RESUMEN
The success of deep learning has brought breakthroughs in many fields. However, the increased performance of deep learning models is often accompanied by an increase in their depth and width, which conflicts with the storage, energy consumption, and computational power of edge devices. Knowledge distillation, as an effective model compression method, can transfer knowledge from complex teacher models to student models. Self-distillation is a special type of knowledge distillation, which does not to require a pre-trained teacher model. However, existing self-distillation methods rarely consider how to effectively use the early features of the model. Furthermore, most self-distillation methods use features from the deepest layers of the network to guide the training of the branches of the network, which we find is not the optimal choice. In this paper, we found that the feature maps obtained by early feature fusion do not serve as a good teacher to guide their own training. Based on this, we propose a selective feature fusion module and further obtain a new self-distillation method, knowledge fusion distillation. Extensive experiments on three datasets have demonstrated that our method has comparable performance to state-of-the-art distillation methods. In addition, the performance of the network can be further enhanced when fused features are integrated into the network.
RESUMEN
Olfactory ensheathing glia (OEG) play an important role in regulating the regeneration of an injured nervous system. However, chronic inflammation damage reduces the viability of OEG via poorly understood mechanisms. We aimed to investigate the pathological responses of OEG in response to LPS-mediated inflammation stress in vitro. The results indicated that lipopolysaccharide (LPS) treatment significantly reduced the viability of OEG in a dose-dependent fashion. Mechanistically, LPS stimuli induced mitochondrial oxidative damage, mitochondrial fragmentation, mitochondrial metabolism disruption, and mitochondrial apoptosis activation. Furthermore, we verified that LPS modulated mitochondrial apoptosis by promoting Bax upregulation, and this process was regulated by the JNK-Bnip3 pathway. Inhibition of the JNK-Bnip3 pathway prevented LPS-mediated Bax activation, thus attenuating OEG apoptosis. Altogether, our data illustrated that LPS-mediated inflammation injury evoked mitochondrial abnormalities in OEG damage via the JNK-Bnip3-Bax pathway. This finding provides a potential target to protect OEG against chronic inflammation stress.
