Recent empirical and theoretical works on collective behaviors based on a topological interaction are beginning to offer some explanations as for the physical reasons behind the selection of a particular number of nearest neighbors locally affecting each individual's dynamics. Recently, flocking starlings have been shown to topologically interact with a very specific number of neighbors, between six to eight, while metric-free interactions were found to govern human crowd dynamics. Here, we use network- and graph-theoretic approaches combined with a dynamical model of locally interacting self-propelled particles to study how the consensus reaching process and its dynamics are influenced by the number k of topological neighbors. Specifically, we prove exactly that, in the absence of noise, consensus is always attained with a speed to consensus strictly increasing with k. The analysis of both speed and time to consensus reveals that, irrespective of the swarm size, a value of k ~ 10 speeds up the rate of convergence to consensus to levels close to the one of the optimal all-to-all interaction signaling. Furthermore, this effect is found to be more pronounced in the presence of environmental noise.

This letter considers the resilient consensus problem for switched multi-agent systems composed of continuous-time and discrete-time subsystems. We propose a switched filtering strategy for cooperative nodes based upon available local information, withstanding the threat of noncooperative nodes. We provide conditions that guarantee resilient consensus in the presence of locally bounded Byzantine nodes in directed networks under arbitrary switching. Resilient scaled consensus and resilient scaled formation generation problems for switched multi-agent systems are solved as generalizations. Simulations are also provided to illustrate the effectiveness of the theoretical results.

Hederagenin (HED) has poor anticancer activity whose mechanism remains unclear and unsystematic. Free drugs for cancer treatment exhibit disadvantages such as poor targeting and efficacy. To address this problem, we constructed a nanoplatform of black phosphorus quantum dots (BPQDs) camouflaged with a platelet membrane (PLTm) carrying HED, termed PLT@BPQDs-HED. PLTm vesicles serve as a shell to encapsulate multiple high-efficiency drug-loaded nanocores, which can target tumor sites and significantly improve antitumor activity. Compared with free HED, this platform significantly reduced tumor cell viability and the mitochondrial membrane potential (MMP), while increasing the production of intracellular reactive oxygen species (ROS). The platform also significantly increased the amounts of terminal deoxyribonucleotide transferase mediated dUTP nick-end-labeling (TUNEL)-positive cells and decreased the number of Ki-67-positive cells. In addition, the platform upregulated proapoptotic factor Bax, downregulated the anti-apoptotic molecule Bcl-2, activated Caspase-9 and Caspase-3, and stimulated Cytochrome C release. Moreover, the platform promoted the formation of autophagosomes, upregulated Beclin-1, and promoted LC3-I conversion into LC3-II. This study demonstrated that the above platform significantly enhances tumor targeting and promotes mitochondria-mediated cell apoptosis and autophagy in tumor cells.