Fatigue is a universal and challenging problem in a nurse's career, particularly for those working in the emergency department. Through analyzing the current status of emergency department nurses’ fatigue, the purpose of this study is to provide guidance for occupational health promotion strategies making and fatigue relief. Cross-sectional study was conducted among nurses working in emergency department in 6 grade III A hospitals in Xi’an, China. Convenience sample of 346 nurses agreed to participate in this study. Data collection was based on the questionnaires. Descriptive statistics, hypothesis tests and correlation analysis were used to describe the samples’ characteristics and identify associations amongst participants’ characteristics. The fatigue score of those emergency nurses from grade III A hospitals in Xian was 8.71 ± 3.01, a high fatigue level. Moreover, there were significant differences in fatigue scores of different age groups, sleep qualities, work stress levels and physical states ( P < .01). Further, the dimension of physical fatigue in various age groups, job title, marital status, sleep qualities, work stress levels and physical states was significantly different ( P < .05) and the dimension of mental fatigue with different sleep qualities, work stress levels and physical states was significantly different ( P < .01). The results of correlation analysis showed that fatigue was positively correlated with perceived stress while negatively correlated with social support and self-efficacy ( P < .01). The multiple stepwise linear regression analysis indicated that the independent variables in the fatigue regression equation were perceived stress, physical condition and work stress in turn ( P < .01), and the independent variables in the the dimensions of physical fatigue regression equation were perceived stress, physical condition,work stress and job title in turn ( P < .05); the independent variables in the the dimensions of mental fatigue regression equation were perceived stress,subjective support and physical condition in turn ( P < .05). The current status of high fatigue level of emergency nurses should be taken seriously. It is imperative to take effective measures to help emergency nurses reduce stress, improve social support, promote the self-efficacy, and thus relieve fatigue.

Purpose Previous studies have not determined the interactive effects of stress and coping style on cognitive function in patients with schizophrenia, and the current studies have been restricted to the relationship between stress and stress response, which may be associated with cognitive impairment in individuals with schizophrenia. The present research was aimed to determine whether stress is related to cognitive function in patients with schizophrenia. In addition, this research further investigates the moderating effects of coping style on the relationship between stress and cognitive function in patients with schizophrenia on the basis of stress and coping theory. Patients and methods Our sample consisted of 274 patients with a confirmed diagnosis of schizophrenia, and all of them completed the Simple Cope Style Questionnaire, Social Readjustment Rating Scale, and cognitive function assessment. A multivariate regression analysis was performed to investigate the possible correlations between cognitive function and stress, and the moderating effects of coping style on the relationship between stress and cognitive function were tested using the PROCESS macro for SPSS. Results Stress was negatively correlated with working memory. Negative coping but not positive coping moderated the relationship between stress and working memory in patients with schizophrenia, and the Johnson–Neyman technique showed that the moderating effect was significant only above this cutoff (38.32% of all negative coping scores). This means that when exposed to similar stress, patients adopting high negative coping had worse working memory than those who did not. Conclusion These findings suggested that the assessment of stress and coping style may help estimate working memory impairment risk in patients with schizophrenia, and reducing negative coping may be a crucial intervention target to prevent further impairment of working memory in patients with schizophrenia suffering from great stress.

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Pregnancy exposure of valproic acid (VPA) is widely adopted as a model of environmental factor induced autism spectrum disorder (ASD). Increase of excitatory/inhibitory synaptic transmission ratio has been proposed as the mechanism of VPA induced ASD. How this happened, particularly at the level of excitatory neuron differentiation in human neural progenitor cells (NPCs) remains largely unclear. Here, we report that VPA exposure remarkably inhibited human NPC proliferation and induced excitatory neuronal differentiation without affecting inhibitory neurons. Following VPA treatment, mitochondrial dysfunction was observed before neuronal differentiation, as showed by ultrastructural changes, respiratory complex activity, mitochondrial membrane potential and oxidation levels. Meanwhile, extracellular acidification assay revealed an elevation of glycolysis by VPA stimulation. Interestingly, inhibiting glycolysis by 2-deoxy-d-glucose-6-phosphate (2-DG) efficiently blocked the excitatory neuronal differentiation of human NPCs induced by VPA. Furthermore, 2-DG treatment significantly compromised the VPA-induced expression of H3ac and H3K9ac, and the VPA-induced binding of H3K9ac on the promoter of Ngn2 and Mash1, two key transcription factors of excitatory neuron fate determination. These data, for the first time, demonstrated that VPA biased excitatory neuron differentiation by glycolysis-mediated histone acetylation of neuron specific transcription factors.

Social dysfunction is the core syndrome of autism spectrum disorder (ASD) and lacks effective medicine. Although numerous risk genes and relevant environmental factors have been identified, the convergent molecular mechanism underlying ASD‐associated social dysfunction remains largely elusive. Here, we report aberrant activation of canonical Wnt signaling and increased glycolysis in the anterior cingulate cortex (ACC, a key brain region of social function) of two ASD mouse models (Shank3−/− and valproic acid‐treated mice) and their corresponding human neurons. Overexpressing β‐catenin in the ACC of wild‐type mice induces both glycolysis and social deficits. Suppressing glycolysis in ASD mice partially rescued synaptic and social phenotype. Axin2, a key inhibitory molecule in Wnt signaling, interacts with the glycolytic enzyme enolase 1 (ENO1) in ASD neurons. Surprisingly, an Axin2 stabilizer, XAV939, effectively blocked Axin2/ENO1 interaction, switched glycolysis/oxidative phosphorylation balance, promoted synaptic maturation, and rescued social function. These data revealed excessive neuronal Wnt‐glycolysis signaling as an important underlying mechanism for ASD synaptic deficiency, indicating Axin2 as a potential therapeutic target for social dysfunction.