Magnetically actuated aphid-inspired dry adhesion is developed with rapid tunability and high reversibility and demonstrated in transfer printing both in air and in a vacuum.

Possessing the attributes of high adaptability and low cost, soft robotic individuals can further coordinate and form into a swarming system, enhancing the performances as well as functions in practical applications. However, the formation control of soft robotic swarm remains challenging mainly due to the limitation in relatively low precision and slow response of the soft actuators. In this work, a soft robotic fish swarm system with global vision positioning was studied. The soft robotic fish used in the project is driven by a hybrid powercontrol system, in which the soft dielectric elastomers and the rigid electrical servo provide forward propulsion and controllable steering function, respectively. Results show that soft robotic fish swarm can quickly shift their formations, mimicking three typical swarming behaviors of natural creatures: highly parallel group, encircling, and torus. The system design and controlling principles of the soft robotic fish swarm may guide the future research of soft robots and robotic swarms, specifically for underwater applications.

TcpC is a multifunctional virulence factor of Uropathogenic Escherichia coli (UPEC). Macrophages can differentiate into two different subsets M1 and M2 that play distinct roles in anti-infection immunity. Here, we investigate the influence of TcpC on M1/M2 polarization and the potential mechanisms. Our data showed that M1 markers CD86 and iNOS were significantly inhibited, while the M2 markers CD163, CD206 and Arg-1 were enhanced in macrophages in kidneys from the TcpC-secreting wild-type CFT073 (CFT073wt)-infected pyelonephritis mouse model, compared with those in macrophages in kidneys from TcpC knockout CFT073 mutant (CFT073Δtcpc)-infected mice. CFT073wt or recombinant TcpC (rTcpC) treatment inhibits LPS + IFN-γ-induced CD80, CD86, TNF-α and iNOS expression, but promotes IL-4-induced CD163, CD206, Arg-1 and IL-10 expression in both human and mouse macrophage cell lines THP-1 and J774A.1. Moreover, rTcpC significantly attenuated LPS + IFN-γ-induced phosphorylation of p38, ERK, p50 and p65 but enhanced IL-4-induced phosphorylation of Akt and STAT6. These data suggest that TcpC inhibits M1 but promotes M2 macrophage polarization by down-regulation of p38, ERK/NF-κB and up-regulation of the Akt/STAT6 signaling pathway, respectively. Our findings not only illuminate the regulatory effects of TcpC on macrophage M1/M2 polarization and its related signaling pathways, but also provide a novel mechanism underlying TcpC-mediated immune evasion of macrophage-mediated innate immunity.