Evaluation of Vertebral Function and Long-Term Quality of Life after Percutaneous Minimally Invasive Surgery in Patients with Thoracolumbar Spine Fractures.

OBJECTIVE: To investigate the changes in vertebral function after minimally invasive surgery in patients with thoracolumbar spinal fractures and investigate the impact of percutaneous minimally invasive surgery on patients' quality of life by following up the patients in the long term. METHODS: A retrospective analysis was performed to select 80 patients with thoracolumbar spinal fractures treated in our hospital from April 2013 to October 2018, and the patients were divided into a study group and a control group according to the difference in their choice of procedure. The two groups were compared in terms of perioperative wound pain, serum creatine kinase (CK) activity, and C-reactive protein (CRP) levels, and the two groups were followed up for 2 years to compare the changes in anterior vertebral body height and Cobb's angle during the follow-up period and to compare the differences in quality of life between the two groups. RESULTS: (1) The pain level of patients in the study group was significantly lower than that of the control group at the 1st and 3rd postoperative days (p < 0.05). (2) The CK activity and CPR level of patients in the study group were significantly lower than that of the control group at the 1st and 3rd postoperative days (p < 0.05). (3) Compared with the preoperative period, the height of the anterior border of the vertebral body and the Cobb's angle in both groups showed significant changes at 7 d, 6 months, one year, and two years after surgery (p < 0.05), suggesting that both procedures can significantly restore the height of the injured vertebra and improve the function of the vertebral body. (4) The somatic, physical, and psychological functions of patients in the study group were significantly greater than those in the control group at 6 months postoperatively (p > 0.05). CONCLUSION: Compared to traditional open surgery, minimally invasive percutaneous surgery for thoracolumbar fractures can significantly reduce perioperative pain and improve perioperative stress in patients, while achieving better surgical outcomes and a significantly improved quality of life in patients at long-term follow-up.

A naturally derived small molecule NDSM253 inhibits IKK1 to suppress inflammation response and promote bone healing after fracture.

Bone fracture induces an acute inflammatory response in the resident and peripheral monocyte/macrophage cells. Excessive amounts of proinflammatory cytokines can cause severe tissue damage and inhibit bone healing. The proinflammatory cytokine genes are mainly controlled by TLR4/NF-κB (Toll-like receptor 4/Nuclear factor κB). Thus, targeting the molecules in this signaling pathway to decrease the expression of proinflammatory cytokines is an effective strategy to inhibit the inflammatory response. Herein, we identified a naturally derived small molecule NDSM253 that specifically inhibited IKKα (Inhibitor of NF-κB kinase subunit-alpha), a critical component of TLR4/NF-κB signaling. Biochemically, NDMS253 decreased phosphorylation of IκB (Inhibitor of NF-κB), thereby increasing the binding of IκB-NF-κB and suppressing the proinflammatory cytokine gene expression. NDMS253 showed a much stronger inhibitory effect on proinflammatory cytokine gene expression than did the known IKK inhibitors, including ACHP (2-Amino-6-[2-(cyclopropylmethoxy)-6-hydroxyphenyl]-4-(4-piperidinyl)-3-pyridinecarbonitrile), IKK16, and Amlexanox. Administration of these IKK inhibitors in a mouse femoral fracture model showed that NDSM253 suppressed proinflammatory cytokine genes, thereby promoting bone healing, while the other three IKK inhibitors showed a weaker improvement of both bone healing and circulating proinflammatory cytokines. Collectively, our data suggested that NDSM253 might be an effective inhibitor of IKKα that could inhibit inflammatory cytokine action in bone injury.

TLR4/NF-κB axis signaling pathway-dependent up-regulation of miR-625-5p contributes to human intervertebral disc degeneration by targeting COL1A1.

The activation of the toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB) signaling pathway has been found to play a critical role in many inflammatory diseases by controlling the expression of many cytokines. However, this pathway's role in the pathological process of intervertebral disc degeneration (IDD) has not been reported to date. In the present study, we found universal activation of the TLR4/NF-κB signaling pathway and elevated levels of pro-inflammatory cytokines in IDD patients. The in vitro analyses in human nucleus pulposus cells (hNPC) and annulus fibrosus cells (hAFC) also indicated that Lipopolysaccharide (LPS) treatment could activate TLR4/NF-κB signaling and induce pro-inflammatory cytokine levels. By comparing the results of two microRNA (miRNA)-based microarrays, we identified 15 miRNAs that were dysregulated in both IDD tissues and LPS-treated cells. Of these miRNAs, the most prominently up-regulated was miR-625-5p, which was predicted to bind to the three prime untranslated region (3'-UTR) of collagen type I alpha 1 (COL1A1). In vitro overexpression or down-regulation of miR-625-5p was able to repress or induce the expression of COL1A1, respectively. The in vitro analyses showed that treatment with LPS, recombinant IL-6 or TNF-α could induce miR-625-5p levels but decrease COL1A1 expression. In contrast, the treatments with their corresponding inhibitors, CLI095, siltuximab and D2E7, respectively, resulted in the exact opposite effects. Taken together, our results suggest that activation of the TLR4/NF-κB signaling pathway induces pro-inflammatory cytokines, which further up-regulates the expression of miR-625-5p, resulting in the down-regulation of COL1A1 and eventually contributing to the pathological process of IDD.

Value of high-frequency ultrasound in diagnosing carpal tunnel syndrome.

This study aimed to evaluate the diagnostic value of high-frequency ultrasound examination for carpal tunnel syndrome (CTS). A total of 63 wrists from 45 patients diagnosed with CTS were selected as the study group, and 43 asymptomatic wrists of 40 cases were included as the normal control group. Parameters such as the transverse diameter, vertical diameter, cross-sectional area (CSA), and flattening rate (FR) of the carpal tunnel radioulnar joint, postular bone, and median nerve in the hamate bone hook plane were measured, and the differences between the two groups were compared. The median nerve CSA in the postular bone plate was significantly greater in the study group than in the normal control group (0.17±0.05 vs. 0.09±0.02, P<0.01), and the FR at the hook of the hamate was significantly higher in the study group (3.52±0.86 vs. 3.21±0.26, P<0.01). Our results suggest that ultrasonography can effectively provide dynamic real-time images of the wrist in addition to being painless, non-invasive, and associated with relatively low costs. Based on our findings, we believe that ultrasonography is an effective examination method for CTS. When the threshold of the median nerve CSA in the postular bone plate was set as 10 mm(2), the diagnostic sensitivity and specificity were 92% and 86%, respectively. Therefore, the median nerve CSA may represent a good clinical indicator of CTS.

Subclass opioid receptors associated with the cardiovascular depression after traumatic shock and the antishock effects of its specific receptor antagonists.

The present available opioid receptor antagonists such as naloxone and naltrexone are not highly receptor selective. They may antagonize mu opioid receptors to affect the pain threshold of the patients with traumatic shock while they exert antishock effects. Therefore, they are not suitable for traumatic shock. It is very important to elucidate the subclass of opioid receptors that are closely associated with cardiovascular depression of traumatic shock and then choose their specific receptor antagonists to treat it. Traumatic shock was used in pentobarbital-anesthetized Wistar rats by right femur fracture plus hemorrhage (fixed hemorrhage at a rate of 20 mL/kg in experiment 1 or hemorrhage to 40 mmHg mean arterial blood pressure for 60 min in experiments 2 and 3), and the changes of myocardial and brain opioid receptors after traumatic shock, the antagonizing effects of mu, delta, and kappa opioid receptor antagonists on the cardiovascular depression of traumatic shock and the antishock effects of delta and kappa opioid receptor antagonists ICI174,864 and Nor-binaltorphimine (Nor-BNI) were observed. The results indicate that after traumatic shock, the number of myocardial and brain delta and kappa opioid receptors were significantly increased that were significantly associated with the decreased cardiovascular functions. mu Opioid receptors in the heart and brain did not change significantly. Intracerebral ventricular administration of ICI174,864 and Nor-BNI significantly antagonized the decreased cardiovascular function after traumatic shock and increased the survival rate of traumatic shock rats, but mu opioid receptor antagonist beta-funaltrexamine did not. Meanwhile, intravenous administration of delta and kappa opioid receptor antagonists ICI174,864 and Nor-BNI also significantly increased the mean arterial blood pressure, improved the hemodynamic parameters, and prolonged the survival rate of traumatic shock rats. These findings suggest that opioid receptors are involved in the cardiovascular depression of traumatic shock, and the subclass receptors are mainly delta and kappa opioid receptors. delta and kappa opioid receptor antagonists have good beneficial effects on traumatic shock.