Nowadays, motor imagery (MI) electroencephalogram (EEG) signal classification has become a hotspot in the research field of brain computer interface (BCI). More recently, deep learning has emerged as a promising technique to automatically extract features of raw MI EEG signals and then classify them. However, deep learning-based methods still face two challenging problems in practical MI EEG signal classification applications: (1) Generally, training a deep learning model successfully needs a large amount of labeled data. However, most of the EEG signal data is unlabeled and it is quite difficult or even impossible for human experts to label all the signal samples manually. (2) It is extremely time-consuming and computationally expensive to train a deep learning model from scratch. To cope with these two challenges, a deep transfer convolutional neural network (CNN) framework based on VGG-16 is proposed for EEG signal classification. The proposed framework consists of a VGG-16 CNN model pre-trained on the ImageNet and a target CNN model which shares the same structure with VGG-16 except for the softmax output layer. The parameters of the pre-trained VGG-16 CNN model are directly transferred to the target CNN model used for MI EEG signal classification. Then, front-layers parameters in the target model are frozen, while later-layers parameters are fine-tuned by the target MI dataset. The target dataset is composed of timefrequency spectrum images of EEG signals. The performance of the proposed framework is verified on the public benchmark dataset 2b from the BCI competition IV. The experimental results show that the proposed framework improves the accuracy and efficiency performance of EEG signal classification compared with traditional methods, including support vector machine (SVM), artificial neural network (ANN), and standard CNN. INDEX TERMS Motor imagery (MI), electroencephalogram (EEG), signal classification, short time Fourier transform (STFT), VGG-16, transfer learning.

Aims: Apoptosis plays a critical role in cardiomyocyte loss during ischaemic heart injury. A detailed understanding of the mechanism involved has a substantial impact on the optimization and development of treatment strategies. Here, we report that the expression of SIRT4, a mitochondrial sirtuin, is markedly down-regulated in hypoxia-induced apoptosis of H9c2 cardiomyoblast cells. Methods and Results: SIRT4 interference significantly alters H9c2 cell viability, apoptotic cell number and caspase-3/7 activity. Furthermore, SIRT4 expression can affect the ratio of pro-caspase 9/caspase 9 or pro-caspase 3/caspase 3, an affect Bax translocation, which in turn alters the development of H9c2 cell apoptosis. Conclusion: These results suggest that SIRT4 is a key player in hypoxia-induced cardiomyocyte apoptosis, and that strategies based on its enhancement might be of benefit in the treatment of ischaemic heart disease.

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