ABSTRACT
Force changes in axially loaded members can be monitored by quantifying variations in impedance signatures. However, statistical damage metrics, which are not physically related to the axial load, often lead to difficulties in accurately estimating the amount of axial force changes. Inspired by the wearable technology, this study proposes a novel wearable piezoelectric interface that can be used to monitor and quantitatively estimate the force changes in axial members. Firstly, an impedance-based force estimation method was developed for axially loaded members. The estimation was based on the relationship between the axial force level and the peak frequencies of impedance signatures, which were obtained from the wearable piezoelectric interface. The estimation of the load transfer capability from the axial member to the wearable interface was found to be an important factor for the accurate prediction of axial force. Secondly, a prototype of the wearable piezoelectric interface was designed to be easily fitted into existing axial members. Finally, the feasibility of the proposed technique was established by assessing tension force changes in a numerical model of an axially loaded cylindrical member and a lab-scale model of a prestressed cable structure.
ABSTRACT
Despite its significant clinical implications, physiological hypertrophy remains poorly understood. In this study, the transcription coactivator Eya2 was shown to be up-regulated during physiological hypertrophy. Transgene- or adenovirus-mediated overexpression of Eya2 led to up-regulation of mTOR, a critical mediator of physiological hypertrophy. Luciferase reporter and chromatin immunoprecipitation assays revealed that Eya2 directly binds to and activates mTOR expression. The phosphorylation of mTOR downstream molecules was significantly enhanced in Eya2 transgenic (TG) hearts, implying that the Eya2-mediated induction of mTOR expression leads to an elevated mTOR activity. The transcription factor Six1 was also up-regulated during physiological hypertrophy and formed a complex with Eya2. Luciferase reporter and electrophoretic mobility shift assays revealed that the Eya2-Six1 complex binds to and enhances the expression of mTOR in a synergistic manner. Under pressure overload, Eya2 transgenic hearts developed hypertrophy which exhibited important molecular signatures of physiological hypertrophy, as assessed by gene expression profiling and measurements of expression levels of physiological hypertrophy-related genes by quantitative (q) RT-PCR. Examination of heart sections under electron microscopy revealed that the mitochondrial integrity remained largely intact in Eya2 transgenic mice, but not in wild-type littermates, under pressure overload. This finding was confirmed by measurements of mitochondrial DNA contents and the expression levels of mitochondrial function-related genes by qRT-PCR. These data suggest that Eya2 in a physical complex with Six1 plays a critical role in physiological hypertrophy. The cardioprotective effect of Eya2 appears to be due, at least in part, to its preservation of mitochondrial integrity upon pressure overload.
