As an important part of the professional courses in China, cross-border e-commerce plays an important role in improving students’ professional ability. The OBE concept is effectively used for ...cross-border e-commerce course teaching. The evaluation and assessment system helps to improve the shortcomings of the current teaching and improve the learning effect of students. At present, cross-border e-commerce major in our country universities in the process of course teaching has paid attention to the OBE concept effectively used in it, through analysis from multiple dimensions and check the students ‘learning results, the teaching objectives, teaching implementation and teaching guarantee, and other links to cover, can provide dynamic support for students’ learning results. Based on this, this study will analyze the construction of the cross-border E-commerce teaching evaluation and assessment system under the OBE concept from the perspective of the OBE concept, so as to help improve the existing teaching deficiencies, so as to establish a diversified teaching evaluation and teaching assessment system.
Siamese network based the tracker is a hot topic in the field of visual object tracking. However, Siamese trackers still have a robustness gap compared with state‐of‐the‐art algorithms. Therefore, ...focusing on the issue, this letter adds Frequency Channel Attention (FCA) and adaptive template feature map to the framework of Siamese neural network. FCA can enhance feature representation of effective channels and improve feature discrimination by modeling the correlation between each channel of the image. In this algorithm, by theoretical analysis and experimental validation, restriction is broken through a simple yet effective FCA network sampling strategy and a Siamese‐FCA tracker with significant performance gain is successfully trained. Meanwhile, in order to better adjust the proportion between target and background, the tracker selects suitable size of the target feature map. Moreover, extensive ablation studies are conducted to demonstrate the effectiveness of the proposed tracker. Fairly, the experimental results of five test benchmarks, including OTB2013, OTB2015, VOT2016, VOT2018 and UAV123 datasets, shows that the proposed algorithm performs outstanding. In particular, the issue of similarity and small target tracking failure is overcome. The average running frame rate reaches 86 frames per second, which can meet the real‐time requirements.
As an important forest type, deciduous broad-leaved forest is crucial for estimating forest carbon sequestration capacity and evaluating forest carbon balance. This study focuses on the natural ...deciduous broad-leaved forest of Mazongling Nature Reserve in Jinzhai County of China. WorldView-2 images were selected as data source. 36 candidate factors including vegetation indices, texture features, and topographic factors were used for modelling. Three machine learning algorithms (i.e., random forest, k-nearest neighbor, and artificial neural network) were used to establish the optimal quantitative retrieval model for natural deciduous broad-leaved biomass. Results showed that the ANN model was the best predictor with R
2
= 0.69 and RMSE = 31.53 (Mg·ha
−1
). Combining the ANN model with the complete spatial coverage of remote sensing data, we developed a distribution map of natural deciduous broad-leaved biomass in the Mazongling forest farm. The estimated average biomass of the study area was 90.34 ± 47.96 Mg·ha
−1
. In addition, the influence of light saturation on model accuracy is also discussed. This study confirms that remote sensing data in temporal and spatial space can improve the model estimation accuracy.
Mitochondrial dysfunction and lung cellular senescence are significant features involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) stands as the ...primary contributing factor to COPD. This study examined mitochondrial dynamics, mitophagy and lung cellular senescence in COPD patients and investigated the effects of modulation of mitochondrial fusion mitofusin2 (MFN2) and Optic atrophy 1 (OPA1) on CS extract (CSE)-induced lung cellular senescence.
Senescence-associated secretory phenotype (SASP) component mRNAs (IL-1β, IL-6, CXCL1 and CXCL8), mitochondrial morphology, mitophagy and mitochondria-related proteins (including phosphorylated-DRP1(p-DRP1), DRP1, MFF, MNF2, OPA1, PINK1, PARK2, SQSTM1/p62 and LC3b) and senescence-related proteins (including P16, H2A.X and Klotho) were measured in lung tissues or primary alveolar type II (ATII) cells of non-smokers, smokers and COPD patients. Alveolar epithelial (A549) cells were exposed to CSE with either pharmacologic inducer (leflunomide and BGP15) or genetic induction of MFN2 and OPA1 respectively.
There were increases in mitochondrial number, and decreases in mitochondrial size and activity in lung tissues from COPD patients. SASP-related mRNAs, DRP1 phosphorylation, DRP1, MFF, PARK2, SQSTM1/p62, LC3B II/LC3B I, P16 and H2A.X protein levels were increased, while MFN2, OPA1, PINK1 and Klotho protein levels were decreased in lung tissues from COPD patients. Some similar results were identified in primary ATII cells of COPD patients. CSE induced increases in oxidative stress, SASP-related mRNAs, mitochondrial damage and dysfunction, mitophagy and cellular senescence in A549 cells, which were ameliorated by both pharmacological inducers and genetic overexpression of MFN2 and OPA1.
Impaired mitochondrial fusion, enhanced mitophagy and lung cellular senescence are observed in the lung of COPD patients. Up-regulation of MFN2 and OPA1 attenuates oxidative stress, mitophagy and lung cellular senescence, offering potential innovative therapeutic targets for COPD therapy.
Exposure to particulate matter (PM) with an aerodynamic diameter less than 2.5 mum (PM.sub.2.5) is a risk factor for developing pulmonary diseases and the worsening of ongoing disease. Mitochondrial ...fission and fusion are essential processes underlying mitochondrial homeostasis in health and disease. We examined the role of mitochondrial fission and fusion in PM.sub.2.5-induced alveolar epithelial cell damage and lung injury. Key genes in these processes include dystrophin-related protein 1 (DRP1) and optic atrophy 1 (OPA1) respectively. Alveolar epithelial (A549) cells were treated with PM.sub.2.5 (32 microg/ml) in the presence and absence of Mdivi-1 (10microM, a DRP1 inhibitor) or BGP-15 (10microM, an OPA1 activator). Results were validated using DRP1-knockdown (KD) and OPA1-overexpression (OE). Mice were injected intraperitoneally with Mdivi-1 (20 mg/kg), BGP-15 (20 mg/kg) or distilled water (control) one hour before intranasal instillation of PM.sub.2.5 (7.8 mg/kg) or distilled water for two consecutive days. PM.sub.2.5 exposure of A549 cells caused oxidative stress, enhanced inflammation, necroptosis, mitophagy and mitochondrial dysfunction indicated by abnormal mitochondrial morphology, decreased mitochondrial membrane potential (DELAΨm), reduced mitochondrial respiration and disrupted mitochondrial fission and fusion. Regulating mitochondrial fission and fusion pharmacologically using Mdivi-1 and BGP-15 and genetically using DRP1-KD and OPA1-OE prevented PM.sub.2.5-induced celluar damage in A549 cells. Mdivi-1 and BGP-15 attenuated PM.sub.2.5-induced acute lung injury in mice. Increased mitochondrial fission and decreased mitochondrial fusion may underlie PM.sub.2.5-induced alveolar epithelial cell damage in vitro and lung injury in vivo.
Transient receptor potential (TRP) ankyrin 1 (TRPA1) could mediate ozone-induced lung injury. Optic Atrophy 1 (OPA1) is one of the significant mitochondrial fusion proteins. Impaired mitochondrial ...fusion, resulting in mitochondrial dysfunction and ferroptosis, may drive the onset and progression of lung injury. In this study, we examined whether TRPA1 mediated ozone-induced bronchial epithelial cell and lung injury by activating PI3K/Akt with the involvement of OPA1, leading to ferroptosis.
Wild-type, TRPA1-knockout (KO) mice (C57BL/6 J background) and ferrostatin-1 (Fer-1)-pretreated mice were exposed to 2.5 ppm ozone for 3 h. Human bronchial epithelial (BEAS-2B) cells were treated with 1 ppm ozone for 3 h in the presence of TRPA1 inhibitor A967079 or TRPA1-knockdown (KD) as well as pharmacological modulators of PI3K/Akt-OPA1-ferroptosis. Transcriptome was used to screen and decipher the differential gene expressions and pathways. Oxidative stress, inflammation and ferroptosis were measured together with mitochondrial morphology, function and dynamics.
Acute ozone exposure induced airway inflammation and airway hyperresponsiveness (AHR), reduced mitochondrial fusion, and enhanced ferroptosis in mice. Similarly, acute ozone exposure induced inflammatory responses, altered redox responses, abnormal mitochondrial structure and function, reduced mitochondrial fusion and enhanced ferroptosis in BEAS-2B cells. There were increased mitochondrial fusion, reduced inflammatory responses, decreased redox responses and ferroptosis in ozone-exposed TRPA1-KO mice and Fer-1-pretreated ozone-exposed mice. A967079 and TRPA1-KD enhanced OPA1 and prevented ferroptosis through the PI3K/Akt pathway in BEAS-2B cells. These in vitro results were further confirmed in pharmacological modulator experiments.
Exposure to ozone induces mitochondrial dysfunction in human bronchial epithelial cells and mouse lungs by activating TRPA1, which results in ferroptosis mediated via a PI3K/Akt/OPA1 axis. This supports a potential role of TRPA1 blockade in preventing the deleterious effects of ozone.
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•Acute ozone exposure causes bronchial epithelial cell and lung injury.•Acute ozone exposure activates TRPA1 through PI3K/Akt, disrupts mitochondrial function, and leads to ferroptosis.•Mitochondrial fusion protein--OPA1 is essential in regulating mitochondrial function and ferroptosis.•Ferroptosis plays an important role in acute ozone exposure-induced lung injury.•TRPA1 is a novel ferroptosis regulator in ozone-induced bronchial epithelial cell and lung injury.
Target tracking is a significant topic in the field of computer vision. In this paper, the target tracking algorithm based on deep Siamese network is studied. Aiming at the situation that the ...tracking process is not robust, such as drift or miss the target, the tracking accuracy and robustness of the algorithm are improved by improving the feature extraction part and online update part. This paper adds SE-block and temporal attention mechanism (TAM) to the framework of Siamese neural network. SE-block can refine and extract features; different channels are given different weights according to their importance which can improve the discrimination of the network and the recognition ability of the tracker. Temporal attention mechanism can update the target state by adjusting the weights of samples at current frame and historical frame to solve the model drift caused by the existence of similar background. We use cross-entropy loss to distinguish the targets in different sequences so that their distance in the feature domains is longer and the features are easier to identify. We train and test the network on three benchmarks and compare with several state-of-the-art tracking methods. The experimental results demonstrate that the algorithm proposed is superior to other methods in tracking effect diagram and evaluation criteria. The proposed algorithm can solve the occlusion problem effectively while ensuring the real-time performance in the process of tracking.
BackgroundTransient receptor potential (TRP) ankyrin 1 (TRPA1) and vanilloid 1 (TRPV1) mediate the development of lung injury and inflammation. This study investigated the role and mechanism of the ...TRPA1/TRPV1 pathway in airway inflammation and bronchial hyperresponsiveness (BHR) induced by acute ozone exposure. MethodsC57BL/6 mice (8-10 weeks) were intraperitoneally injected with phosphate buffered saline (PBS), A967079 (TRPA1 inhibitor) or AMG9810 (TRPV1 inhibitor) 1 h before or after ozone exposure (2.5 ppm, 3 h). BHR, cell counts in bronchoalveolar lavage (BAL) fluid, oxidative stress biomarkers, inflammatory cytokines, TRPA1 and TPRV1 protein levels, mitochondrial dynamics- and mitophagy-related protein levels, and activities of mitochondrial respiratory chain (MRC) in lung were measured. ResultsThe preventive treatment effect was similar to the therapeutic treatment effect. Both A967079 and AMG9810 intervention suppressed BHR, inflammatory cytokines, total BAL fluid cells, malondialdehyde (MDA) levels and inflammatory cytokines mRNA including Substance P (SP), Keratinocyte-Derived Chemokine (KC), interleukin-18 (IL-18) and chemokine (C-X-C motif) ligand 8 (CXCL8) expression, and enhanced reduced glutathione (GSH)/oxidized glutathione (GSSG) levels compared with ozone-exposed mice. A967079 and AMG9810 intervention inhibited dynamin-related protein (DRP1), mitochondrial fission factor (MFF), Parkinson protein 2 E3 ubiquitin protein ligase (PARK2) and Sequestosome 1 (SQSTM1)/p62 expression, increased Optic atrophy 1 (OPA1), mitofusin 2 (MFN2) and PTEN-induced putative kinase 1 (PINK1) expression, and up-regulated the activities of MRC complex III and V in lung tissue. ConclusionsThe results show that both TRPA1 and TRPV1 pathways are involved in acute ozone exposure-induced airway inflammation and BHR and influence oxidative stress, mitochondrial quality control and MRC activity, which could be a potential target for clinical therapy of respiratory diseases.
Chronic obstructive pulmonary disease (COPD) is a common chronic lung disease and its incidence is steadily increasing. COPD patients and mouse models of COPD share some similarities in lung ...pathology and physiology. We performed this study to explore the potential metabolic pathways involved in the pathogenesis of COPD and to discover the COPD-associated biomarkers. Furthermore, we aimed to examine how much the mouse model of COPD was similar and different to human COPD in terms of the altered metabolites and pathways.
Twenty human lung tissue samples (ten COPD and ten controls) and twelve mice lung tissue samples (six COPD and six controls) were analyzed by targeted HM350 metabolomics, and multivariate and pathway analysis were performed by Kyoto Encyclopedia of Genes and Genomes (KEGG) database.
The counts of many metabolites such as amino acids, carbohydrates and carnitines were changed in both COPD patients and mice compared to controls, respectively. While lipid metabolism was changed only in COPD mice. After KEGG analysis, we found these altered metabolites involved in COPD through aging, apoptosis, oxidative stress and inflammation pathways.
The expressions of metabolites changed in both COPD patients and cigarette smoke exposed (CS-exposed) mice. And there were also some differences between COPD patients and mouse models due to the differences between species. Our study suggested the dysregulation in amino acid metabolism, energy production pathway and perhaps lipid metabolism may be significantly related to the pathogenesis of COPD.
Exposure to particulate matter (PM) with an aerodynamic diameter less than 2.5 μm (PM
) is a risk factor for developing pulmonary diseases and the worsening of ongoing disease. Mitochondrial fission ...and fusion are essential processes underlying mitochondrial homeostasis in health and disease. We examined the role of mitochondrial fission and fusion in PM
-induced alveolar epithelial cell damage and lung injury. Key genes in these processes include dystrophin-related protein 1 (DRP1) and optic atrophy 1 (OPA1) respectively.
Alveolar epithelial (A549) cells were treated with PM
(32 µg/ml) in the presence and absence of Mdivi-1 (10µM, a DRP1 inhibitor) or BGP-15 (10µM, an OPA1 activator). Results were validated using DRP1-knockdown (KD) and OPA1-overexpression (OE). Mice were injected intraperitoneally with Mdivi-1 (20 mg/kg), BGP-15 (20 mg/kg) or distilled water (control) one hour before intranasal instillation of PM
(7.8 mg/kg) or distilled water for two consecutive days.
PM
exposure of A549 cells caused oxidative stress, enhanced inflammation, necroptosis, mitophagy and mitochondrial dysfunction indicated by abnormal mitochondrial morphology, decreased mitochondrial membrane potential (ΔΨm), reduced mitochondrial respiration and disrupted mitochondrial fission and fusion. Regulating mitochondrial fission and fusion pharmacologically using Mdivi-1 and BGP-15 and genetically using DRP1-KD and OPA1-OE prevented PM
-induced celluar damage in A549 cells. Mdivi-1 and BGP-15 attenuated PM
-induced acute lung injury in mice.
Increased mitochondrial fission and decreased mitochondrial fusion may underlie PM
-induced alveolar epithelial cell damage in vitro and lung injury in vivo.
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