Repair effect of neurotrophic factor III (NT-3) on rats with spinal injury model and its mechanism.

The present study aimed to study the repair effect of neurotrophic factor III (NT-3) on spinal injury model rats and its mechanism. Wistar rats with spinal injury were established by accelerated compression stroke after the operation and divided into control group, model group, and NT-3 intervention group. The motor function of rats in each group was evaluated at different postoperative time points (3, 7, 14 d). HE staining was used to detect the changes in tissue structure and morphology of the injured spinal column in each group. The changes of SOD, MDA and GSH in serum of rats were detected. The concentrations of inflammatory cytokines IL-1ß, IL-6, IL-17 and TNF-α in serum were detected by enzyme-linked immunosorbent assay (ELISA). Western blot was used to detect the expression changes of anti-apoptotic protein (Bcl-2) and pro-apoptotic protein (Bax) in injured spinal tissue of rats in each group. Compared with model group, motor function score of NT-3 intervention group increased gradually, and had statistical significance at 7 and 14 days (5.29±1.62 vs 9.33±2.16, 5.92±1.44 vs 14.56±2.45, T =7.386, 9.294, P =0.004, 0.000). The levels of SOD and GSH in serum of NT-3 intervention group were significantly increased (t=9.117, 12.207, P=0.000, 0.000), while the level of MDA was significantly decreased (t=5.089, P=0.011). Serum levels of inflammatory cytokines IL-1ß, IL-6, IL-17 and TNF-α in NT-3 intervention group were significantly decreased (T =6.157, 7.958, 6.339, 6.288, P=0.008, 0.005, 0.005, 0.007). In the NT-3 treatment group, Bax protein was significantly decreased (0.24±0.05 vs 0.89±0.12, T =8.579, P=0.001), and the relative expression of Bcl-2 protein was significantly increased (0.75±0.06 vs 0.13±0.05, T =9.367, P=0.001). Neurotrophic factor III can promote spinal injury repair in spinal injury model rats, and play a role by enhancing antioxidant stress ability, inhibiting inflammatory factors, promoting Bcl-2 and decreasing Bax expression.

The Efficacy of Targeted Perioperative Management for Diabetic Patients with Traumatic Calcaneal Fractures.

Objective: To assess the efficacy of targeted perioperative management for diabetic patients with traumatic calcaneal fractures. Methods: Between April 2020 and December 2020, 100 diabetic patients with traumatic calcaneal fractures treated in our institution satisfying the inclusion criteria were enrolled and assigned to receive either conventional treatment with surgery or plaster fixation (observation group) or targeted treatment with surgery or plaster fixation (experimental group) via the random number table method, with 50 patients in each group. All eligible patients were followed up for 1 year postoperatively. Outcome measures included length of hospital stay, recovery time, fracture healing, duration of postoperative wound drainage, complication rate, blood glucose, and treatment satisfaction. The Maryland score was used for the assessment of foot function. Results: The duration of postoperative wound drainage, length of hospital stay, and recovery time in the experimental group (3.63 ± 1.04 d, 12.13 ± 3.77 d, and 111.22 ± 16.24 d) were significantly shorter than those in the observation group (5.71 ± 2.34 d, 15.28 ± 4.42 d, 123.10 ± 22.82 d) (P < 0.01). The experimental group obtained a markedly higher complete healing rate versus the observation group (P < 0.001). A significantly lower complication rate was observed in the experimental group than in the observation group (P < 0.05). The Maryland scores results were dichotomized into good (≥75 points) and poor (<75 points). The experimental group showed significantly higher Maryland scores good rate and treatment satisfaction versus the observation group (P < 0.01). The experimental group patients were associated with better postoperative fasting glucose and 2 h postprandial glucose versus those in the observation group (P < 0.05). Conclusion: Targeted treatment in the perioperative management of diabetic patients with traumatic calcaneal fractures significantly promotes the recovery of patients, reduces the incidence of complications, increases treatment satisfaction, and ameliorates the doctor-patient relationship.

PFK15, a PFKFB3 antagonist, inhibits autophagy and proliferation in rhabdomyosarcoma cells.

Due to the high-level of metastatic and relapsed rates, rhabdomyosarcoma (RD) patients have a poor prognosis, and novel treatment strategies are required. Thereby, the present study evaluated the efficacy of PFK15, a PFKFB3 inhibitor, in RD cells to explore its potential underlying mechanism on the regulation of autophagy and proliferation in these cells. The effects of PFK15 on cell viability loss and cell death in different treatment groups, were evaluated by MTS assay, colony growth assay and immunoblotting, respectively. In addition, the autophagy levels were detected by electron microscopy, fluorescence microscopy and immunoblotting following PFK15 treatment, and the autophagic flux was analyzed with the addition of chloroquine diphosphate salt or by monitoring the level of p62. PFK15 was observed to evidently decrease the viability of RD cells, inhibit the colony growth and cause abnormal nuclear morphology. Furthermore, PFK15 inhibited the autophagic flux and cell proliferation, as well as induced apoptotic cell death in RD cells through downregulation of the adenosine monophosphate­activated protein kinase (AMPK) signaling pathway. An AMPK agonist rescued the inhibited cell proliferation and autophagy induced by PFK15. In conclusion, PFK15 inhibits autophagy and cell proliferation via downregulating the AMPK signaling pathway in RD cells.

Expression of osteoprotegerin, RNAK and RANKL genes in femoral head avascular necrosis and related signaling pathway.

Femoral head avascular necrosis (AVN) causes the damage of hip joint and related dysfunctions, thus consisting of a clinical challenge. Osteoprotegerin (OPG), receptor activator of nuclear factor κB (RANK) and its ligand (RANKL) all regulate the formation of bones via gene transcriptional regulation for the balance between osteoblasts and osteoclasts. This study thus investigated the expressional profiles of OPG, RANK and RANKL genes in AVN patients, and explored related molecular mediating pathways. Real-time qPCR was used to measure the gene expression of OPG, RANK and RANKL genes in AVN femoral head tissue samples from 42 patients, along with normal tissues. Western blotting analysis was performed to quantify protein levels of OPG and RANKL. There was a trend but not statistically significant elevation of mRNA levels of OPG in femoral head AVN tissues compared to normal tissues (P>0.05). The expression of RNAK and RNAKL, however, was significantly elevated in necrotic tissues (P<0.05). No significant difference in protein levels of OPG or RANKL between groups. The expression of OPG, RANK and RANKL genes exert a crucial role in the progression of AVN, suggesting their roles in mediating bone homeostasis and potential effects on bone destruction.