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Acute respiratory distress syndrome (ARDS) refers to the injury of alveolar epithelial cells and capillary endothelial cells due to various injury factors. Research on the pathogenesis of ARDS has made great progress, but the exact pathogenesis of ARDS has not been fully elucidated. Up to now, the prevention and treatment of ARDS is still an important scientific problem that needs to be solved urgently. In this work, we analyzed the effect of uridine on ARDS. An ARDS model was successfully constructed by lipopolysaccharide (LPS) stimulation. Western-blotting, IFA, ELISA, RT-PCT and CLSM were conducted to investigate the effect of uridine on ARDS and insulin resistance, and the results showed that lung histopathological alterations were significantly attenuated by uridine treatment. Further work showed that the levels of proinflammatory cytokines were significantly down-regulated in the lung tissue after treatment with uridine. Additionally, the numbers of total cells and neutrophils in the bronchoalveolar lavage fluid (BALF) were also decreased in the uridine-treated ARDS mice. We further explored the potential mechanism by which uridine could treat ARDS, and the results indicated that NF-κB signaling was down-regulated by uridine treatment. Next, we studied insulin sensitivity in the ARDS mice, and found that insulin signaling was significantly down-regulated, and uridine could enhance insulin sensitivity in the ARDS mice model. Furthermore, we found that the levels of inflammation and oxidative stress were decreased by uridine treatment, which may be the potential mechanism by which uridine could improve insulin sensitivity. Taken together, the current work provides evidence that uridine can serve as a potential drug to treat ARDS and insulin resistance.

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Journal of Behavioral Addictions
Chang Liu
Lei Ren
Kristian Rotaru
Xufeng Liu
Kuiliang Li
Wei Yang
Ye Li
Xinyi Wei
Murat Yücel
, and
Lucy Albertella



Existing research has demonstrated that problematic smartphone use (PSU) may reflect a composition of heterogeneous symptoms, with individual PSU symptoms uniquely related to predisposing variables. The Big Five personality traits represent one of the most frequently examined predisposing variables in relation to PSU. However, no studies to date have examined the trait-to-symptom association between the Big Five personality traits and PSU. Using a network analysis approach, we aimed to understand: 1) specific pathways linking each of the Big Five personality traits to PSU symptoms and 2) the bridging effects of each Big Five personality trait on the PSU symptom cluster.


A regularised graphical Gaussian model was estimated among 1,849 Chinese university students. PSU symptoms were assessed with items from the Problematic Smartphone Use Scale. Facets of the Big Five personality traits were assessed with the subscales of the Chinese Big Five Personality Inventory-15. An empirical index (i.e., bridge expected influence) was used to quantify bridge nodes.


Results revealed specific and distinct pathways between the Big Five personality traits and PSU symptoms (e.g., Neuroticism-Escapism/Avoidance, Conscientiousness-Preoccupation and Extraversion-Escapism/Avoidance). Further, Neuroticism showed the highest positive bridge centrality among the Big Five personality traits, while Conscientiousness had the highest negative bridge centrality.

Discussion and conclusions

The current study provided direct empirical evidence concerning specific pathways between the Big Five personality traits and PSU symptoms and highlighted the influential role of Neuroticism and Conscientiousness as potential targets for early detection and treatment of PSU.

Open access