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This study divided into three portions to provide performance requirements; overview and development of various engine mounts; and the optimization of engine mount systems. The first part provides an insight about the ideal engine mount system that should isolate vibration caused by engine disturbance force in various speed range and prevent engine bounce from shock excitation. This implies that the dynamic stiffness and damping of the engine mount should be frequency and amplitude dependent. Therefore, the development of engine mounting systems has mostly concentrated on improvement of frequency and amplitude dependent properties. The second part starts discussion on the conventional elastomeric mounts that offer a trade-off between static deflection and vibration isolation. The next level, passive hydraulic mounts can provide a better performance than elastomeric mounts especially in the low frequency range. Subsequently, semi-active and active techniques are used to improve performance of hydraulic mounts by making them more tunable. The active engine mounting system can be very stiff at low frequency and be tuned to be very soft at the higher frequency range to isolate the vibration. The final part is about the optimization of engine mounting systems. An overview of the current work on this optimization shows some limitations. Further study is needed to consider the nonlinearities and variations in properties of different types of mounting systems.

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The function of miR-592 has been investigated in many types of cancer, however its roles in breast cancer remain unclear. We therefore investigated the biological function and underlying mechanism of miR-592 in breast cancer. In the present study, a marked downregulation of miR-592 was observed in breast cancer tissues and cell lines compared to the matched adjacent non-tumor tissues and normal breast cell line. Statistical analysis revealed that decreased miR-592 was negatively associated with advanced clinical stage, distant metastasis and lymph node metastases. Function analysis demonstrated that overexpression of miR-592 significantly inhibited cell proliferation, clone formation, migration and invasion in breast cancer cells in vitro, as well as suppressed tumor growth in vivo. Furthermore, transforming growth factor β-2 (TGFβ-2), a known oncogene, was identified as a direct target of miR-592, and its mRNA expression level was inversely correlated with the expression level of miR-592 in human breast cancer specimens. Restoration of TGFβ-2 expression rescued the inhibitory effect in breast cancer cells caused by miR-592. Collectively, these data suggest that miR-592 may exert it suppressive role in breast cancer, at least in part, by targeting TGFβ-2, and that miR-592 may be a novel target for breast cancer treatment.