Analysis of Influencing Factors of Repair Effect after Peripheral Nerve Injury.

In order to improve the repair effect after peripheral nerve injury, this paper analyzes the related influencing factors. The regeneration of peripheral nerve includes two continuous and overlapping processes: the acute wound healing period and the axon seeking target tissue period. The complete and effective process of peripheral nerve regeneration includes the sprouting, growth and extension of regenerated axons, and the reconstruction of synaptic connections (neuromuscular junctions) with target organs to realize the reinnervation of nerves and restore function. This process includes three indicators of success in regeneration: structural reconstruction, metabolic regeneration, and functional recovery. In order to improve the repair effect of peripheral nerve injury, relevant influencing factors can be analyzed, and effective improvement of these influencing factors can improve the recovery effect of peripheral nerve injury. Finally, this paper analyzes multiple factors to provide theoretical references for follow-up clinical diagnosis and treatment.

RNA Sequencing of Peripheral Blood Revealed that the Neurotropic TRK Receptor Signaling Pathway Shows Apparent Correlation in Recovery Following Spinal Cord Injury at Small Cohort.

Spinal cord injury (SCI) can be lethal; however, the precise mechanisms underlying healing are unclear, limiting the development of effective therapies. In this study, the molecular mechanisms involved in SCI were investigated. Clinical peripheral blood samples from normal individuals and patients with incomplete SCI (ISCI) and complete SCI (CSCI) were analyzed by RNA-Seq. The expression levels of EPHA4, CDK16, BAD, MAP2 Normal 2, EGR, and RHOB differed significantly between the SCI group and normal individuals, and these results were verified by q-PCR. A gene ontology (GO) enrichment analysis showed that differentially expressed genes were mostly enriched for the neurotrophin TRK receptor signaling pathway. We verified the expression of neurotrophic factors and found that they were all expressed most highly in the SCI group. The results of this study demonstrate that neurotrophic factors are highly expressed after SCI and the neurotrophin TRK receptor signaling pathway may be involved in the initiation of nerve system regeneration.

MicroRNA-34a alleviates steroid-induced avascular necrosis of femoral head by targeting Tgif2 through OPG/RANK/RANKL signaling pathway.

The study aims to investigate the effect of microRNA-34a (miR-34a) targeting Tgif2 on steroid-induced avascular necrosis of femoral head (SANFH) by regulating OPG/RANK/RANKL signaling pathway. SD rats were divided into normal control and model (RNAKL rat models) groups. The model group was further assigned into model control, negative control, miR-34a mimics and miR-34a inhibitors groups. QRT-PCR was applied to detect miR-34a, Tgif2, OPG, RANK and RNAKL mRNA expressions. Femoral head tissues were collected for Micro-CT scanning and HE staining. QRT-PCR and Western blotting were used to detect expressions of miR-34a, Tgif2, OPG, RANK, RANKL and Runx2, OPN and OC in bone tissues. Dual-luciferase reporter gene assay was used to testify the target relationship between miR-34a and Tgif2. Compared with the normal control group, the model group showed increased Tgif2, RANK and RANKL mRNA expressions, but decreased miR-34a and OPG mRNA expressions. Tgif2 mRNA expression was negatively correlated with miR-34a and OPG mRNA expressions. Micro-CT showed cystic degeneration of femoral head, with decreased bone volume/total volume (BV/TV), bone surface area/bone volume and trabecular number in the model control group compared with the normal control group. Compared with the model control group, the miR-34a mimics group showed increased BV/TV and trabecular thickness and Runx2, OPN and OC expressions, while the parameters decreased in the miR-34a inhibitors group. Compared with the normal control group, the other groups showed increased Tgif2, RANK and RANKL expressions but decreased miR-34a and OPG expressions. Compared with the model control group, Tgif2, RANK and RANKL expressions decreased and miR-34a and OPG expressions increased in the miR-34a mimics group, while the miR-34a inhibitors group had a reverse trend in contrast to the miR-34a mimics group. Tgif2 is a target gene of miR-34a. In conclusion, miR-34a can alleviate SANFH through targeting Tgif2 and further regulating OPG/RANK/RANKL signaling pathway. Impact statement miR-34a can alleviate SANFH through targeting Tgif2 and further regulating OPG/RANK/RANKL signaling pathway, which can be used as a new theoretical basis for SANFH treatment.