ObjectiveTo explore the level and influencing factors of frontline nurses’ post-traumatic growth (PTG) during COVID-19 epidemic.MethodsA cross-sectional survey was conducted in February 2020 in three hospitals in China. The Post-traumatic Growth Inventory (PTGI) was used to investigate the PTG of frontline nurses. Data on related factors, including demographic characteristics and subjective variables, were collected. The Event-Related Rumination Inventory was used to assess rumination. Pearson’s or Spearman’s correlation was calculated for bivariate analysis. Independent sample t-tests or one-way analysis of variance and multiple linear regression analysis were used to examine the related factors.ResultsA total of 179 frontline nurses were recruited, and 167 were included in the analyses. The mean PTG score was 70.53±17.26. The bivariate analyses showed that deliberate rumination was modestly positively correlated with PTG (r=0.557, p<0.01), while intrusive rumination had a modest negative correlation with PTG (r=−0.413, p<0.01). Multiple linear regression demonstrated that working years, self-confidence in frontline work, awareness of risk, psychological intervention or training during the epidemic and deliberate rumination were the main influencing factors of PTG among frontline nurses and accounted for 42.5% of the variance (F=31.626, p<0.001).ConclusionsThe PTG of frontline nurses was at a medium to high level and was influenced by working years, self-confidence in frontline work, awareness of risk, psychological intervention or training and deliberate rumination. It is necessary to strengthen psychological guidance and training for frontline nurses and promote their deliberate rumination on epidemic events to improve their PTG.

Background Neuroinflammation and immune responses occurring minutes to hours after stroke are associated with brain injury after acute ischemic stroke (AIS). PPARγ coactivator-1α (PGC-1α), as a master coregulator of gene expression in mitochondrial biogenesis, was found to be transiently upregulated in microglia after AIS. However, the role of microglial PGC-1α in poststroke immune modulation remains unknown. Methods PGC-1α expression in microglia from human and mouse brain samples following ischemic stroke was first determined. Subsequently, we employed transgenic mice with microglia-specific overexpression of PGC-1α for middle cerebral artery occlusion (MCAO). The morphology and gene expression profile of microglia with PGC-1α overexpression were evaluated. Downstream inflammatory cytokine production and NLRP3 activation were also determined. ChIP-Seq analysis was performed to detect PGC-1α-binding sites in microglia. Autophagic and mitophagic activity was further monitored by immunofluorescence staining. Unc-51-like autophagy activating kinase 1 (ULK1) expression was evaluated under the PGC-1α interaction with ERRα. Finally, pharmacological inhibition and genomic knockdown of ULK1 were performed to estimate the role of ULK1 in mediating mitophagic activity after ischemic stroke. Results PGC-1α expression was shortly increased after ischemic stroke, not only in human brain samples but also in mouse brain samples. Microglia-specific PGC-1α overexpressing mice exhibited significantly decreased neurologic deficits after ischemic injury, with reduced NLRP3 activation and proinflammatory cytokine production. ChIP-Seq analysis and KEGG pathway analysis revealed that mitophagy was significantly enhanced. PGC-1α significantly promoted autophagic flux and induced autolysosome formation. More specifically, the autophagic clearance of mitochondria was enhanced by PGC-1α regulation, indicating the important role of mitophagy. Pharmacological inhibition or knockdown of ULK1 expression impaired autophagic/mitophagic activity, thus abolishing the neuroprotective effects of PGC-1α. Conclusions Mechanistically, in AIS, PGC-1α promotes autophagy and mitophagy through ULK1 and reduces NLRP3 activation. Our findings indicate that microglial PGC-1α may be a promising therapeutic target for AIS.

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This study investigated the effects of brain ischemia on sodium channel gene (NaCh) expression in rats. Using quantitative RT-PCR, our findings demonstrated the expression ratio of NaCh genes in normal rat brain to be Na(v)1.1 > Na(v)1.8 > Na(v)1.3 > Na(v)1.7 (rBI > PN3 > rBIII > PN1). In contrast, brain injury caused by middle cerebral artery occlusion (MCAo) for 2 h followed by reperfusion significantly down-regulated Na(v)1.3 and Na(v)1.7 genes in both injured and contralateral hemispheres; whereas the Na(v)1.8 gene was down regulated in only the injured hemisphere (though only acutely at 2 or 2-6 h post-MCAo). However, the time-course of NaCh gene expression revealed a significant down-regulation of Na(v)1.1 only in the ischemic hemisphere beginning 6 h post-MCAo and measured out to 48 h post-MCAo. In a separate preliminary study Na(v)1.2 (rBII) gene was found to be expressed at levels greater than that of Na(v)1.1 in normal rats and was significantly down regulated at 24 h post-MCAo). Our findings document, for the first time, quantitative and relative changes in the expression of various NaCh genes following ischemic brain injury and suggest that the Na(v)1.1 sodium channel gene may play a key role in ischemic injury/recovery.