Current Status and Factors Influencing Emergency Response Capability of Shared Nurses in the Internet + Nursing Service Model: A Descriptive Cross-Sectional Study.

Aim: To evaluate the existing level of emergency capabilities among shared nurses and analyze the factors influencing these capabilities. Methods: An descriptive cross-sectional survey was conducted from September to October 2023, a purposive sampling method was employed to select 340 shared nurses as the subjects for investigation in Nanchang and Ganzhou cities of Jiangxi Province, as well as Wenzhou city in Zhejiang Province. A self - designed questionnaire on the emergency capabilities of shared nurses was utilized for data collection. Results: This investigation encompassed the collection of 340 valid questionnaires, assessing the overall emergency response proficiency of shared nurses. The cumulative score amounted to (170.81±24.62), averaging (4.27±0.62). It is noteworthy that the dimension scoring the highest was preparedness (4.33±0.68), whereas the recovery capability dimension received the lowest score (4.17±0.75). Through multiple linear regression analysis, it was determined that marital status, participation in emergency capability training, and experience in home nursing services significantly influenced the emergency capabilities of shared nurses (P<0.05). Conclusion: Shared nurses in China demonstrate a moderately high level of emergency response capability. The marital status, participation in emergency capacity training, and on-site nursing service experience are pivotal factors influencing the emergency capabilities of shared nurses. Nursing administrators should prioritize the development of emergency capacity training and team building for shared nurses, establishing a scientifically standardized mechanism for training, assessment, and management. The implementation of performance evaluation mechanisms for shared nurses is crucial to enhance professional awareness within the workforce.

LncRNA FOXC2 antisense transcript accelerates non-small-cell lung cancer tumorigenesis via silencing p15.

Non-coding RNAs (ncRNAs) have been demonstrated to modulate the oncogenesis of non-small cell lung cancer (NSCLC), especially the long non-coding RNAs (lncRNAs). However, the role of lncRNA FOXC2-AS1 in the NSCLC is still unclear. In this research, we find that lncRNA FOXC2-AS1 is involved to NSCLC oncogenesis. The ectopic high-expression level of FOXC2-AS1 is closely correlated with the limited NSCLC patients' survival. In the functional experiments, the knockdown of FOXC2-AS1 dramatically suppressed the NSCLC cells' (A549, H460) proliferation, accelerated the apoptosis and induced the cycle arrest at G0/G1 phase. Mechanistic experiments revealed that FOXC2-AS1 repressed the p15 expression via recruiting the polycomb repressive complex 2 (PRC2) to the promoter of p15. The interaction within FOXC2-AS1 and p15 was validated using the rescue experiments. In conclusion, the results in this work confirmed that FOXC2-AS1 could aggravate NSCLC oncogenesis through repressing p15 expression via interacting EZH2, which provide new idea for the NSCLC therapeutic strategy.

A317491 relieved HIV gp120-associated neuropathic pain involved in P2X3 receptor in dorsal root ganglia.

Glycoprotein 120 (gp120) is an HIV envelope glycoprotein. Gp120 can directly stimulate the primary sensory afferent neurons and cause hyperalgesia. The P2X3 receptor in dorsal root ganglia (DRG) is involved in the transmission of pain. In this study, we aimed to explore the role of the P2X3 receptor in gp120-induced neuropathic pain. Our data showed that mechanical and thermal hyperalgesia in rats treated with gp120 were increased compared to those in the control group. The expression levels of the P2X3 mRNA and protein in rats treated with gp120 were higher than those in the control group. The P2X3 antagonist A317491 decreased mechanical hyperalgesia and thermal hyperalgesia and the up-regulated expression levels of P2X3 mRNA and protein in rats treated with gp120. A317491 decreased ERK1/2 phosphorylation levels in the gp120-treated rat DRG. In addition, P2X3 agonist α,ß-methylene ATP (α,ß-meATP)-activated currents in DRG neurons cultured with gp120 were higher than those in control neurons. The inhibitory effect of A317491 on α,ßme-ATP-induced currents in DRG neurons from the gp120-treated neurons was larger than that for control neurons. Molecular docking data showed that A317491 may be acted in the gp120 protein to inhibit the gp120 initiated the P2X3 activation, decrease the sensitizing DRG primary afferents and reduce the signal transmission of neuropathic pain in gp120-treated rats. Therefore, the inhibition of the P2X3 receptor in rat DRG neurons relieved gp120-induced mechanical hyperalgesia.