Temperature variations have significant effects on propagation of Lamb wave and therefore can severely limit the damage detection for Lamb wave. In order to mitigate the temperature effect, a temperature compensation method based on baseline signal reconstruction is developed for Lamb wave-based damage detection. The method is a reconstruction of a baseline signal at the temperature of current signal. In other words, it compensates the baseline signal to the temperature of current signal. The Hilbert transform is used to compensate the phase of baseline signal. The Orthogonal matching pursuit (OMP) is used to compensate the amplitude of baseline signal. Experiments were conducted on two composite panels to validate the effectiveness of the proposed method. Results show that the proposed method could effectively work for temperature intervals of at least 18 °C with the baseline signal temperature as the center, and can be applied to the actual damage detection.

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In engineering applications, the robustness and effectiveness of damage diagnostic imaging for guided wave-based structural health monitoring could be affected by the complexity of structures. In this study, an elliptical ring distribution probability-based diagnostic imaging algorithm is proposed to mitigate this effect using the estimated wave velocity and damage index. This algorithm improves the ability of damage localization by modifying the defect distribution probability of probability-based diagnostic imaging. The elliptical ring distribution probability of the presence of defect is used for each sensing path in the algorithm. The width of the elliptical ring distribution probability is determined by the range of estimated wave velocity. The amplitude of the elliptical ring distribution probability is determined by the damage index. The damage location is determined by the cross region of different elliptical rings for different sensing paths. The capability of the algorithm is validated by identifying damages at different locations on a complex composite fuselage panel. The results show that the proposed algorithm can identify a single damage accurately and it can identify multiple damages effectively as well.

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As a classic immunoregulatory cytokine, interleukin-10 (IL-10) can provide in vivo and in vitro neuroprotection respectively during cerebral ischemia and after the oxygen-glucose deprivation (OGD)-induced injury. However, its role in cortical neuronal survival at different post-ischemic phases remains unclear. The current study found that IL-10 had distinct effects on the neuronal apoptosis at different OGD stages: at an early stage after OGD, IL-10 promoted the OGD-induced neuronal apoptosis in the cultured primary cortical neurons by activating p65 subunit, which up-regulated Bax expression and down-regulated Bcl-xL expression; at a late OGD stage, however, it attenuated the OGD-induced neuronal apoptosis by activating c-Rel, which up-regulated Bcl-xL expression and down-regulated Bax expression. The early-stage pro-apoptosis and late-stage anti-apoptosis were both partly abolished by PDTC, an NF-κB inhibitor, and promoted by PMA, an NF-κB activator. The optimal anti-apoptotic effect appeared when the cultured neurons were treated with IL-10 at 9-24 h after OGD. Taken together, our findings suggest that IL-10 exerts a dual effect on the survival of the cultured neurons by activating the NF-κB pathway at different stages after OGD injury and that PMA treatment at a late stage can facilitate the IL-10-conferred neuroprotection against OGD-induced neuronal injury.