Multi-sensor information fusion localization of rare-earth suspended permanent magnet maglev trains based on adaptive Kalman algorithm.

Since the positioning accuracy of sensors degrades due to noise and environmental interference when a single sensor is used to localize a suspended rare-earth permanent magnetically levitated train, a multi-sensor information fusion method using multiple sensors and self-correcting weighting is proposed for permanent magnetic levitated train localization. A decay memory factor is introduced to reduce the weight of the influence of historical measurement data on the fusion estimation, thus enhancing the robustness of the fusion algorithm. The Kalman filtering results suffer from inaccuracy when process noise is present in the system. In this paper, we use a covariance adaptive scheme that replaces the prediction step of the Kalman filter with covariance. It uses the covariance adaptive scheme to search the posterior sequence online and reconstruct the prior error covariance. Since the process noise covariance is not used in the new adaptive scheme, the negative impact of the mismatch noise statistics is greatly reduced. Simulation and experimental results show that the use of multi-sensor information fusion and covariance adaptive Kalman algorithm has significant advantages in terms of adaptability, accuracy and simplicity.

Effects of chronic realgar exposure on liver lipidome in mice and identification sensitive lipid biomarker model for realgar-induced liver damage.

Chronic or excessive use of realgar induced liver damage. The biomarkers and exact mechanism have not been fully investigated. We performed an untargeted lipidomics study to investigate the effects of realgar on liver lipidome in mice and explore the sensitive biomarker model of realgar induced liver damage. It was found that realgar exposure induced arsenic accumulation in the liver, increased ROS generation, elevated MDA levels, decreased antioxidant enzymes levels, induced cell apoptosis, changed hepatocyte ultrastructure and morphology, and altered ALT, AST levels. Lipidomics study detected 30 classes and 1457 molecules in mice liver. The numbers of 49 and 103 lipid molecules were significantly altered (FDR<0.05) in the livers of 0.45 g/kg and 1.35 g/kg realgar-exposed mice. The glycerophospholipid and sphingomyelin were the most affected lipid class. We focused on the effect of chronic realgar exposure on the mutual transformation of lipid subclasses and the fatty acid chain composition of lipids in mouse liver, and found that realgar affected the mutual transformation of PE-PC, PC-LPC and SM-Cer. Notably, we found that realgar exposure increased PUFAs linked phospholipids in mouse liver tissues. We identified two sensitive lipid molecules [PE (44:2p) and PE (16:0/22:5)] in combination can accurately distinguish and predict realgar induced liver damage, they are associated with oxidative damage and mitochondrial respiration in liver tissue. Our study provides an experimental basis for the mechanism research and early detection of realgar-induced liver damage.

Development of functional hydroxyethyl cellulose-based composite films for food packaging applications.

Cellulose-based functional composite films can be a good substitute for conventional plastic packaging to ensure food safety. In this study, the semi-transparent, mechanical strengthened, UV-shielding, antibacterial and biocompatible films were developed from hydroxyethyl cellulose Polyvinyl alcohol (PVA) and ε-polylysine (ε-PL) were respectively used as reinforcing agent and antibacterial agent, and chemical cross-linking among these three components were constructed using epichlorohydrin The maximum tensile strength and elongation at break were 95.9 ± 4.1 MPa and 148.8 ± 2.6%, respectively. TG-FTIR and XRD analyses indicated that chemical structure of the composite films could be well controlled by varying component proportion. From UV-Vis analysis, the optimum values of the percentage of blocking from UV-A and UV-B and ultraviolet protection factor values were 98.35%, 99.99% and 60.25, respectively. Additionally, the composite films exhibited good water vapor permeability, swelling behavior, antibacterial activity and biocompatibility. In terms of these properties, the shelf life of grapes could be extended to 6 days after packing with the composite film.

An Experimental Study Reveals the Protective Effect of Autophagy against Realgar-Induced Liver Injury via Suppressing ROS-Mediated NLRP3 Inflammasome Pathway.

Realgar, a poisonous traditional Chinese medicine, has been shown to cause liver injury when used for long periods or overdoses. However, the underlying molecular mechanisms and therapeutic targets have not been fully elucidated. The aim of this study is to explore the role of autophagy in sub-chronic realgar exposure-induced liver injury. Here, the liver injury model was established by continuously administrating mice with 1.35 g/kg realgar for 8 weeks. 3-methyladenine (3-MA) and rapamycin (RAPA) were used to regulate autophagy. The results showed that realgar induced abnormal changes in liver function, pathological morphology, expression of inflammatory cytokines, and upregulated NLRP3 inflammasome pathway in mouse livers. RAPA treatment (an inducer of autophagy) significantly improved realgar-induced liver injury and NLRP3 inflammasome activation, while 3-MA (an inhibitor of autophagy) aggravated the realgar-induced liver injury and NLRP3 inflammasome activation. Furthermore, we found that realgar-induced NLRP3 inflammasome activation in mouse livers is mediated by ROS. RAPA eliminates excessive ROS, inhibits NF-κB nuclear translocation and down-regulates the TXNIP/NLRP3 axis, consequently suppressing ROS-mediated NLRP3 inflammasome activation, which may be the underlying mechanism of the protective effect of autophagy on realgar-induced liver injury. In conclusion, the results of this study suggest that autophagy alleviates realgar-induced liver injury by inhibiting ROS-mediated NLRP3 inflammasome activation. Autophagy may represent a therapeutic target in modulating realgar-induced liver injury.

Metabolic characteristics related to the hazardous effects of environmental arsenic on humans: A metabolomic review.

Arsenic (As) is a toxic metalloid exist ubiquitously in environment. Epidemiological studies and laboratory animal studies have verified that As damages multiple organs or tissues in the body and is associated with a variety of diseases. Changes in metabolites usually indicate disturbances in metabolic pathways and specific metabolites are considered as biomarkers of diseases or drugs/toxins or environmental effects. Metabolomics is the quantitative measurement of the dynamic multi-parameter metabolic responses of biological systems due to pathophysiological or genetic changes. Current years, some metabolomic studies on the hazardous effect of environmental As on humans have been reported. In this paper, we first overviewed the metabolomics studies of environmental As exposure in humans since 2011, emphasizing on the data mining process of metabolic characteristics related to the hazardous effects of environmental As on humans. Then, the relationship between metabolic characteristics and the toxic mechanism of environmental As exposure in humans were discussed, and finally, the prospects of metabolomics studies on populations exposed to environmental As were put forward. Our paper may shed light on the study of mechanisms, prevention and individualized treatment of As poisoning.

Sub-chronic exposure to realgar induces liver injury via upregulating the TXNIP/NLRP3 pathway and disturbing bile acid homeostasis in mice.

ETHNOPHARMACOLOGICAL RELEVANCE: Realgar is a traditional Chinese medicine used in China for a long history. Long-time or excessive use of realgar causes liver injury. However, its underlying mechanism is not fully clarified. AIM OF THE STUDY: In this study, we investigated the toxic effect of sub-chronic exposure to realgar on mice liver, and further revealed its underlying mechanism focused on the TXNIP/NLRP3 pathway and bile acid homeostasis. MATERIAL AND METHODS: Mice were divided into control and different doses of sub-chronic realgar exposed groups. Total arsenic levels in the blood and liver were determined by atomic fluorescence spectrometry. The effect of realgar on liver function was evaluated by biochemical analysis and histopathological examination. Assay kits were applied for the measurement of oxidative stress indexes, MPO and plasma inflammatory cytokines. The mRNA and proteins involved in the TXNIP/NLRP3 and NF-κB pathways were determined by RT-qPCR, western blot, Immunofluorescence and Immunohistochemistry. UHPLC/MS/MS was used for the quantitative analysis of bile acids (BAs) in mice plasma, liver and urine. The genes related to BAs metabolism were measured by RT-qPCR. RESULTS: Sub-chronic exposure to realgar led to arsenic accumulation and caused oxidative damage and inflammatory infiltration in mouse liver, finally resulting in liver injury. Realgar treatment activated the NF-κB pathway and significantly upregulated the TXNIP/NLRP3 pathway in mouse liver. Realgar altered the metabolic balance of BAs, which is related to the abnormal expression of BAs transporters and enzymes. CONCLUSION: Sub-chronic exposure to realgar caused liver injury in mouse, and the mechanism may involve the upregulation of the TXNIP/NLRP3 pathway and disordered BAs homeostasis.