This paper presents an overview of AiDIN-VI, a force-controllable quadruped robot system with incorporated mandatory abilities of speed, efficiency, and mobility for providing real-world services. This paper describes the design methodologies and principles employed to implement these requisite capabilities on a single robot platform; particularly, the torque sensing method, along with the components and modularization method of the torque-controllable actuator unit are elucidated herein. The developed robot platform is equipped with all necessary components, including onboard PCs (for motion generation and vision mapping), a battery, modular actuator units, a wireless network router, and a remote e-stop controller for autonomous and manual locomotion control. The robot is subdivided into joints, legs, and robots, and its performance is experimentally tested. The capability of the robot with regard to joint torque control (± 70 Nm), leg force control (350 N along the z-axis), robot (vertical loading 25 kg, pulling force 200 N) were experimentally verified, and locomotive performances (walk, pace, trot, and jump) on various terrains were executed. A maximum trot gait speed of 1.2 m/s was recorded, along with minimum costs of transport of 1.187 and 1.15 at a speed of 1.0 m/s and under loading conditions, respectively.

As cellular senescence, reactive oxygen species (ROS) accumulate excessively, causing cellular damage. Flavonoids derived from natural products are known for their antioxidant effects and their ability to delay cellular senescence. Previous studies have attempted to mitigate cellular senescence using flavonoids from natural sources. However, the detailed mechanisms and regulatory targets of some flavonoids exhibiting antioxidant effects have not been fully elucidated. Therefore, we screened a library of flavonoids for antioxidant properties. Isoschaftoside, a glycosidic flavonoid, significantly reduced ROS levels in senescent cells. It was found that mitochondrial function was restored, and dependence on glycolysis was reduced in senescent cells treated with isoschaftoside. Additionally, we identified that isoschaftoside suppresses ROS by reducing the expression of RAC2 and LINC00294 in senescent cells. Taken together, this study establishes a novel mechanism for ROS inhibition and the regulation of cellular senescence by isoschaftoside. Our findings contribute important insights to antioxidant and anti-senescence research.

Oxidative stress caused by reactive oxygen species (ROS) is one of the major causes of senescence. Strategies to reduce ROS are known to be important factors in reversing senescence, but effective strategies have not been found. In this study, we screened substances commonly used as cosmetic additives to find substances with antioxidant effects. Polygonum cuspidatum (P. cuspidatum) extract significantly reduced ROS levels in senescent cells. A novel mechanism was discovered in which P. cuspidatum extract reduced ROS, a byproduct of inefficient oxidative phosphorylation (OXPHOS), by increasing OXPHOS efficiency. The reduction in ROS by P. cuspidatum extract restored senescence-associated phenotypes and enhanced skin protection. Then, we identified polydatin as the active ingredient of P. cuspidatum extract that exhibited antioxidant effects. Polydatin, which contains stilbenoid polyphenols that act as singlet oxygen scavengers through redox reactions, increased OXPHOS efficiency and subsequently restored senescence-associated phenotypes. In summary, our data confirmed the effects of P. cuspidatum extract on senescence rejuvenation and skin protection through ROS reduction. This novel finding may be used as a treatment in senescence rejuvenation in clinical and cosmetic fields.

Background: Reactive oxygen species (ROS) generated by mitochondrial dysfunction damage cellular organelles and contribute to skin aging. Therefore, strategies to reduce mitochondrial ROS production are considered important for alleviating skin aging, but no effective methods have been identified. Methods: In this study, we evaluated substances utilized as cosmetic ingredients and discovered Camellia sinensis (C. sinensis) as a substance that reduces mitochondrial ROS levels. Results: C. sinensis extracts were found to act as senolytics that selectively kill senescent fibroblasts containing dysfunctional mitochondria. In addition, C. sinensis extracts facilitated efficient electron transport in the mitochondrial electron transport chain (ETC) by increasing the efficiency of oxidative phosphorylation (OXPHOS), thereby reducing mitochondrial ROS production, a byproduct of the inefficient ETC. This novel mechanism of C. sinensis extracts led to the restoration of skin aging and the skin barrier. Furthermore, epigallocatechin gallate (EGCG) was identified as an active ingredient that plays a key role in C. sinensis extract-mediated skin aging recovery. Indeed, similar to C. sinensis extracts, EGCG reduced ROS and improved skin aging in an artificial skin model. Conclusions: Our data uncovered a novel mechanism by which C. sinensis extract reverses skin aging by reducing mitochondrial ROS production via selective senescent cell death/increased OXPHOS efficiency. Our results suggest that C. sinensis extract or EGCG may be used as a therapeutic agent to reverse skin aging in clinical and cosmetic applications.

One of the major causes of senescence is oxidative stress caused by ROS, which is mainly generated from dysfunctional mitochondria. Strategies to limit mitochondrial ROS production are considered important for reversing senescence, but effective approaches to reduce them have not yet been developed. In this study, we screened the secondary metabolites that plants produce under oxidative stress and discovered sauchinone as a potential candidate. Sauchinone induced mitochondrial function recovery, enabling efficient electron transport within the electron transport chain (ETC). This led to a decrease in ROS production, a byproduct of inefficient electron transport. The reduction in ROS by sauchinone rejuvenated senescence-associated phenotypes. To understand the underlying mechanism by which sauchinone rejuvenates senescence, we carried out RNA sequencing and found VAMP8 as a key gene. VAMP8 was downregulated by sauchinone. Knockdown of VAMP8 decreased mitochondrial ROS levels and subsequently rejuvenated mitochondrial function, which was similar to the effect of sauchinone. Taken together, these studies revealed a novel mechanism by which sauchinone reduces mitochondrial ROS production by regulating mitochondrial function and VAMP8 expression. Our results open a new avenue for aging research to control senescence by regulating mitochondrial ROS production.