Search

Aiming at the formation problem of the multi-rotor UAV swarm, this paper adopts a multi-rotor UAV swarm formation control method based on a stress matrix to ensure the stability of multi-rotor UAV swarm formation. On the basis of achieving the target formation through a stress matrix, the formation of a multi-rotor UAV swarm can be rotated, scaled, and sheared. When the obstacles are known, the multi-rotor UAV swarm can pass through the obstacle environment smoothly through rotation, scaling, and shearing transformations. However, this transformation cannot cope with the situation where the obstacles are known. This paper proposes an active obstacle avoidance function for multi-rotor UAV swarm formation based on a stress matrix. Through the detection capability of the UAV itself, the obstacle avoidance function is realized autonomously after the UAV detects an unknown obstacle. Due to the effect of a stress matrix, when the navigator performs the active obstacle avoidance function, the formation of the multi-rotor UAV swarm will be destroyed. This paper designs a virtual UAV and only retains the UAV that controls the flight trajectory of the multi-rotor UAV swarm as the only real UAV to ensure that the UAV swarm formation is not destroyed. This paper proves the stability of the multi-rotor UAV swarm formation through simulation experiments, and the multi-rotor UAV swarm can pass through the obstacle environment smoothly when facing known obstacles and unknown obstacles. [ABSTRACT FROM AUTHOR]

Background: To identify biomarkers and develop an inflammatory score based on proper integration to improve risk prediction of delayed cerebral ischemia (DCI) and poor outcome in patients with aneurysmal subarachnoid hemorrhage (aSAH). We also further explore the mediation and interaction of DCI within the chain of events using the four-way effect decomposition. Methods: Machine learning algorithms are used for biomarker selection and constructed the inflammatory score. Multivariate logistic regression was performed to identify the association of inflammatory score with DCI and poor outcome. Next, we employed a four‐way decomposition to assess the extent to which the inflammation effect on the risk of poor outcome is mediated by or interacts with DCI. Finally, the additive value of inflammatory score was measured using the area under the curve (AUC), net reclassification improvement (NRI) and integrated discrimination improvement (IDI). Results: In total, 368 aSAH patients were included. The inflammatory score was calculated with the combination of lymphocyte, pan-immune-inflammation value (PIV), red blood cell distribution width (RDW), and lactate dehydrogenase (LDH). Multivariate analysis identified that inflammatory score was independently associated with DCI and poor outcome. The effect of high inflammatory score on poor outcome may be partly explained by DCI, where there is both pure mediation and mediated interaction. With DCI as a potential mediator, the excess relative risk could be decomposed into 30.86% controlled direct effect, 3.60% mediation only, 26.64% interaction only, and 38.89% mediated interaction. Adding the inflammatory score to the predictive model improved the AUC from 0.772 to 0.822, with an NRI of 5.3% and IDI of 6.9%. Conclusion: The inflammatory score was significantly associated with DCI and poor outcome in patients with aSAH. Not only may be a potential synergistic interaction between high inflammatory score and DCI on the risk of poor outcome but also where DCI is an important mediating mechanism. [ABSTRACT FROM AUTHOR]

The repair of DNA double-strand breaks (DSBs) through homologous recombination (HR) is vital for maintaining the stability and integrity of the genome. RNA binding proteins (RBPs) intricately regulate the DNA damage repair process, yet the precise molecular mechanisms underlying their function remain incompletely understood. In this study, we highlight the pivotal role of RPS15, a representative RBP, in homologous recombination repair. Specifically, we demonstrate that RPS15 promotes DNA end resection, a crucial step in homologous recombination. Notably, we identify an interaction between RPS15 and CtIP, a key factor in homologous recombination repair. This interaction is essential for CtIP recruitment to DSB sites, subsequent RPA coating, and RAD51 replacement, all critical steps in efficient homologous recombination repair and conferring resistance to genotoxic treatments. Functionally, suppressing RPS15 expression sensitizes cancer cells to X-ray radiation and enhances the therapeutic synergistic effect of PARP1 inhibitors in breast cancer cells. In summary, our findings reveal that RPS15 promotes DNA end resection to ensure effective homologous recombination repair, suggesting its potential as a therapeutic target in cancer treatment. [ABSTRACT FROM AUTHOR]

In the present study, the toxicity of nicosulfuron to Danio rerio embryos was evaluated in three experiments through standardized toxicity tests according to OECD TG236 guidelines. In the first experiment, six concentrations of nicosulfuron (0, 0.1, 1, 10, 100, 1000 mg/L) were tested under optimal conditions (26 °C, pH 7.0) to assess the general sensitivity of zebrafish embryos to nicosulfuron. The second and third experiment examined the effects of different pH levels (5.0 and 9.0) and temperatures (21 °C and 31 °C) on the toxicity at four nicosulfuron concentrations (0, 10, 100, 1000 mg/L). Additionally, the sub-organismic effects of nicosulfuron on stress protein levels (Hsp70) of fish embryos were analyzed. Throughout the embryo experiments, no malformations were observed in all experiments. The survival rate exceeded 80% in all groups except for the 21 °C (pH 7.0) treatment groups. No significant effect of nicosulfuron on the survival rate was found at the same temperature or pH (p > 0.05). No significant difference in the heart rate was found among all nicosulfuron groups (p > 0.05) at 21 °C. The heart rate of fish embryos at 31 °C, pH 5.0 and pH 9.0 increased with nicosulfuron concentrations. Except for the pH 5.0 (26 °C) and 21 °C (pH 7.0) treatment groups, nicosulfuron was found to increase the hatching rate of embryos in other treatments; however, the corresponding times of action were different. At 21 °C (pH 7.0), the embryos did not hatch until 144 h post-fertilization. In terms of proteotoxicity, nicosulfuron was found to be more toxic to zebrafish embryos in the 21 °C, pH 5.0 and pH 9.0 treatment groups. However, at 31 °C, no significant difference in Hsp70 levels was found among all the different nicosulfuron concentrations (p > 0.05). Our results show that nicosulfuron exerts a weak toxicity to zebrafish embryos; however, this toxicity is amplified by inappropriate pH or temperature conditions. [ABSTRACT FROM AUTHOR]