Fault Diagnosis of Rolling Element Bearings with a Two-Step Scheme Based on Permutation Entropy and Random Forests.

This study presents a two-step fault diagnosis scheme combined with statistical classification and random forests-based classification for rolling element bearings. Considering the inequality of features sensitivity in different diagnosis steps, the proposed method utilizes permutation entropy and variational mode decomposition to depict vibration signals under single scale and multiscale. In the first step, the permutation entropy features on the single scale of original signals are extracted and the statistical classification model based on Chebyshev's inequality is constructed to detect the faults with a preliminary acquaintance of the bearing condition. In the second step, vibration signals with fault conditions are firstly decomposed into a collection of intrinsic mode functions by using variational mode decomposition and then multiscale permutation entropy features derived from each mono-component are extracted to identify the specific fault types. In order to improve the classification ability of the characteristic data, the out-of-bag estimation of random forests is firstly employed to reelect and refine the original multiscale permutation entropy features. Then the refined features are considered as the input data to train the random forests-based classification model. Finally, the condition data of bearings with different fault conditions are employed to evaluate the performance of the proposed method. The results indicate that the proposed method can effectively identify the working conditions and fault types of rolling element bearings.

NOD2 mediates isoflurane preconditioning-induced protection of myocardial injury.

Anesthetic cardioprotection reduces myocardial infarct size following ischemia-reperfusion injury. However, the underlying mechanisms that drive ischemia-reperfusion injury in cardiomyocytes remain unclear. In this study, we report that isoflurane, a commonly used inhaled anesthetic, can protect cardiomyocytes from anoxia/reoxygenation injury by a nucleotide binding oligomerization domain containing 2 (NOD2)-dependent mechanism. The results showed that isoflurane increased cell viability, and decreased autophagosome generation in primary cardiomyocytes under anoxia/reoxygenation conditions. In addition, western blot revealed that isoflurane reduces the expression of NOD2. Overexpression of NOD2 is accompanied by an increased expression of autophagy-related genes, decreased cell viability, and enhanced expression of phosphorylation p38-mitogen-activated protein kinase (p38MAPK), while NOD2 knockdown exerted the opposite effect. Following preconditioning with SB203580, a p38MAPK inhibitor, the inhibitory effect of isoflurane on cardiomyocytes autophagy was further enhanced, which suggests that p38MAPK is involved in the mechanism of cardioprotection provided by isoflurane. These findings reveal a novel mechanism underlying isoflurane-afford protection of myocardial injury.