A Nonlinear Ultrasonic Modulation Method for Crack Detection in Turbine Blades

In modern gas turbines, efforts are being made to improve efficiency even further. This is achieved primarily by increasing the generated pressure ratio in the compressor and by increasing the turbine inlet temperature. This leads to enormous loads on the components in the hot gas region in the turbine. As a result, non-destructive testing and structural health monitoring (SHM) processes are becoming increasingly important to gas turbine manufacturers. Initial cracks in the turbine blades must be identified before catastrophic events occur. A proven method is the linear ultrasound method. By monitoring the amplitude and phase fluctuations of the input signal, structural integrity of the components can be detected. However, closed cracks or small cracks cannot be easily detected due to a low impedance mismatch with the surrounding materials. By contrast, nonlinear ultrasound methods have shown that damages can be identified at an early stage by monitoring new signal components such as sub- and higher harmonics of the fundamental frequency in the frequency spectrum. These are generated by distortion of the elastic waveform due to damage/nonlinearity of the material. In this paper, new global nonlinear parameters were derived that result from the dual excitation of two different ultrasound frequencies. These nonlinear features were used to assess the presence of cracks as well as their qualitative sizes. The proposed approach was tested on several samples and turbine blades with artificial and real defects. The results were compared to samples without failure. Numerical simulations were conducted to investigate nonlinear elastic interaction of the stress waves with the damage regions. The results show a clear trend of nonlinear parameters changing as a function of the crack size, demonstrating the capability of the proposed approach to detect in-service cracks

Molecular Cloning and Functional Characterization of a Unique Mammalian Cardiac Na v Channel Isoform with Low Sensitivity to the Synthetic Inactivation Inhibitor (Ϫ)-(S)-6-Amino-␣-[(4- diphenylmethyl-1-piperazinyl)-methyl]-9H-purine-9-ethanol (SDZ 211-939

ABSTRACT Cardiac voltage-dependent sodium channels (Na v ) are drug targets for synthetic inactivation inhibitors typified by (Ϯ)-4-[3-(4-diphenylmethyl-1-piperazinyl)-2-hydroxy propoxy]-1H-indole-2-carbonitrile (DPI 201-106), of which the molecular mode of action is not yet defined. The previous observation by Mevissen and coworkers in 2001 of the electrophysiological ineffectiveness of DPI 201-106 in the bovine heart, in contrast to other species, offers the opportunity for investigating these open questions. We now report about the molecular cloning, expression in Xenopus laevis oocytes, and electrophysiological characterization of a unique bovine heart sodium channel. Although the predicted 2022-amino acid bovine heart sodium channel (bH1) shares 92% identity with the rat and human isoforms and normal gating properties, it displays drastically reduced sensitivity to (Ϫ)-(S)-6-amino-␣-[(4-diphenylmethyl-1-piperazinyl)-methyl]-9H-purine-9-ethanol (SDZ 211-939). Experimental results with Anemonia sulcata toxin II (0.1-2.5 M) exclude the possibility of an overall insensitivity of this isoform to various sodium channel modulators. The binding of SDZ 211-939 seems to be largely unaffected (EC 50 of 10.3 and 10.6 M for bovine and rat isoforms, respectively) but the corresponding efficacy in bovine (V m of 0.15) is approximately 5 times smaller compared with the rat heart isoform (V m of 0.69). The comparison of the primary structure of bH1 to other sodium channels and the gating properties obtained in presence or absence of SDZ 211-939 revealed a high degree of similarity. Whether the mechanism of channel modulation depends on the interaction of synthetic modulators with some possibly voltageindependent part of the inactivation machinery needs to be determined