Path Planning for a Wheel-Foot Hybrid Parallel-Leg Walking Robot.

Mobile robots require the ability to plan collision-free paths. This paper introduces a wheel-foot hybrid parallel-leg walking robot based on the 6-Universal-Prismatic-Universal-Revolute and 3-Prismatic (6UPUR + 3P) parallel mechanism model. To enhance path planning efficiency and obstacle avoidance capabilities, an improved artificial potential field (IAPF) method is proposed. The IAPF functions are designed to address the collision problems and issues with goals being unreachable due to a nearby problem, local minima, and dynamic obstacle avoidance in path planning. Using this IAPF method, we conduct path planning and simulation analysis for the wheel-foot hybrid parallel-legged walking robot described in this paper, and compare it with the classic artificial potential field (APF) method. The results demonstrate that the IAPF method outperforms the classic APF method in handling obstacle-rich environments, effectively addresses collision problems, and the IAPF method helps to obtain goals previously unreachable due to nearby obstacles, local minima, and dynamic planning issues.

The Critical Role of The Piezo1/ß-catenin/ATF4 Axis on The Stemness of Gli1+ BMSCs During Simulated Microgravity-Induced Bone Loss.

Disuse osteoporosis is characterized by decreased bone mass caused by abnormal mechanical stimulation of bone. Piezo1 is a major mechanosensitive ion channel in bone homeostasis. However, whether intervening in the action of Piezo1 can rescue disuse osteoporosis remains unresolved. In this study, a commonly-used hindlimb-unloading model is employed to simulate microgravity. By single-cell RNA sequencing, bone marrow-derived mesenchymal stem cells (BMSCs) are the most downregulated cell cluster, and coincidentally, Piezo1 expression is mostly enriched in those cells, and is substantially downregulated by unloading. Importantly, activation of Piezo1 by systemically-introducing yoda1 mimics the effects of mechanical stimulation and thus ameliorates bone loss under simulated microgravity. Mechanistically, Piezo1 activation promotes the proliferation and osteogenic differentiation of Gli1+ BMSCs by activating the ß-catenin and its target gene activating transcription factor 4 (ATF4). Inhibiting ß-catenin expression substantially attenuates the effect of yoda1 on bone loss, possibly due to inhibited proliferation and osteogenic differentiation capability of Gli1+ BMSCs mediated by ATF4. Lastly, Piezo1 activation also slightly alleviates the osteoporosis of OVX and aged mice. In conclusion, impaired function of Piezo1 in BMSCs leads to insufficient bone formation especially caused by abnormal mechanical stimuli, and is thus a potential therapeutic target for osteoporosis.