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As the mobile Internet improves by leaps and bounds, the model of traditional offline used car trading has gradually lost the ability to live up to the needs of consumers, and online used car trading platforms have emerged as the times require. Second-hand car price assessment is the premise of second-hand car trading, and a reasonable price can reflect the objective, fair, and true nature of the second-hand car market. In order to standardize the evaluation standards of used car prices and improve the accuracy of used car price forecasts, the linear correlation between vehicle parameters, vehicle conditions, and transaction factors and used car price was comprehensively investigated, grey relational analysis was applied to filter the feature variables of factors affecting used car price, the traditional BP neural network was also optimized by combining the particle swarm optimization algorithm, and a used car price prediction method based on PSO-GRA-BPNN was proposed. The results show that only the correlation coefficient of new car price, engine power, and used car price is greater than 0.6, which has a certain linear correlation. The correlation between new car price, displacement, mileage, gearbox type, fuel consumption, and registration time on used car prices is greater than 0.7, and the impact of other indicators on used car prices is negligible. Compared with the traditional BPNN model and the multiple linear regression, random forest, and support vector machine regression models proposed by other researchers, the MAPE of the PSO-GRA-BPNN model proposed in this paper is 3.936%, which is 30.041% smaller than the error of the other three models. The MAE of the PSO-GRA-BPNN model is 0.475, which is a maximum reduction of 0.622 compared to the other three models. R can reach up to 0.998, and R2 can reach 0.984. Although the longest training time is 94.153 s, the overall prediction effect is significantly better than other used car price prediction models, providing a new idea and method for used car evaluation.

Background The fear of insecurity and uncertainty caused by the 2019 coronavirus disease (COVID-19), the separation and loss of certain important relationships, and great changes in lifestyle have awakened strong emotional responses, which may cause psychological problems in the general population. However, there is little research on how people who pay attention to anxiety and depression cope with the negative psychological impact during an epidemic or major disaster. This study aimed to identify what behaviors can effectively reduce negative emotions during an epidemic. Methods From 1 February to 8 March 2020, we conducted a web-based survey and collected information on general demographic data. Probable depression, anxiety symptoms, and coping behaviors were assessed with the Patient Health Questionnaire-9, Generalized Anxiety Disorder-7, and self-made coping behaviors questionnaires. Result Among 17 249 responders, 7923 and 9326 completed assessments of depression and anxiety respectively, and all responders completed the coping behaviors questionnaires. Our survey population showed a high prevalence rate of possible depression disorders (2746 of 7923, 34.66%) and anxiety disorders (5309 of 9326, 56.93%). Compared with other groups, the elderly, women, people of lower education, and people with lower income were more likely to suffer depression and/or anxiety. In terms of marital status, the cohabiting group showed the highest rate of depression and/or anxiety. Among the careers, students and housewives were high-risk groups suffering from depression and/or anxiety. After adjusting for social-demographic factors (e.g. age, sex), depression and anxiety were positively associated with self-injury, doing housework, and having sex or masturbating, and negatively associated with singing, drawing, or writing, dating friends online, singing, attending lectures, and doing yoga. Conclusion Our findings identified some spontaneous coping behaviors that can probably relieve the psychological impact of vulnerable groups during the COVID-19 epidemic.

In this paper, we propose an attention-based multi-task neural network model for text classification and sequence tagging and then apply it to the named entity recognition and the intent analysis of Chinese online medical questions. We found that the use of both attention and multi-task learning improved the performance of these tasks. Our method achieved superior performance in named entity recognition and intent analysis compared with other baseline methods; the method is a light-weight solution that is suitable for deployment on small servers. Furthermore, we took advantage of the model's capabilities for these two tasks and built a simple question-answering system for cardiovascular issues. Users and service providers can monitor the logic of the answers generated by this system.

TGF-β1 induces an increase in paracellular permeability and actin stress fiber formation in lung microvascular endothelial and alveolar epithelial cells via small Rho GTPase. The molecular mechanism involved is not fully understood. Neuronal Wiskott-Aldrich syndrome protein (N-WASP) has an essential role in actin structure dynamics. We hypothesized that N-WASP plays a critical role in these TGF-β1-induced responses. In these cell monolayers, we demonstrated that N-WASP down-regulation by short hairpin RNA prevented TGF-β1-mediated disruption of the cortical actin structure, actin stress filament formation, and increased permeability. Furthermore, N-WASP down-regulation blocked TGF-β1 activation mediated by IL-1β in alveolar epithelial cells, which requires actin stress fiber formation. Control short hairpin RNA had no effect on these TGF-β1-induced responses. TGF-β1-induced phosphorylation of Y256 of N-WASP via activation of small Rho GTPase and focal adhesion kinase mediates TGF-β1-induced paracellular permeability and actin cytoskeleton dynamics. In vivo, compared with controls, N-WASP down-regulation increases survival and prevents lung edema in mice induced by bleomycin exposure-a lung injury model in which TGF-β1 plays a critical role. Our data indicate that N-WASP plays a crucial role in the development of TGF-β1-mediated acute lung injury by promoting pulmonary edema via regulation of actin cytoskeleton dynamics.-Wagener, B. M., Hu, M., Zheng, A., Zhao, X., Che, P., Brandon, A., Anjum, N., Snapper, S., Creighton, J., Guan, J.-L., Han, Q., Cai, G.-Q., Han, X., Pittet, J.-F., Ding, Q. Neuronal Wiskott-Aldrich syndrome protein regulates TGF-β1-mediated lung vascular permeability.

Fibroblast migration plays an important role in the normal wound healing process; however, dysregulated cell migration may contribute to the progressive formation of fibrotic lesions in the diseased condition. To examine the role of focal-adhesion-kinase (FAK)-related non-kinase (FRNK) in regulation of fibrotic lung fibroblast migration, we examined cell migration, FRNK expression, and activation of focal adhesion kinase (FAK) and Rho GTPase (Rho and Rac) in primary lung fibroblasts derived from both idiopathic pulmonary fibrosis (IPF) patients and normal human controls. Fibrotic (IPF) lung fibroblasts have increased cell migration when compared to control human lung fibroblasts. FRNK expression is significantly reduced in IPF lung fibroblasts, while activation of FAK, Rho and Rac are increased in IPF lung fibroblasts. Endogenous FRNK expression is inversely correlated with FAK activation and cell migration rate in IPF lung fibroblasts. Forced exogenous FRNK expression abrogates the increased cell migration, and blocked the activation of FAK and Rho GTPase (Rho and Rac), in IPF lung fibroblasts. These data for the first time provide evidence that downregulation of endogenous FRNK plays a role in promoting cell migration through FAK and Rho GTPase in fibrotic IPF lung fibroblasts.

Myofibroblasts are implicated in pathological stromal responses associated with lung fibrosis. One prominent phenotypic marker of fully differentiated myofibroblasts is the polymerized, thick cytoplasmic filaments containing newly synthesized α-smooth muscle actin (α-SMA). These α-SMA-containing cytoplasmic filaments are important for myofibroblast contractility during tissue remodeling. However, the molecular mechanisms regulating the formation and maturation of α-SMA-containing filaments have not been defined. This study demonstrates a critical role for neuronal Wiskott-Aldrich syndrome protein (N-WASP) in regulating the formation of α-SMA-containing cytoplasmic filaments during myofibroblast differentiation and in myofibroblast contractility. Focal adhesion kinase (FAK) is activated by transforming growth factor-β1 (TGF-β1) and is required for phosphorylation of tyrosine residue 256 (Y256) of N-WASP. Phosphorylation of Y256 of N-WASP is essential for TGF-β1-induced formation of α-SMA-containing cytoplasmic filaments in primary human lung fibroblasts. In addition, we demonstrate that actin-related protein (Arp) 2/3 complex is downstream of N-WASP and mediates the maturation of α-SMA-containing cytoplasmic filaments. Together, this study supports a critical role of N-WASP in integrating FAK and Arp2/3 signaling to mediate formation of α-SMA-containing cytoplasmic filaments during myofibroblast differentiation and maturation.

Idiopathic pulmonary fibrosis (IPF) is a progressive fibrotic lung disease whose underlying molecular mechanisms are largely unknown. Herein, we show that focal adhesion kinase–related nonkinase (FRNK) plays a key role in limiting the development of lung fibrosis. Loss of FRNK function in vivo leads to increased lung fibrosis in an experimental mouse model. The increase in lung fibrosis is confirmed at the histological, biochemical, and physiological levels. Concordantly, loss of FRNK function results in increased fibroblast migration and myofibroblast differentiation and activation of signaling proteins that drive these phenotypes. FRNK-deficient murine lung fibroblasts also have an increased capacity to produce and contract matrix proteins. Restoration of FRNK expression in vivo and in vitro reverses these profibrotic phenotypes. These data demonstrate the multiple antifibrotic actions of FRNK. More important, FRNK expression is down-regulated in human IPF, and down-regulation of FRNK in normal human lung fibroblasts recapitulates the profibrotic phenotype seen in FRNK-deficient cells. The effect of loss and gain of FRNK in the experimental model, when taken together with its down-regulation in human IPF, suggests that FRNK acts as an endogenous negative regulator of lung fibrosis by repressing multiple profibrotic responses.

Recent studies recognize that Hypocretin system (also known as Orexin) plays a critical role in sleep/wake disorders and feeding behaviors. However, little is known about the regulation of the Hypocretin system. It is also known that tumor necrosis factor alpha (TNF-α) is involved in the regulation of sleep/wake cycle. Here, we test our hypothesis that the Hypocretin system is regulated by TNF-α. Prepro-Hypocretin and Hypocretin receptor 2 (HcrtR2) can be detected at a very low level in rat B35 neuroblastoma cells. In response to TNF-α, Prepro-Hypocretin mRNA and protein levels are down-regulated, and also HcrtR2 protein level is down-regulated in B35 cells. To investigate the mechanism, exogenous rat Prepro-Hypocretin and rat HcrtR2 were overexpressed in B35 cells. In response to TNF-α, protein and mRNA of Prepro-Hypocretin are significantly decreased (by 93% and 94%, respectively), and the half-life of Prepro-Hypocretin mRNA is decreased in a time- and dose-dependent manner. The level of HcrtR2 mRNA level is not affected by TNF-α treatment; however, HcrtR2 protein level is significantly decreased (by 86%) through ubiquitination in B35 cells treated with TNF-α. Downregulation of cellular inhibitor of apoptosis protein-1 and -2 (cIAP-1 and -2) abrogates the HcrtR2 ubiquitination induced by TNF-α. The control green fluorescent protein (GFP) expression is not affected by TNF-α treatment. These studies demonstrate that TNF-α can impair the function of the Hypocretin system by reducing the levels of both Prepro-Hypocretin and HcrtR2.