimental values, and the accuracy of the theoretical values was improved. Comparing the theoretical values for nonwoven fabrics without high ventilation resistance, the sound absorption coefficient was greater when vibration was not considered. Therefore, it was suggested that the vibration of the nonwoven fabric hinders sound absorption.
RESUMEN
Activating transcription factor 5 (ATF5) is a stress-responsive transcription factor that belongs to the cAMP response element-binding protein (CREB)/ATF family, and is essential for the differentiation and survival of sensory neurons in murine olfactory organs. However, the study of associated proteins and target genes for ATF5 has been hampered due to the limited availability of immunoprecipitation-grade ATF5 antibodies. To overcome this issue, we generated hemagglutinin (HA)-tag knock-in mice for ATF5 using CRISPR/Cas9-mediated genome editing with one-step electroporation in oviducts (i-GONAD). ATF5-HA fusion proteins were detected in the nuclei of immature and some mature olfactory and vomeronasal sensory neurons in the main olfactory epithelium and vomeronasal organ, respectively, as endogenous ATF5 proteins were expressed, and some ATF5-HA proteins were found to be phosphorylated. Chromatin immunoprecipitation (ChIP) experiments revealed that ATF5-HA bound to the CCAAT/enhancer-binding protein (C/EBP)-ATF response element site in the promotor region of receptor transporting protein 1 (Rtp1), a chaperone gene responsible for proper olfactory receptor expression. These knock-in mice may be used to examine the expression, localization, and protein-protein/-DNA interactions of endogenous ATF5 and, ultimately, the function of ATF5 in vivo.
