RESUMO
Standard alternating leg motions serve as the foundation for simple bipedal gaits, and the effectiveness of the fixed stimulus signal has been proved in recent studies. However, in order to address perturbations and imbalances, robots require more dynamic gaits. In this paper, we introduce dynamic stimulus signals together with a bipedal locomotion policy into reinforcement learning (RL). Through the learned stimulus frequency policy, we induce the bipedal robot to obtain both three-dimensional (3D) locomotion and an adaptive gait under disturbance without relying on an explicit and model-based gait in both the training stage and deployment. In addition, a set of specialized reward functions focusing on reliable frequency reflections is used in our framework to ensure correspondence between locomotion features and the dynamic stimulus. Moreover, we demonstrate efficient sim-to-real transfer, making a bipedal robot called BITeno achieve robust locomotion and disturbance resistance, even in extreme situations of foot sliding in the real world. In detail, under a sudden change in torso velocity of -1.2 m/s in 0.65 s, the recovery time is within 1.5-2.0 s.
RESUMO
Yersinia pestis, the causative agent of plague, expresses a capsule-like antigen, fraction 1 (F1), at 37 degrees C. F1 is encoded by the caf1 gene located on the large 100-kb pFra plasmid, which is unique to Y. pestis. F1 is a surface polymer composed of a protein subunit, Caf1, with a molecular mass of 15.5 kDa. The secretion and assembly of F1 require the caf1M and caf1A genes, which are homologous to the chaperone and usher protein families required for biogenesis of pili. F1 has been implicated to be involved in the ability of Y. pestis to prevent uptake by macrophages. In this study we addressed the role of F1 antigen in inhibition of phagocytosis by the macrophage-like cell line J774. The Y. pestis strain EV76 was found to be highly resistant to uptake by J774 cells. An in-frame deletion of the caf1M gene of the Y. pestis strain EV76 was constructed and found to be unable to express F1 polymer on the bacterial surface. This strain had a somewhat lowered ability to prevent uptake by J774 cells. Strain EV76C, which is cured for the virulence plasmid common to the pathogenic Yersinia species, was, as expected, much reduced in its ability to resist uptake. A strain lacking both the virulence plasmid and caf1M was even further hampered in the ability to prevent uptake and, in this case, essentially all bacteria (95%) were phagocytosed. Thus, F1 and the virulence plasmid-encoded type III system act in concert to make Y. pestis highly resistant to uptake by phagocytes. In contrast to the type III effector proteins YopE and YopH, F1 did not have any influence on the general phagocytic ability of J774 cells. Expression of F1 also reduced the number of bacteria that interacted with the macrophages. This suggests that F1 prevents uptake by interfering at the level of receptor interaction in the phagocytosis process.
