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The path following of underactuated autonomous surface vehicle (ASV) with line-of-sight (LOS)-based heading and velocity guidance is studied thoroughly in the presence of complex uncertainties and asymmetric input saturation that actuators are likely to suffer from. On the basis of the extended-state-observer-based LOS (ELOS) principle and guided velocity design strategies, a finite-time heading and velocity guidance control (HVG) scheme is presented. Firstly, an improved ELOS (IELOS) is developed such that the unknown sideslip angle can be estimated directly, instead of requiring one more step to calculate it by the output of observers and relying on the equivalent assumption between actual heading angle and guidance angle. Secondly, a new form of velocity guidance is designed by considering magnitude and rate constraints and path's curvature, keeping in line with ASV's manoeuvrability and agility. Then asymmetric saturation is considered and studied by designing projection-based finite-time auxiliary systems to avoid parameter drift. All error signals of the closed-loop system of ASV are forced to converge to an arbitrarily small neighbourhood of the origin within a finite settling time by the HVG scheme. The expected performance of the presented strategy is demonstrated via a series of simulations and comparisons. In addition, to show the strong robustness of the presented scheme, stochastic noises modelled by Markov process, bidirectional step signals and faults both multiplication and addition types are considered in simulations.
RESUMO
An amendment to this paper has been published and can be accessed via a link at the top of the paper.
RESUMO
Postmortem diagnosis of cantharidin-induced myocardial injury and postmortem interval estimation (PMI) are the challenges in forensic science. Cardiac biomarkers play an important role in the prediction and diagnosis of myocardial injury and can be used to determine the PMI. Based on the evidence, we aimed to explore the biomarkers which may be used for the postmortem diagnosis of cantharidin-induced myocardial injury and PMI estimation using the study of the proteins expression of TN-T, VEGF and HIF-1α by ELISA. Results of this study suggested that postmortem pathological changes were difficult to identify due to the autolysis of myocardium 72 h after death in cantharidin poisoning group. The plasma levels of TN-T and HIF-1α/TN-T are cardiac biomarkers with higher diagnostic accuracy for postmortem diagnosis of cantharidin-induced myocardial injury, VEGF/HIF-1α promises to be a biomarker for PMI estimation. Further studies are needed to verify these biomarkers, based on population, for being a useful tool in postmortem diagnosis of cantharidin-induced myocardial injury and PMI estimation.
RESUMO
Cantharidin is of high medicinal value but has strong toxicity. Nowadays, multiple research has focused on the mechanism of its antitumor activity while research on toxicological profiles associated with cantharidin poisoning is still limited. Its hepatotoxicity has attracted attention recently for the crucial role of the liver in detoxification. Here, we aim to find a potential mechanism for cantharidin-induced acute hepatotoxicity with a view to assisting subsequent research or clinical use or detoxification. Twenty-one male Sprague-Dawley rats were randomly divided into control, low-dose (1.34 mg/kg) and high-dose (2.67 mg/kg) cantharidin exposure groups. We used hematoxylin-eosin to observe pathological changes and used immunofluorescent staining, western blotting and real-time quantitative polymerase chain reaction to detect the expression of the markers. The main pathological changes in livers of cantharidin-treated rats were necrosis, inflammatory infiltration and hemorrhage. We found coexpression of tumor necrosis factor alpha (TNF-α), IkappaB kinase-alpha (IKK-α) and caspase3 by immunofluorescent staining in livers of cantharidin-treated rats. Compared with the control, the levels of TNF-α, IKK-α and caspase3 increased significantly in the experimental groups (P < .05). The ratio of B-cell lymphoma-2 (Bcl-2)/Bax increased in the low-dose group but decreased in the high-dose group (P < .05). Cantharidin exposure raised IKK-α mRNA and caspase3 mRNA levels (P < .05). In conclusion, the participation of TNF-α, IKK-α, Bcl-2, Bax and caspase3 uncovered a novel mechanism underlying cantharidin-induced acute hepatotoxicity, and the mechanism needs to be studied further.
