Estimation of dispersion curves of water-loaded structures by using approximated acoustic mass.

For coupled structures surrounded by heavy fluids, it is difficult to obtain dispersion curves from an eigenvalue analysis, because the external fluid term in the coupled equation includes transcendental functions for frequency and wavenumber. Thus, in this study, the acoustic mass of the external fluid was approximated as a function of frequency or wavenumber only. The coupled equation can then be used to calculate eigenvalues, and can estimate dispersion curves from an eigenvalue analysis. Because of this assumption, those dispersion curves will contain errors. Accordingly, those errors were evaluated in this study through a comparison with a dispersion curve derived from forced responses. The acoustic mass was also evaluated for a water-loaded plate; this can be formulated theoretically. As a result, the acoustic mass is less sensitive to frequency changes than wavenumber changes, and using the fluid term defined at a low frequency has advantages when estimating the dispersion curve. Finally, the generality of the proposed method was identified through the application for a submerged cylindrical shell.

MicroRNA-302 induces proliferation and inhibits oxidant-induced cell death in human adipose tissue-derived mesenchymal stem cells.

Mesenchymal stem cells (MSCs) are a heterogeneous population of cells that proliferate in vitro as plastic-adherent cells, have a fibroblast-like morphology, form colonies in vitro and can differentiate into bone, cartilage and fat cells. The abundance, ease and repeatable access to subcutaneous adipose tissue and the simple isolation procedures provide clear advantages for the use of human adipose tissue-derived mesenchymal stem cells (hASDCs) in clinical applications. We screened microRNAs (miRNAs) that affected the proliferation and survival of hADSCs. Transfection of miR-302d mimic increased cell proliferation and protected cells from oxidant-induced cell death in hADSCs, which was supported by flow-cytometric analysis. miR-302d did not affect the expression of Bcl-2 family members or anti-oxidant molecules. The Nrf2-Keap1 system, which is one of the major mechanisms for the cellular defense against oxidative stress, was not altered by transfection of miR-302d mimic. To identify the target of the miR-302d actions on proliferation and survival of hADSCs, a microarray analysis was performed using miR-302d-overexpressing hADSCs. Real-time PCR analysis showed that transfection of miR-302d mimic inhibited the CDKN1A and CCL5 expression. Downregulation of CDKN1A with a specific siRNA mimicked the effect of miR-302d on hADSCs proliferation, but did not affect miR-302d-induced cell survival. Downregulation of CCL5 protected oxidant-induced cell death as miR-302d, inhibited oxidant-induced reactive oxygen species (ROS) generation and the addition of recombinant CCL5 inhibited the protective action of miR-302d on oxidant-induced cell death. This study indicates that miR-302 controls proliferation and cell survival of hADSCs through different targets and that this miRNA can be used to enhance the therapeutic efficacy of hADSCs transplantation in vivo.