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[Objectives] Both the mechanical impedance of the foundation and the homogenization of foundation impedance among loading points can affect the radiation noise of underwater structures.[Methods] The mechanical impedance of a typical long underwater foundation was studied. A mathematical topology model in which the density of web plate was set to be the design variable was established to improve the homogenization of foundation impedance. An effective form of web perforation was put forward according to the result of topology optimization. On this basis,a multi-objective size optimization mathematical model based on tolerance ranking method was proposed. The thicknesses of plates constituting the foundation were used as design variables while the objective was to maximize the mechanical impedance and impedance uniformity simultaneously. Finally an optimum proposal of thicknesses of face plates,webs and knee plates was found.[Results] The result of topology optimization indicates that hole formed on foundation webs are not the same,and the centers of holes do not coincide with web centers. The size optimization result shows that the maximum dispersion of foundation impedance can be reduced by 9.37% with 33.31% weight saving,while the minimum mechanical impedance remains nearly unchanged by redistributing the material in plates of the foundation by matching thicknesses of face plates,webs and knee plates.[Conclusions] In order to improve the impedance homogenization among loading points, forms of perforations on foundation webs should not be the same. And foundation components in different areas can be different in order to take into account both the mechanical impedance and impedance homogenization. The study in this paper can provide reference for the optimal design of underwater structure foundation.

The dynamic changes of RNA N6-methyladenosine (m6A) during cancer progression participate in various cellular processes. However, less is known about a possible direct connection between upstream regulator and m6A modification, and therefore affects oncogenic progression. Here, we have identified that a key enzyme in N4-acetylcytidine (ac4C) acetylation NAT10 is highly expressed in human osteosarcoma tissues, and its knockdown enhanced m6A contents and significantly suppressed osteosarcoma cell growth, migration and invasion. Further results revealed that NAT10 silence inhibits mRNA stability and translation of m6A reader protein YTHDC1, and displayed an increase in glucose uptake, a decrease in lactate production and pyruvate content. YTHDC1 recognizes differential m6A sites on key enzymes of glycolysis phosphofructokinase (PFKM) and lactate dehydrogenase A (LDHA) mRNAs, which suppress glycolysis pathway by increasing mRNA stability of them in an m6A methylation-dependent manner. YTHDC1 partially abrogated the inhibitory effect caused by NAT10 knockdown in tumor models in vivo, lentiviral overexpression of YTHDC1 partially restored the reduced stability of YTHDC1 caused by lentiviral depleting NAT10 at the cellular level. Altogether, we found ac4C driven RNA m6A modification can positively regulate the glycolysis of cancer cells and reveals a previously unrecognized signaling axis of NAT10/ac4C-YTHDC1/m6A-LDHA/PFKM in osteosarcoma. 6WoSibQBSZGZLQEcMB75Lw Video Abstract [ABSTRACT FROM AUTHOR]