A bioinspired jumping robot has a strong ability to overcome obstacles. It can be applied to the occasion with complex and changeable environment, such as detection of planet surface, postdisaster relief, and military reconnaissance. So the bioinspired jumping robot has broad application prospect. The jumping process of the robot can be divided into three stages: takeoff, air posture adjustment, and landing buffer. The motivation of this review is to investigate the research results of the most published bioinspired jumping robots for these three stages. Then, the movement performance of the bioinspired jumping robots is analyzed and compared quantitatively. Then, the limitation of the research on bioinspired jumping robots is discussed, such as the research on the mechanism of biological motion is not thorough enough, the research method about structural design, material applications, and control are still traditional, and energy utilization is low, which make the robots far from practical applications. Finally, the development trend is summarized. This review provides a reference for further research of bioinspired jumping robots.

The GKN2 is a secretory protein, whose levels decrease in gastric cancer. The present study aimed to investigate the expression, function and mechanism of action of GKN2 in gastric cancer. Molecular biology assays were performed to elucidate the function and underlying mechanisms of GKN2 in gastric cancer under stress-induced condition in vivo and in vitro. Clinical specimens were used to assess the correlation of GKN2 and prognosis. We found that overexpression of GKN2 significantly enhanced apoptosis and growth arrest in vitro. GKN2 expression increased in gastric cancer cells exposed to hydrogen peroxide and promoted reactive oxygen species-induced mitochondrial dysfunction and resulted in increased cell apoptosis via inhibition of NF-κB signaling pathway and activation of JNK signaling pathway through the direct interaction of GKN2 with Hsc70. Trefoil factor 1 might contribute to the tumor suppressing effects of GKN2. MiR-216a downregulated GKN2 expression. GKN2 also inhibited xenograft tumor growth and was an independent and significant prognostic factor for patients with gastric cancer treated with oxaliplatin. Taken together, our data indicate that GKN2 may increase sensitivity of GC cells to the drugs which increase ROS levels in tumors. Inhibition of the interaction between GKN2 and Hsc70 could attenuate the effects induced by GKN2. GKN2 overexpression could be used to determine the subgroup of patients to obtain the more favorable outcome of oxaliplatin treatment and may be used as biomarker of the prognosis of this cancer.