Learning agile soccer skills for a bipedal robot with deep reinforcement learning.

We investigated whether deep reinforcement learning (deep RL) is able to synthesize sophisticated and safe movement skills for a low-cost, miniature humanoid robot that can be composed into complex behavioral strategies. We used deep RL to train a humanoid robot to play a simplified one-versus-one soccer game. The resulting agent exhibits robust and dynamic movement skills, such as rapid fall recovery, walking, turning, and kicking, and it transitions between them in a smooth and efficient manner. It also learned to anticipate ball movements and block opponent shots. The agent's tactical behavior adapts to specific game contexts in a way that would be impractical to manually design. Our agent was trained in simulation and transferred to real robots zero-shot. A combination of sufficiently high-frequency control, targeted dynamics randomization, and perturbations during training enabled good-quality transfer. In experiments, the agent walked 181% faster, turned 302% faster, took 63% less time to get up, and kicked a ball 34% faster than a scripted baseline.

Modulating the functional contributions of c-Myc to the human endothelial cell cyclic strain response.

This study addresses whether pathological levels of cyclic strain activate the c-Myc promoter, leading to c-Myc transcription and downstream gene induction in human umbilical vein endothelial cells (HUVEC) or human aortic endothelial cells (HAEC). mRNA and protein expression of c-Myc under physiological (6-10%) and pathological cyclic strain conditions (20%) were studied. Both c-Myc mRNA and protein expression increased 2-3-fold in HUVEC cyclically strained at 20%. c-Myc protein increased 4-fold in HAEC. In HUVEC, expression of mRNA peaked at 1.5-2 h. Subsequently, the effect of modulating c-Myc on potential downstream gene targets was determined. A small molecular weight compound that binds to and stabilizes the silencer element in the c-Myc promoter attenuates cyclic strain-induced c-Myc transcription by about 50%. This compound also modulates c-Myc downstream gene targets that may be instrumental in induction of vascular disease. Cyclic strain-induced gene expression of vascular endothelial growth factor, proliferating cell nuclear antigen and heat shock protein 60 are attenuated by this compound. These results offer a possible mechanism and promising clinical treatment for vascular diseases initiated by increased cyclic strain.