Real-Time Video Synopsis via Dynamic and Adaptive Online Tube Resizing.

Nowadays, with the increased numbers of video cameras, the amount of recorded video is growing. Efficient video browsing and retrieval are critical issues when considering the amount of raw video data to be condensed. Activity-based video synopsis is a popular approach to solving the video condensation problem. However, conventional synopsis methods always consists of complicated and pairwise energy terms that involve a time-consuming optimization problem. In this paper, we propose a simple online video synopsis framework in which the number of collisions of objects is classified first. Different optimization strategies are applied according to different collision situations to maintain a balance among the computational cost, condensation ratio, and collision cost. Secondly, tube-resizing coefficients that are dynamic in different frames are adaptively assigned to a newly generated tube. Therefore, a suitable mapping result can be obtained in order to represent the proper size of the activity in each frame of the synopsis video. The maximum number of activities can be displayed in one frame with minimal collisions. Finally, in order to remove motion anti-facts and improve the visual quality of the condensed video, a smooth term is introduced to constrain the resizing coefficients. Experimental results on extensive videos validate the efficiency of the proposed method.

Senescence-associated secretory factors induced by cisplatin in melanoma cells promote non-senescent melanoma cell growth through activation of the ERK1/2-RSK1 pathway.

Although targeted therapy and immunotherapy greatly improve the outcome of melanoma, drug resistance and low response rates still maintain the unsubstitutability of traditional chemotherapy. Cisplatin (CDDP) is widely used in different types of tumours with high response rates, but it generally has low efficiency in melanoma. The mechanisms underpinning the phenomena are not sufficiently understood. Here we demonstrated that various melanoma cell lines adopted senescence phenotype after CDDP treatment in contrast to the other types of tumour cells. CDDP treatment induced melanoma A375 cells into senescence through the sequential activation of the DNA damage response and the P53/P21 pathway. All the senescent melanoma cells induced by CDDP alone or the combination of CDDP and dacarbazine developed robust senescence-associated secretory phenotype (SASP), that is, the secretion of multiple cytokines. IL-1α was an early component and an upstream regulator of SASP. Similarly, CDDP either alone or combined with dacarbazine could induce melanoma cell senescence and SASP in either A375 or B16F10 melanoma xenograft mice. The supernatant of senescent A375 cells promoted the growth of normal non-senescent A375 cells and enhanced their expression and secretion of IL-8 through the activation of the ERK1/2-RSK1 pathway. The transplantation of non-senescent and senescent A375 cells together into nude mice showed accelerated tumour growth compared with transplanting non-senescent cells alone; no tumours developed when transplanting senescent cells alone. Following CDDP administration in A375-bearing mice, the intratumour injection of neutralisation antibodies targeting the SASP factors IL-1α or IL-8 evidently delayed tumour growth. The results suggest that the CDDP-induced senescent melanoma cells promote non-senescent cells proliferation through the activation of ERK1/2-RSK1 pathway by the SASP factors. Cell senescence and concomitant SASP may be the particular mechanisms for melanoma to resist chemotherapeutics.

IL-1α inhibits proliferation and adipogenic differentiation of human adipose-derived mesenchymal stem cells through NF-κB- and ERK1/2-mediated proinflammatory cytokines.

Dysfunctional adipogenesis such as subcutaneous lipoatrophy is closely related to insulin resistance and metabolic disorders. Although the expression or release of the cytokine interleukin-1α (IL-1α) is known to increase in adipose tissue in response to cell death, cell senescence, aging, or solar radiation, the regulatory role of IL-1α in adipogenesis has not been sufficiently investigated. To investigate the problem, we explored the effect of IL-1α on the proliferation and adipogenic differentiation of human adipose-derived mesenchymal stem cells (ADSCs) using cell counting, alamarBlue assay, oil red O staining, Western blot, among others. The results showed that IL-1α evidently inhibited the proliferation and adipogenic differentiation of ADSCs, which might be related with the activated nuclear factor-κB (NF-κB) and extracellular signal-regulated kinase (ERK) 1/2 pathways. Early-stage adipogenic differentiation was more sensitive to IL-1α than late-stage differentiation. After differentiation of ADSCs into mature adipocytes, adding of IL-1α had no obvious influence on the cellular morphology, including lipid droplet accumulation. IL-1α enhanced the expression of proinflammatory cytokines, such as IL-8, IL-6, CCL2 (C-C motif chemokine ligand 2), and IL-1ß, when added into the adipogenic medium of ADSCs. Blocking IL-8 and IL-6 with neutralizing antibodies partially alleviated the inhibitory effect of IL-1α on the proliferation and adipogenic differentiation. The results suggest that IL-1α inhibits adipogenesis through activation of NF-κB and ERK1/2 pathways and subsequent upregulation of proinflammatory cytokines in ADSCs. IL-1α might play an important role in mediating lipoatrophy by regulation of ADSCs.

[Induction of robust senescence-associated secretory phenotype in mouse NIH-3T3 cells by mitomycin C].

Senescence-associated secretory phenotype (SASP) is often a concomitant result of cell senescence, embodied by the enhanced function of secretion. The SASP factors secreted by senescent cells include cytokines, proteases and chemokines, etc, which can exert great influence on local as well as systemic environment and participate in the process of cell senescence, immunoregulation, angiogenesis, cell proliferation and tumor invasion, etc. Relative to the abundance of SASP models in human cells, the in vitro SASP model derived from mouse cells is scarce at present. Therefore, the study aimed to establish a mouse SASP model to facilitate the research in the field. With this objective, we treated the INK4a-deficient mouse NIH-3T3 cells and the wildtype mouse embryonic fibroblasts (MEF) respectively with mitomycin C (MMC), an anticarcinoma drug which could induce DNA damage. The occurring of cell senescence was evaluated by cell morphology, ß-gal staining, integration ratio of EdU and Western blot. Quantitative RT-PCR and ELISA were used to detect the expression and secretion of SASP factors, respectively. The results showed that, 8 days after the treatment of NIH-3T3 cells with MMC (1 µg/mL) for 12 h or 24 h, the cells became enlarged and the ratios of ß-gal-positive (blue-stained) cells significantly increased, up to 77.4% and 90.4%, respectively. Meanwhile, the expression of P21 protein increased and the integration ratios of EdU significantly decreased (P < 0.01). Quantitative RT-PCR detection showed that the mRNA levels of several SASP genes, including IL-6, TNF-α, IL-1α and IL-1ß increased evidently. ELISA detection further observed an enhanced secretion of IL-6 (P < 0.01). On the contrary, although wildtype MEF could also be induced into senescence by MMC treatment for 12 h or 24 h, embodied by the enlarged cell volume, increased ratios of ß-gal-positive cells (up to 71.7% and 80.2%, respectively) and enhanced expression of P21 protein, the secretion of IL-6 displayed no significant change. Our study indicated that, although MMC could induce senescence in both mouse NIH-3T3 cells and wildtype MEF, only senescent NIH-3T3 cells displayed the canonical SASP phenomena. Current study suggested that senescent NIH-3T3 cells might be an appropriate in vitro SASP model of mouse cells.

Sufficient and necessary conditions for Lyapunov stability of genetic networks with SUM regulatory logic.

In this paper, a nonlinear model for genetic regulator networks (GRNs) with SUM regulatory logic is presented. Four sufficient and necessary conditions of global asymptotical stability and global exponential stability for the equilibrium point of the GRNs are proposed, respectively. Specifically, three weak sufficient conditions and corresponding corollaries are derived by using comparing theorem and Dini derivative method. Then, a famous GRN model is used as the example to illustrate the effectiveness of our theoretical results. Comparing to the results in the previous literature, some novel ideas, study methods and interesting results are explored.

Unconditional global exponential stability in Lagrange sense of genetic regulatory networks with SUM regulatory logic.

In this paper, the global exponential stability in Lagrange sense for genetic regulatory networks (GRNs) with SUM regulatory logic is firstly studied. By constructing appropriate Lyapunov-like functions, several criteria are presented for the boundedness, ultimate boundedness and global exponential attractivity of GRNs. It can be obtained that GRNs with SUM regulatory logic are unconditionally globally exponentially stable in Lagrange sense. These results can be applied to analyze monostable as well as multistable networks. Furthermore, to analyze the stability for GRNs more comprehensively, the existence of equilibrium point of GRNs is proved, and some sufficient conditions of the global exponential stability in Lyapunov sense for GRNs are derived. Finally two numerical examples are given to illustrate the application of the obtained results.

Global dissipativity of continuous-time recurrent neural networks with time delay.

This paper addresses the global dissipativity of a general class of continuous-time recurrent neural networks. First, the concepts of global dissipation and global exponential dissipation are defined and elaborated. Next, the sets of global dissipativity and global exponentially dissipativity are characterized using the parameters of recurrent neural network models. In particular, it is shown that the Hopfield network and cellular neural networks with or without time delays are dissipative systems.