Objective To summarize the nursing intervention for patients with root canal retreatment. Methods A total of 70 patients who received retreatment of the root canal by ProTaper file were selected as the research objects and randomly divided into the control group and the treatment group. The patients in the control group were given routine nursing care. On the basis of the control group, comprehensive nursing was performed and perfected before, during and after the whole process in the treatment group. The treatment time, complication incidence and patient's satisfaction were compared between the two groups. Results The treatment time was (10.11±3.11) minutes in the treatment group and (13.11±5.28) minutes in the control group, and the difference was statistically significant (t=-2.636, P=0.011). The incidence of complication in the treatment group was 6.90%, which was lower than that of the control group 20.69%, however, there was no statistical significance in the difference (χ2=2.32,P=0.128). Conclusions In the retreatment of root canal, strengthening preoperative, intraoperative and postoperative nursing can effectively improve the effect of root canal dredging and reduce the incidence of complications.

Mesenchymal stem cell (MSC)-based therapy has emerged as a promising treatment for spinal cord injury (SCI), but improving the neurogenic potential of MSCs remains a challenge. Mixed lineage leukemia 1 (MLL1), an H3K4me3 methyltransferases, plays a critical role in regulating lineage-specific gene expression and influences neurogenesis. In this study, we investigated the role and mechanism of MLL1 in the neurogenesis of stem cells from apical papilla (SCAPs). We examined the expression of neural markers, and the nerve repair and regeneration ability of SCAPs using dynamic changes in neuron-like cells, immunofluorescence staining, and a SCI model. We employed a coimmunoprecipitation (Co-IP) assay, real-time RT-PCR, microarray analysis, and chromatin immunoprecipitation (ChIP) assay to investigate the molecular mechanism. The results showed that MLL1 knock-down increased the expression of neural markers, including neurogenic differentiation factor (NeuroD), neural cell adhesion molecule (NCAM), tyrosine hydroxylase (TH), βIII-tubulin and Nestin, and promoted neuron-like cell formation in SCAPs. In vivo, a transplantation experiment showed that depletion of MLL 1 in SCAPs can restore motor function in a rat SCI model. MLL1 can combine with WD repeat domain 5 (WDR5) and WDR5 inhibit the expression of neural markers in SCAPs. MLL1 regulates Hairy and enhancer of split 1 (HES1) expression by directly binds to HES1 promoters via regulating H3K4me3 methylation by interacting with WDR5. Additionally, HES1 enhances the expression of neural markers in SCAPs. Our findings demonstrate that MLL1 inhibits the neurogenic potential of SCAPs by interacting with WDR5 and repressing HES1. These results provide a potential therapeutic target for promoting the recovery of motor function in SCI patients.
Animals ; Humans ; Rats ; Cell Differentiation ; Intracellular Signaling Peptides and Proteins/therapeutic use* ; Leukemia/metabolism* ; Mesenchymal Stem Cells ; Neurogenesis ; Stem Cells ; Transcription Factor HES-1/metabolism*