Rotor fault classification technique and precision analysis with kernel principal component analysis and multi-support vector machines

To solve the diagnosis problem of fault classification for aero-engine vibration over standard during test, a fault diagnosis classification approach based on kernel principal component analysis (KPCA) feature extraction and multi-support vector machines (SVM) is proposed, which extracted the feature of testing cell standard fault samples through exhausting the capability of nonlinear feature extraction of KPCA. By computing inner product kernel functions of original feature space, the vibration signal of rotor is transformed from principal low dimensional feature space to high dimensional feature spaces by this nonlinear map. Then, the nonlinear principal components of original low dimensional space are obtained by performing PCA on the high dimensional feature spaces. During muti-SVM training period, as eigenvectors, the nonlinear principal components are separated into training set and test set, and penalty parameter and kernel function parameter are optimized by adopting genetic optimization algorithm. A high classification accuracy of training set and test set is sustained and over-fitting and under-fitting are avoided. Experiment results indicate that this method has good performance in distinguishing different aero-engine fault mode, and is suitable for fault recognition of a high speed rotor

Knockdown of FABP3 Impairs Cardiac Development in Zebrafish through the Retinoic Acid Signaling Pathway

Fatty acid-binding protein 3 (FABP3) is a member of the intracellular lipid-binding protein family, and is primarily expressed in cardiac muscle tissue. Previously, we found that FABP3 is highly expressed in patients with ventricular-septal defects and is often used as a plasma biomarker in idiopathic dilated cardiomyopathy, and may play a significant role in the development of these defects in humans. In the present study, we aimed to investigate the role of FABP3 in the embryonic development of the zebrafish heart, and specifically how morpholino (MO) mediated knockdown of FABP3 would affect heart development in this species. Our results revealed that knockdown of FABP3 caused significant impairment of cardiac development observed, including developmental delay, pericardial edema, a linear heart tube phenotype, incomplete cardiac loop formation, abnormal positioning of the ventricles and atria, downregulated expression of cardiac-specific markers and decreased heart rate. Mechanistically, our data showed that the retinoic acid (RA) catabolizing enzyme Cyp26a1 was upregulated in FABP3-MO zebrafish, as indicated by in situ hybridization and real-time PCR. On the other hand, the expression level of the RA synthesizing enzyme Raldh2 did not significantly change in FABP3-MO injected zebrafish. Collectively, our results indicated that FABP3 knockdown had significant effects on cardiac development, and that dysregulated RA signaling was one of the mechanisms underlying this effect. As a result, these studies identify FABP3 as a candidate gene underlying the etiology of congenital heart defects