This paper studies the problem of distributed output tracking consensus control for a class of high-order stochastic nonlinear multiagent systems with unknown nonlinear dead-zone under a directed graph topology. The adaptive neural networks are used to approximate the unknown nonlinear functions and a new inequality is used to deal with the completely unknown dead-zone input. Then, we design the controllers based on backstepping method and the dynamic surface control technique. It is strictly proved that the resulting closed-loop system is stable in probability in the sense of semiglobally uniform ultimate boundedness and the tracking errors between the leader and the followers approach to a small residual set based on Lyapunov stability theory. Finally, two simulation examples are presented to show the effectiveness and the advantages of the proposed techniques.

This paper studies the dynamic output feedback tracking control problem for stochastic interconnected time-delay systems with the prescribed performance. The subsystems are in the form of triangular structure. First, we design a reduced-order observer independent of time delay to estimate the unmeasured state variables online instead of the traditional full-order observer. Then, a new state transformation is proposed in consideration of the prescribed performance requirement. Using neural network to approximate the composite unknown nonlinear function, the corresponding decentralized output tracking controller is designed. It is strictly proved that the resulting closed-loop system is stable in probability in the sense of uniformly ultimately boundedness and that both transient-state and steady-state performances are preserved. Finally, a simulation example is given, and the result shows the effectiveness of the proposed control design method.

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Colorectal cancer (CRC) is the third most common type of cancer. MicroRNAs have been reported to participate in the progression of various cancers. In previous studies, miR‐301a‐3p expression was shown to be upregulated in CRC tissues. However, the underlying mechanism of miR‐301a‐3p in CRC has not yet been elucidated. Herein, the level of miR‐301a‐3p was found to be significantly upregulated in CRC clinical tissues and cell lines (HT29 and SW620). In addition, overexpression of miR‐301a‐3p obviously promoted cell proliferation, migration and invasion, and inhibited cell apoptosis in CRC cells. Meanwhile, upregulated miR‐301a‐3p expression also enhanced the expressions of Bax, caspase‐3, caspase‐9, matrix metalloproteinase (MMP)‐2, and MMP‐9, while the expression of Bax‐2 was decreased. Furthermore, deleted in liver cancer‐1 (DLC‐1) and runt‐related transcription factor 3 (RUNX3) were verified to be direct target genes of miR‐301a‐3p. Furthermore, overexpression of DLC‐1 and RUNX3 revealed antitumor effects in CRC cell lines with the inhibition of cell proliferation, migration and invasion, and the induction of cell apoptosis. In addition, the expressions of Bax, caspase‐3, caspase‐3, MMP‐2, and MMP‐9 could be decreased after upregulating the expressions of DLC‐1 and RUNX3, along with the upregulation of Bax‐2. Moreover, overexpression of miR‐301a‐3p could promote the growth of xenograft tumors and liver metastasis in vivo, along with reducing the expressions of DLC‐1 and RUNX3. Overall, miR‐301a‐3p might act as a tumor inducer in CRC cells through negatively regulating DLC‐1 and RUNX3.