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Abstract Visual-Inertial Odometry (VIO) has been developed from Simultaneous Localization and Mapping (SLAM) as a low-cost and versatile sensor fusion approach and attracted increasing attention in ground vehicle positioning. However, VIOs usually have the degraded performance in challenging environments and degenerated motion scenarios. In this paper, we propose a ground vehicle-based VIO algorithm based on the Multi-State Constraint Kalman Filter (MSCKF) framework. Based on a unified motion manifold assumption, we derive the measurement model of manifold constraints, including velocity, rotation, and translation constraints. Then we present a robust filter-based algorithm dedicated to ground vehicles, whose key is the real-time manifold noise estimation and adaptive measurement update. Besides, GNSS position measurements are loosely coupled into our approach, where the transformation between GNSS and VIO frame is optimized online. Finally, we theoretically analyze the system observability matrix and observability measures. Our algorithm is tested on both the simulation test and public datasets including Brno Urban dataset and Kaist Urban dataset. We compare the performance of our algorithm with classical VIO algorithms (MSCKF, VINS-Mono, R-VIO, ORB_SLAM3) and GVIO algorithms (GNSS-MSCKF, VINS-Fusion). The results demonstrate that our algorithm is more robust than other compared algorithms, showing a competitive position accuracy and computational efficiency.

This paper addresses cooperative control for a class of multi-agent networks. An interesting feature of such network is that each agent possesses the characteristic of multi-time-scale. By developing the relative states or the relative outputs based consensus protocols, some well-conditioned consensus criteria in terms of linear matrix inequalities are derived successively based on the $\varepsilon $ -strict Lyapunov function. Compared with undirected graphs or strongly connected digraphs in existing works, a more general digraph that it contains at least a directed spanning tree is considered herein. Moreover, a fully distributed consensus protocol with time-varying coupling strength is proposed to avoid using global information. Finally, the obtained theoretical results are validated by two examples including standard and nonstandard agents.

IntroductionMyocardial infarction (MI) is a fatal manifestation of coronary heart disease, and its underlying mechanism is still largely unknown. Lipid levels and composition alterations predict the risk of MI complications. Glycerophospholipids (GPLs) are important bioactive lipids and play a crucial role in the development of cardiovascular diseases. However, the metabolic changes in the GPLs profile during post-MI injury remain unknown.MethodsIn the current study, we constructed a classic MI model by ligating the left anterior descending branch and assessed the alterations in both plasma and myocardial GPLs profiles during the reparative phase post-MI by liquid chromatography–tandem mass spectrometry analysis.ResultsWe found that myocardial GPLs, but not plasma GPLs, were markedly changed after MI injury. Importantly, MI injury is associated with decreased phosphatidylserine (PS) levels. Consistently, the expression of phosphatidylserine synthase 1 (PSS1), which catalyzes the formation of PS from its substrate phosphatidylcholine, was significantly reduced in heart tissues after MI injury. Furthermore, oxygen-glucose deprivation (OGD) inhibited PSS1 expression and reduced PS levels in primary neonatal rat cardiomyocytes, while overexpression of PSS1 restored the inhibition of PSS1 and the reduction in PS levels caused by OGD. Moreover, overexpression of PSS1 abrogated, whereas knockdown of PSS1 aggravated, OGD-induced cardiomyocyte apoptosis.ConclusionsOur findings revealed that GPLs metabolism was involved in the reparative phase post-MI, and cardiac decreased PS levels, resulting from inhibition of PSS1, are important contributor to the reparative phase post-MI. PSS1 overexpression represents a promising therapeutic strategy to attenuate MI injury.

Abstract Background Chronic inflammatory pain significantly reduces the quality of life and lacks effective interventions. In recent years, human umbilical cord mesenchymal stem cells (huc-MSCs)-derived exosomes have been used to relieve neuropathic pain and other inflammatory diseases as a promising cell-free therapeutic strategy. However, the therapeutic value of huc-MSCs-derived exosomes in complete Freund's adjuvant (CFA)-induced inflammatory pain remains to be confirmed. In this study, we investigated the therapeutic effect and related mechanisms of huc-MSCs-derived exosomes in a chronic inflammatory pain model. Methods C57BL/6J male mice were used to establish a CFA-induced inflammatory pain model, and huc-MSCs-derived exosomes were intrathecally injected for 4 consecutive days. BV2 microglia cells were stimulated with lipopolysaccharide (LPS) plus adenosine triphosphate (ATP) to investigate the effect of huc-MSCs-derived exosomes on pyroptosis and autophagy. Bioinformatic analysis and rescue experiments were used to demonstrate the role of miR-146a-5p/ TRAF6 in regulating pyroptosis and autophagy. Western blotting, RT-qPCR, small interfering RNA and Yo-Pro-1 dye staining were performed to investigate the related mechanisms. Results Huc-MSCs-derived exosomes alleviated mechanical allodynia and thermal hyperalgesia in CFA-induced inflammatory pain. Furthermore, huc-MSCs-derived exosomes attenuated neuroinflammation by increasing the expression of autophagy-related proteins (LC3-II and beclin1) and inhibiting the activation of NLRP3 inflammasomes in the spinal cord dorsal horn. In vitro, NLRP3 inflammasome components (NLRP3, caspase1-p20, ASC) and gasdermin D (GSDMD-F, GSDMD-N) were inhibited in BV2 cells pretreated with huc-MSCs-derived exosomes. Western blot and Yo-Pro-1 dye staining demonstrated that 3-MA, an autophagy inhibitor, weakened the protective effect of huc-MSCs-derived exosomes on BV2 cell pyroptosis. Importantly, huc-MSCs-derived exosomes transfected with miR-146a-5p mimic promoted autophagy and inhibited BV2 cell pyroptosis. TRAF6, as a target gene of miR-146a-5p, was knocked down via small-interfering RNA, which increased pyroptosis and inhibited autophagy. Conclusion Huc-MSCs-derived exosomes attenuated inflammatory pain via miR-146a-5p/TRAF6, which increased the level of autophagy and inhibited pyroptosis. Graphical Abstract

Spinal cord injury (SCI) is a devastating trauma characterized by serious neuroinflammation and permanent neurological dysfunction. However, the molecular mechanism of SCI remains unclear, and few effective medical therapies are available at present. In this study, multiple bioinformatics methods were used to screen out novel targets for SCI, and the mechanism of these candidates during the progression of neuroinflammation as well as the therapeutic effects were both verified in a rat model of traumatic SCI. As a result, CASP4, IGSF6 and IL1R1 were identified as the potential diagnostic and therapeutic targets for SCI by computational analysis, which were enriched in NF-κB and IL6-JAK-STATA3 signaling pathways. In the injured spinal cord, these three signatures were up-regulated and closely correlated with NLRP3 inflammasome formation and gasdermin D (GSDMD) -induced pyroptosis. Intrathecal injection of inhibitors of IL1R1 or CASP4 improved the functional recovery of SCI rats and decreased the expression of these targets and inflammasome component proteins, such as NLRP3 and GSDMD. This treatment also inhibited the pp65 activation into the nucleus and apoptosis progression. In conclusion, our findings of the three targets shed new light on the pathogenesis of SCI, and the use of immunosuppressive agents targeting these proteins exerted anti-inflammatory effects against spinal cord inflammation by inhibiting NF-kB and NLRP3 inflammasome activation, thus blocking GSDMD -induced pyroptosis and immune activation.

Neuropathic pain is characterized by hyperalgesia and allodynia. Inflammatory response is conducive to tissue recovery upon nerve injury, but persistent and exaggerated inflammation is detrimental and participates in neuropathic pain. Synaptic transmission in the nociceptive pathway, and particularly the balance between facilitation and inhibition, could be affected by inflammation, which in turn is regulated by glial cells. Importantly, glycometabolism exerts a vital role in the inflammatory process. Glycometabolism reprogramming of inflammatory cells in neuropathic pain is characterized by impaired oxidative phosphorylation in mitochondria and enhanced glycolysis. These changes induce phenotypic transition of inflammatory cells to promote neural inflammation and oxidative stress in peripheral and central nervous system. Accumulation of lactate in synaptic microenvironment also contributes to synaptic remodeling and central sensitization. Previous studies mainly focused on the glycometabolism reprogramming in peripheral inflammatory cells such as macrophage or lymphocyte, little attention was paid to the regulation effects of glycometabolism reprogramming on the inflammatory responses in glial cells. This review summarizes the evidences for glycometabolism reprogramming in peripheral inflammatory cells, and presents a small quantity of present studies on glycometabolism in glial cells, expecting to promote the exploration in glycometabolism in glial cells of neuropathic pain.

Chronic pain, such as persistent inflammatory pain, remains a public health problem that has no effective treatment at present. Bromodomain-containing protein 4 (BRD4) inhibition, induced by JQ1 injection or BRD4 knockdown, has been used to attenuate inflammatory pain; However, it remains elusive whether BRD4 aggravates inflammatory pain by regulating inflammasome. Western blot and immunofluorescence staining showed that BRD4 expression increased after administration of complete Freund’s adjuvant (CFA) and reached its peak on day 3. Immunofluorescence staining showed that BRD4 was mainly colocalized with NeuN-positive neurons in the spinal cord, which was accompanied by upregulation of inflammasome component proteins, such as NLRP3, gasdermin D, and caspase-1. JQ1 was intrathecally injected into mice 1 h before CFA administration, and the mechanical and thermal hyperalgesia levels were measured on days 1, 3, and 7 after CFA administration. CFA-induced inflammatory pain, paw inflammation, and swelling were attenuated by pre-treatment with JQ1. To our knowledge, this study was the first to prove that NLRP3 inflammasome-induced neuronal pyroptosis participates in inflammatory pain. BRD4 inhibition decreased the expression of pyroptosis-related proteins by inhibiting the activation of NF-κB signaling pathway, both in vivo and in vitro. Taken together, BRD4 inhibition exerted analgesic and anti-inflammatory effects against inflammatory pain by inhibiting NF-κB and inflammasome activation, which protected neural cells from pyroptosis.

In actual industrial application scenarios, noise pollution makes it difficult to extract fault features accurately via conventional methods. A novel method for rolling bearing fault diagnosis combining a convolutional neural network (CNN), an attention mechanism for a squeeze-and-excitation network (SENet) module and a broad learning system (BLS) is proposed (SECNN–BLS). The one-dimensional bearing vibration signal is processed by using multiple short-time Fourier transforms (STFT); the two-dimensional image in the time-frequency domain is used as the model input. In the CNN fault feature extraction process, SENet is introduced to replace the CNN convolution layer, and global information is obtained through the squeeze operation. Excitation operation captures the importance of image channels, assigns weights adaptively to improve the attention on important information and eliminates the interference of irrelevant features without increasing the spatial and temporal complexity. The weighted feature representation is then transferred to the BLS input. The BLS has the characteristics of a flat structure and ridge regression to quickly solve the weights; as a fault classifier, it can save more computing resources and improve the accuracy of the fault classification. The SECNN–BLS fault diagnosis has achieved more than 98% accuracy on the Society for Machinery Failure Prevention Technology (MFPT) dataset. We also demonstrate the excellent performance of SECNN–BLS in a noisy environment.

The 23rd Winter Olympics Games and the 13th Winter Paralympic Games are held in Pyeongchang, South Korea during 9-25 February 2018 and 8-18 March 2018. Supported by the WMO(World Meteorological Organization) WWRP(World Weather Research Project Group), ICE-POP 2018(International Collaborative Experiments for Pyeongchang 2018 Olympic and Paralympic winter games) is organized by KMA (Korea Meteorological Administration), which aims to improve the forecasting ability of convective scale numerical models for high-impact weather system under complex terrain and to support weather forecasting and meteorological services during the Winter Olympics through international cooperation. GRAPES_3 km, a high-resolution model independently developed by CMA (China Meteorological Administration), participated in this project and provided real-time forecasting products at the specific sites during the Winter Olympics Games. In order to improve the forecasting ability of GRAPES_3 km, a bias correction method named one-order adaptive Kalman filtering is applied, which compensate for the fact that the resolution of GRAPES_3 km is not sufficient to simulate the complex terrain of the Winter Olympic Games and GRAPES_3 km doesn't assimilate Korea's observations due to some objective reasons such as data transmission. 1-24-hour calibration products are provided twice a day, including 2 m temperature, 2 m relative humidity, 10 m wind speed, and 10 m wind direction on sixteen sites. The verification and evaluation are carried out in two aspects. First, it is to check whether the bias correction improves the accuracy of GRAPES_3 km, examined from the model's diurnal cycle, daily variation and the forecast ability of complex terrain. Second, to the performance of calibrated GRAPES_3 km during the Winter Olympic Games is and examined compared to LDAPS model from KMA and NU-WRF from NASA, which shows that the high-resolution GRAPES_3 km model has abilities to simulate the near-ground elements in this service and the bias correction technology makes model products better and effective. After bias correction, the root mean square error of model products is reduced to about 2℃ for the temperature, about 2 m·s-1 for the wind speed, and less than 20% for the relative humidity is reduced to. Compared with, NU-WRF and LDAPS models, the corrected GRAPES_3 km has the best wind speed forecast capability and root mean square error of the wind speed is significantly reduced. For the wind direction forecast of complex terrain, although all numerical models have limited capabilities, and their wind direction forecasting of all the stations are almost dominated by westerly during the Winter Games, the corrected GRAPES_3 km perform relatively well in some non-westerly dominated stations. However, GRAPES_3 km has no significant advantage in temperature and humidity compared with the other two models although they are improved more obviously than wind after the calibration. In addition, the bias correction can attenuate the diurnal variation characteristics of GRPAES_3 km, and to some extent, improve the simulation capability for complex terrain. In short, the application of the bias correction in the Pyeongchang Winter Olympic Games is an effective way for GRAPES_3 km.

Aberrant sphingolipid metabolism contributes to cardiac pathophysiology. Emerging evidence found that an increased level of ceramide during the inflammatory phase of post-myocardial infarction (MI) served as a biomarker and was associated with cardiac dysfunction. However, the alternation of the sphingolipid profile during the reparative phase after MI is still not fully understood. Using a mouse model of the left anterior descending ligation that leads to MI, we performed metabolomics studies to assess the alternations of both plasma and myocardial sphingolipid profiles during the reparative phase post-MI. A total number of 193 sphingolipid metabolites were detected. Myocardial sphingolipids but not plasma sphingolipids showed marked change after MI injury. Ceramide-1-phosphates, which were accumulated after MI, contributed highly to the difference in sphingolipid profiles between groups. Consistently, the expression of ceramide kinase, which phosphorylates ceramides to generate ceramide-1-phosphates, was upregulated in heart tissue after MI injury. Our findings revealed the altering sphingolipid metabolism during the reparative phase post-MI and highlighted the potential role of ceramide kinase/ceramide-1-phosphate in ischemic heart disease.

The flower of Edgeworthia gardneri (Wall.) Meisn is commonly used in beverage products in Tibet and has potential health benefits for diabetes. However, the mechanisms underlying anti-insulin resistance (IR) action of the flower of E. gardneri are not fully understood. This study aims to investigate the effects of the water extract of the flower of E. gardneri (WEE) on IR in palmitate (PA)-exposed HepG2 hepatocytes. WEE was characterized by UPLC analysis. PA-treated HepG2 cells were selected as the IR cell model. The cell viability was determined using MTT assay. Moreover, the glucose consumption and production were measured by glucose oxidase method. The glucose uptake and glycogen content were determined by the 2-NBDG (2-deoxy-2-[(7-nitro-2,1,3-benzoxadiazol-4-yl) amino]-D-glucose) glucose uptake assay and anthrone-sulfuric acid assay, respectively. The intracellular triglyceride content was detected by oxidative enzymic method. Protein levels were examined by Western blotting. Nuclear localization of FoxO1 was detected using immunofluorescence analyses and Western blotting. The expression of FoxO1 target genes was detected by quantitative real-time polymerase chain reaction (qRT-PCR). The viability of PA-treated HepG2 cells was concentration-dependently increased by incubation with WEE for 24 h. WEE treatment remarkably increased the consumption and uptake of glucose in PA-exposed HepG2 cells. Moreover, treatment with WEE significantly decreased the PA-induced over-production of glucose in HepG2 cells. After exposure of HepG2 cells with PA and WEE, the glycogen content was significantly elevated. The phosphorylation and total levels of IRβ, IRS1, and Akt were upregulated by WEE treatment in PA-exposed HepG2 cells. The phosphorylation of GSK3β was elevated after WEE treatment in PA-treated cells. WEE treatment also concentration-dependently downregulated the phosphorylated CREB, ERK, c-Jun, p38 and JNK in PA-exposed HepG2 cells. Furthermore, the nuclear protein level and nuclear translocation of FoxO1 were also suppressed by WEE. Additionally, PA-induced changes of FoxO1 targeted genes were also attenuated by WEE treatment. The GLUT2 and GLUT4 translocation were also promoted by WEE treatment in PA-treated HepG2 cells. Taken together, WEE has potential anti-IR effect in PA-exposed HepG2 cells; the underlying mechanism of this action may be associated with the regulation of IRS1/GSK3β/FoxO1 signaling pathway. This study provides a pharmacological basis for the application of WEE in the treatment of metabolic diseases such as type 2 diabetes mellitus.