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Traditional clustering algorithms are widely used for building bag-of-words (BOW) models to aggregate spatio-temporal feature points extracted from a video for human activity recognition problems. Their performances are restricted by the computational complexity which limits the number of feature points being used. In contrast, deep clustering yields good clustering performance without the limit of the number of feature points. Therefore, this work proposes a dual stacked autoencoders features embedded clustering (DSAFEC) and a BOW construction method based on the DSAFEC (B-DSAFEC) to reduce the computational complexity and to remove the selection restriction. The DSAFEC first transforms feature points extracted from a video to a learned feature space and then probabilities of cluster assignment of feature points are predicted to build BOWs for human activity recognition. A soft clustering is used by assigning each feature point to multiple clusters yielding the largest probabilities instead of only one in hard clustering. Experimental results on three benchmark human activity datasets show that the B-DSAFEC yields better performance compared to five reference methods which are developed based on either traditional clustering methods or deep clustering methods. [ABSTRACT FROM AUTHOR]

Intervertebral degenerative disc disease (IDDD) is a common disease in clinic that causes pain and heavy financial burden on patients with poor prognosis. However, the pathogenesis of IDDD is not clear. Long non-coding RNA (LncRNA) is involved in regulating various body growth and pathological processes by affecting cell proliferation, differentiation, and apoptosis. However, the role of lncRNAs in IDDD is rarely reported. This study aims to investigate the role and mechanism of lncRNA MALAT1 in the development of IDDD. The nucleus pulposus of the intervertebral disc were collected and the primary nucleus pulposus cells were isolated and cultured. The cells were divided into three groups, including IDDD group, empty plasmid group transfected by pcDNA3.1, or MALAT1 group transfected by pcDNA3.1-MALAT1. MALAT1 expression was detected by real-time PCR. Cell proliferation was assessed by MTT assay. Caspase 3 activity was tested by the activity detection kit. IL-1 and IL-6 levels were analyzed by ELISA. The expression of MALAT1 in IDDD nucleus pulposus cells was significantly lower than that in control group (P < 0.05). The expression of MALAT1 was significantly increased after transfection with pcDNA3.1-MALAT1 plasmid in IDDD nucleus pulposus cells, which obviously inhibited cell proliferation, enhanced Caspase 3 activity, and promoted the secretion of IL-1 and IL-6 compared with IDDD group (P < 0.05). MALAT1 level decreased in IDDD nucleus pulposus cells. Upregulation of MALAT1 expression restrained IDDD through suppressing inflammation; inhibiting nucleus pulposus cell apoptosis, and promoting cell proliferation., Competing Interests: None., (IJCEP Copyright © 2017.)