Aim: To examine the relative in uence of fear of COVID-19 on nurses' psychological distress, work satisfaction and intent to leave their organisation and the profession. Background: The emergence of COVID-19 has signi cantly impacted the psychological and mental wellbeing of frontline healthcare workers, including nurses. To date, no studies have been conducted examining how this fear of COVID-19 contributes to health, well-being and work outcomes in frontline nurses. Methods: This is a cross-sectional research design involving 261 frontline nurses in the Philippines. Five standardised scales were used for data collection. Results: Overall, the composite score of the fear of COVID-19 scale was 19.92. Job role and attendance of COVID-19-related training predicted fear of COVID-19. An increased level of fear of COVID-19 was associated with decreased job satisfaction, increased psychological distress, and increased organisational and professional turnover intentions. Conclusions: Frontline nurses who reported not having attended COVID-19-related training and those who held part-time job roles reported increased fears of COVID-19. Addressing the fear of COVID-19 may result in improved job outcomes in frontline nurses, such as increased job satisfaction, decreased stress levels and lower intent to leave the organisation and the profession. Implications for Nursing Management: Organisational measures are vital to support the mental health of nurses and address their fear of COVID-19 through peer and social support, psychological and mental support services (e.g., counselling or psychotherapy), provision of training related to COVID-19, and accurate and regular information updates.

Background Runt-related transcription factor 1 (RUNX1) plays the roles of an oncogene and an anti-oncogene in epithelial tumours, and abnormally elevated RUNX1 has been suggested to contribute to the carcinogenesis of colorectal cancer (CRC). However, the mechanism remains unclear. Methods The expression of RUNX1 in CRC and normal tissues was detected by real-time quantitative PCR and Western blotting. The effect of RUNX1 on CRC migration and invasion was conducted by functional experiments in vitro and in vivo. Chromatin Immunoprecipitation assay verified the direct regulation of RUNX1 on the promoter of the KIT, which leads to the activation of Wnt/β-catenin signaling. Results RUNX1 expression is upregulated in CRC tissues. Upregulated RUNX1 promotes cell metastasis and epithelial to mesenchymal transition (EMT) of CRC both in vitro and in vivo. Furthermore, RUNX1 can activate Wnt/β-catenin signalling in CRC cells by directly interacting with β-catenin and targeting the promoter and enhancer regions of KIT to promote KIT transcription. These observations demonstrate that RUNX1 upregulation is a common event in CRC specimens and is closely correlated with cancer metastasis and that RUNX1 promotes EMT of CRC cells by activating Wnt/β-catenin signalling. Moreover, RUNX1 is regulated by Wnt/β-catenin. Conclusion Our findings first demonstrate that RUNX1 promotes CRC metastasis by activating the Wnt/β-catenin signalling pathway and EMT. Electronic supplementary material The online version of this article (10.1186/s13046-019-1330-9) contains supplementary material, which is available to authorized users.

Inflammatory mediators, many of which activate the signaling of nuclear factor kappa B (NFκB), have received increasing attention in the field of neurogenesis. NFκB signaling regulates neurite outgrowth and neural plasticity as well as the proliferation/apoptosis and terminal differentiation of neural stem cells (NSCs). Early neurogenesis from NSCs produces identical progeny through symmetric division and committed daughter cells through asymmetric division. Here, we show that NFκB signaling is required for NSC initial differentiation. The canonical IKKβ/IκBα/ p65 pathway is activated during the initial stages of neural differentiation induced by treatment with TNFα or with- drawal of epidermal growth factor/basic fibroblast growth factor. NSC-specific inhibition of NFκB in transgenic mice causes an accumulation of Nestin+/Sox2+/glial fibrillary acidic protein+ NSCs. Inhibition of NFκB signaling in vitro blocks differentiation and asymmetric division and maintains NSCs in an undifferentiated state. The induction of initial differentiation and asymmetry by NFκB signaling occurs through the inhibition of C/EBPβ expression. Our data reveal a novel function of NFκB signaling in early neurogenesis and provide insight into the molecular mechanisms underlying neurodevelopmental disorders and neurodegenerative diseases.