No abstract

External-stimuli-driven soft actuators overcome several limitations inherent in traditional mechanical-driven technology considering the coming age of flexible robots, which might face harsh working conditions and rigorous multifunctional requirements. However, how to achieve multi-external-stimuli response, fast speed, and precise control of the position and angle of the actuator, especially working in a toxic liquid or vapor environment, still requires long-term efforts. Here, we report a multi-external-stimuli-driven sandwich actuator with aligned carbon nanotubes as the constructive subject, which can respond to various types of liquids (organic solvents), vapor, and solar light. The actuator has an ultrafast response speed (<10 ms) and can accurately adjust the bending angle range from 0° to 180°. Through manipulating the stimuli positions, actuators can be wound into varied turns when simulating a flexible robotic arm. Hence, liquid/vapor/light-driven actuators are able to support diverse programmable motions, such as periodic blooming, gesture variations, caterpillar crawling, toxic surface evading, and bionic phototaxis. We believe that this multifunctional actuator is promising in supporting a complex scenario to complete a variety of tasks in the fields of healthcare, bioengineering, chip technology, and mobile sensors.

Circular antisense non-coding RNA in the INK4 locus (cANRIL) participated in inflammation of endothelial cells. However, whether cANRIL is associated with inflammatory injury of HK-2 cells, thereby affecting chronic kidney disease has not been investigated. We tested the hypothesis that cANRIL participated in inflammatory response in vitro. HK-2 cells were stimulated by lipopolysaccharides (LPS). RT-qPCR was executed for cANRIL expression assessment. After transfection, cell viability, apoptosis, inflammatory cytokines and ROS generation were appraised to evaluate the impact of silencing cANRIL on LPS-induced inflammatory injury. The regulatory relationship between cANRIL and microRNA-9 (miR-9) was verified. In addition, whether miR-9 affected LPS-induced inflammatory injury was measured after miR-9 inhibitor transfection. Western blot was utilized to detect NF-jB and JNK/p38 pathway-related proteins. The results showed that LPS promoted cANRIL expression and cell injuries in HK-2 cells. Furthermore, silencing cANRIL alleviated inflammatory injuries by promoting viability, suppressing apoptosis, inflammatory cytokines and ROS generation in HK-2 cells. In addition, miR-9 expression was accelerated by silencing cANRIL. Meanwhile, miR-9 down-regulation invalidated the effect of silencing cANRIL on inflammation and NF-jB and JNK/p38 pathways. The study clarified that silencing cANRIL hindered NF-jB and JNK/p38 pathways by positively regulating miR-9, thereby protecting HK-2 cells from LPS-induced injury.

No abstract