BECS-II: an updated bio-inspired electrocommunication system for small underwater robots.

Some weakly electric fish can use electric signals to interact and communicate with each other in dark and complex underwater environments where traditional underwater communication fails. In our previous work, we developed a bio-inspired electrocommunication system (BECS) that serves as an effective alternative to traditional methods in this challenging underwater scenario performing communication at a speed of approximately 1200 bps (bits per second) within approximately 3 m. In this study, a novel underwater wireless communication system (BECS-II) is proposed to upgrade the BECS with much better performance. We first propose theoretical and simulation models for electrocommunication, including the effects of the angular frequency and electrode impedance. A custom-made digital communication system is employed in BECS-II to improve the anti-interference ability and channel capacity of the BECS. In addition, a novel circuit optimization strategy was used to develop a customized circuit to enhance the transmitting and receiving capabilities of the BECS-II. Dual-frequency communication is proposed to meet the communication demands of different tasks by taking inspiration from the task allocation and evolution mechanisms of weakly electric fish. The experimental results showed that BECS-II outperformed BECS in high-frequency mode at both the communication speed (approximately 20 kbps) and distance (approximately 10 m), whereas in low-frequency mode, it extended the communication range by transmitting data up to a distance of approximately 20 m at a speed of approximately 200 bps. A substantial increase in the communication distance can expand the robot motion space in a group and improve group flexibility.

Adiponectin alleviates non-alcoholic fatty liver injury via regulating oxidative stress in liver cells.

BACKGROUND: The aim of the present study was to investigate the role of adiponectin in non-alcoholic fatty liver cell model and its mechanism. METHODS: The serum were collected from patients with non-alcoholic fatty liver disease and healthy controls. Then the expression of APN in the serum was detected using APN kit. Furthermore, an in vitro model of NAFLD was established using mixed fatty acids treated HepG2 cells, and APN was highly expressed in the culture solution to a concentration of 10 µg/mL. The normal control group (Normal) was normal cells, the model group (NAFLD) was mixed fatty acids treated HepG2 cells, the experimental group (NAFLD+APN) was model cells transfected with high APN expression, and the negative control group (NAFLD+PBS) was model cells transfected with PBS. The expression of NOX2 in each group was detected by Western blot. The corresponding kit was used to detect the level of triglyceride (TG), the activity of superoxide dismutase (SOD), the content of malondialdehyde (MDA), and the ratio of GSH/GSSG in each group of cells. RESULTS: The expression level of APN was greatly decreased in the serum of NAFLD patients (P<0.01), and the TG content was significantly increased in HepG2 cells treated with fatty acids (P<0.001), indicating successful modeling. The cells had high expression of APN (P<0.001) showed low expression of NOX2 (P<0.001). The kit test results showed that the high expression of APN could reverse the decrease of SOD activity, the increase of MDA level, the decrease of GSH/GSSG ratio and the increase of TG content (P<0.001), all of which were restored to the modeling level after application of NOX2's activator TBCA. CONCLUSIONS: APN was lowly expressed in the serum of NAFLD patients. Its effect mechanism was to alleviate the injury of NAFLD cells by reducing oxidative stress via regulating NOX2 expression.