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BACKGROUND: Scoliosis causes changes in the thorax, but it is unclear what type of changes occur in the thoracic profile after scoliosis surgery. OBJECTIVE: To investigate changes in rib cage deviation in the postoperative period after adolescent idiopathic scoliosis (AIS) surgery. METHODS: Forty-four patients with AIS with a main right thoracic curvature underwent posterior surgical fusion (PSF), and radiological parameters of the spine and thorax were evaluated. RESULTS: The correction rates of main thoracic curve (MT)-Cobb angle at immediate after surgery and postoperative follow-up (2 years) were 64% and 66%, respectively. At these two postoperative time points, the correction rates of height of thoracic vertebrae 1 to 12 (T1T12) were 10% and 12%; the correction rates of Rib-vertebra angle difference (RVAD) were 59% and 52%; the correction rates of Apical rib hump prominence (RH) were 58% and 76%; while the correction rates of Apical vertebral body-rib ratio (AVB-R) were 23% and 25%, respectively. Statistical analysis showed that all these radiological parameters at the two postoperative time points were significantly different from the preoperative values (p< 0.001). There were significant correlations between MT-Cobb angle and T1-T12 height (p< 0.001), RVAD (p< 0.001), RH (p< 0.001), and AVB-R (p< 0.001). CONCLUSIONS: Posterior spinal fusion appears to be effective at correcting scoliosis, and the correction of rib cage deviation also plays an important role.

Purpose: To investigate the effect of methylbenzoxime on dexamethasone-induced rat model of osteoporosis. Methods: Osteoporosis rat model was prepared by administration of dexamethasone to rats for sixty days. The rats were then divided into five groups of five animals each: normal control, untreated, and 2, 5 and 10 mg/kg treatment groups. All rats were administered dexamethasone for 60 days. Thereafter, rats in the three treatment groups received daily doses of 2, 5 or 10 mg/kg methylbenzoxime for 15 days, while rats in normal control and untreated groups were given equivalent volumes of normal saline in place of methylbenzoxime. After treatment, the rats were sacrificed, and the femur removed for histological assessment of pathological changes using H&E staining. Expressions of Wntn signalling pathway proteins in osteoblasts were assayed using reverse transcriptase-polymerase chain reaction (RT-PCR) and western blot assays. Results: Methylbenzoxime inhibited osteoblast proliferation, as revealed from 3-(4,5-dimethylthiazol-2- yl)-2,5-diphenyltetrazolium bromide (MTT) assay. It increased the expression of osteoprotegerin and downregulated receptor activator for nuclear factor-kappa B ligand. Dexamethasone decreased the expression of Wnt signalling pathway proteins in osteoblasts. However, treatment of the dexamethasone-exposed osteoblasts with methylbenzoxime reversed the inhibition of expressions of Wnt signalling pathway proteins. In vivo studies showed that methylbenzoxime treatment mitigated dexamethasone-induced pathological features in femur. In osteoporotic rats, methylbenzoxime significantly up-regulated the expression of osteocalcin but down-regulated the level of collagen-type I fragments, relative to the untreated group. The effect was significant in the 5 and 10 mg/kg treatment groups, when compared with 2 mg/kg group. Conclusion: Methylbenzoxime prevents dexamethasone-induced osteoporosis in vitro and in rats. Therefore, it is a potential therapeutic agent for the management of osteoporosis.

Background: Osteosarcoma (OS) is one of the most common primary malignant bone tumors in teenagers. Emerging studies demonstrated TWEAK and Fn14 were involved in regulating cancer cell differentiation, proliferation, apoptosis, migration and invasion. Objective: The present study identified differently expressed mRNAs and lncRNAs after anti-TWEAK treatment in OS cells using GSE41828. Methods: We identified 922 up-regulated mRNAs, 863 downregulated mRNAs, 29 up-regulated lncRNAs, and 58 down-regulated lncRNAs after anti-TWEAK treatment in OS cells. By constructing PPI networks, we identified several key proteins involved in anti-TWEAK treatment in OS cells, including MYC, IL6, CD44, ITGAM, STAT1, CCL5, FN1, PTEN, SPP1, TOP2A, and NCAM1. By constructing lncRNAs coexpression networks, we identified several key lncRNAs, including LINC00623, LINC00944, PSMB8-AS1, LOC101929787. Result: Bioinformatics analysis revealed DEGs after anti-TWEAK treatment in OS were involved in regulating type I interferon signaling pathway, immune response related pathways, telomere organization, chromatin silencing at rDNA, and DNA replication. Bioinformatics analysis revealed differently expressed lncRNAs after antiTWEAK treatment in OS were related to telomere organization, protein heterotetramerization, DNA replication, response to hypoxia, TNF signaling pathway, PI3K-Akt signaling pathway, Focal adhesion, Apoptosis, NF-kappa B signaling pathway, MAPK signaling pathway, FoxO signaling pathway. Conclusion: : This study provided useful information for understanding the mechanisms of TWEAK underlying OS progression and identifying novel therapeutic markers for OS.

Activation of reactive oxygen species (ROS) and oxidative stress play an important role in the pathogenesis of spinal cord injury (SCI). Melatonin (MT) has good antioxidant and anti-apoptotic effects. In this study, the oxidative stress model of adrenal pheochromocytoma cells (PC12) was established by hydrogen peroxide (H2O2) in order to evaluate the protective effect of MT on SCI model in vitro and its possible mechanism. PC12 cells were treated with H2O2 to establish cellular oxidative stress model. Cells were treated with different concentrations of MT (control group, 10uM MT + H2O2, 25uM MT + H2O2, 50uM MT + H2O2). Cell viability was detected by CCK-8. Intracellular ROS were detected by dichlorodihydrofluorescein diacetate, and apoptosis rate was detected by flow cytometry. Western blot and immunofluorescence were used to detect Nrf2, HO-1, SOD2, Prxd3, IL-1β, IL-18, iNOS protein expression. The results showed that MT could reduce H2O2-induced oxidative stress injury and cell apoptosis. MT inhibited the expression of IL-1β, IL-18, iNOS and promoted the expression of SOD2 and Prxd3. In addition, MT promoted Nrf2, HO-1 expression. In conclusion, MT pretreatment can protect H2O2-induced oxidative damage of PC12 cells through Nrf2/HO-1 signaling pathway.

Spinal cord injury can lead to severe motor, sensory and autonomic nervous dysfunctions. However, there is currently no effective treatment for spinal cord injury. Neural stem cells and progenitor cells, bone marrow mesenchymal stem cells, olfactory ensheathing cells, umbilical cord blood stem cells, adipose stem cells, hematopoietic stem cells, oligodendrocyte precursor cells, macrophages and Schwann cells have been studied as potential treatments for spinal cord injury. These treatments were mainly performed in animals. However, subtle changes in sensory function, nerve root movement and pain cannot be fully investigated with animal studies. Although these cell types have shown excellent safety and effectiveness in various animal models, sufficient evidence of efficacy for clinical translation is still lacking. Cell transplantation should be combined with tissue engineering scaffolds, local drug delivery systems, postoperative adjuvant therapy and physical rehabilitation training as part of a comprehensive treatment plan to provide the possibility for patients with SCI to return to normal life. This review summarizes and analyzes the clinical trials of cell transplantation therapy in spinal cord injury, with the aim of providing a rational foundation for the development of clinical treatments for spinal cord injury.

Neural stem/progenitor cells (NSPCs) can enhance regeneration after spinal cord injury (SCI), but survival of transplanted cells remains poor. Understanding how NSPCs respond to the chemical mediators of secondary injury thus is essential for treating SCI. Thymosin β4 (Tβ4) has physiological functions that are highly relevant to SCI. We exposed NSPCs to oxidative stress and found reduced expression of Tβ4 in H2O2-injured NSPCs. Using an MTT assay, we found that Tβ4 dose dependently increased viability of the injured NSPCs. Tβ4 also reversed the decreases of intracellular Ca2+ concentration and increases of lactate dehydrogenase in NSPCs induced by H2O2 treatment. H2O2 exposure increased NSPC apoptosis, which Tβ4 decreased. In H2O2-induced NSPCs, ROS production and pro-inflammatory cytokines increased, and again, Tβ4 reversed these effects. We investigated the toll-like receptor 4 (TLR4) and myeloid differentiation primary response 88 (MyD88) signaling pathway as an underlying mechanism in Tβ4's protective effect on H2O2-exposed NSPCs. Our results showed that Tβ4 reduced expression of TLR4 and MyD88. Moreover, H2O2-exposed NSPCs that were treated with the TLR4/MyD88 pathway inhibitor showed a reversal of all the effects caused by H2O2, similar to Tβ4's effects. In conclusion, our study determined that Tβ4 attenuated H2O2-induced oxidative stress injury in NSPCs via the TLR4/MyD88 pathway.

To investigate the effect of Parkinson's disease related protein DJ-1 on the cell proliferation, apoptosis, invasion and migration in human osteosarcoma cells and the underlying molecular mechanisms. Methods: The protein expression levels of DJ-1 were detected in human osteosarcoma cell lines (MG-63, Saos-2, and U2OS) and human osteoblast cell line hFOB1.19 with or without deficiency in phosphatase and tensin homolog deleted from chromosome 10 (PTEN) were detected by Western blot. Osteosarcoma cells were treated with DJ-1 siRNA, and then the protein expression levels of DJ-1 were detected by Western blot. Cell survival rate of osteosarcoma cells was detected by cell counting kit-8 (CCK-8) assay. Cell apoptosis of osteosarcoma cells was measured by annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) double staining method. Cell invasive and migration ability of osteosarcoma cells were examined by transwell invasion and migration assay. Results: Compared with that of human osteoblast cell line (hFOB1.19), the protein expression level of DJ-1 was significantly upregulated in human osteosarcoma cell lines (MG-63, Saos-2, and U2OS) (all P0.05), and U2OS had the highest level of DJ-1 when compared with the other three cell lines (P0.01). DJ-1 siRNA could significantly down-regulate the DJ-1 protein expression in U2OS cells, and also diminish the cell survival rate. Moreover, DJ-1 down-regulation of DJ-1 could promote cell apoptosis, suppress the ability of cell invasion and migration, and increase the PTEN protein expression level (all P0.05). In addition, the protein expression level of PTEN was markedly up-regulated in human osteosarcoma cell lines when compared with that in the hFOB1.19 cells (P0.05). Conclusion: DJ-1 can promote the cell proliferation, inhibit cell apoptosis, and decrease the ability of cell invasion and migration, and the potential underlying mechanisms may be associated with the up-regulation of PTEN protein expression.目的：研究帕金森病相关蛋白DJ-1对人骨肉瘤细胞增殖、凋亡、侵袭和迁移的影响及其作用机制。方法：Western 印迹检测骨肉瘤细胞株(MG-63，Saos-2和U2OS)及正常人成骨细胞株hFOB1.19中DJ-1和第10号染色体上缺失的磷酸酶与张力蛋白同源物(phosphatase and tensin homolog deleted from chromosome 10，PTEN)基因的表达。DJ-1 siRNA处理人骨肉瘤细胞后，采用Western印迹检测DJ-1的蛋白表达水平；细胞计数试剂盒(cell counting kit-8，CCK-8)法检测细胞存活率；膜联蛋白V(annexin V)-异硫氰酸荧光素(fluorescein isothiocyanate，FITC)/碘化吡啶(propidium iodide，PI)双染检测细胞凋亡；Transwell侵袭和迁移实验检测细胞侵袭和迁移水平。结果：与hFOB1.19细胞比较，骨肉瘤细胞DJ-1蛋白表达水平显著升高(均P0.05)，其中U2OS细胞升高最为显著(P0.01)。DJ-1 siRNA可显著降低U2OS细胞中DJ-1蛋白表达水平、降低细胞存活率、促进细胞凋亡、抑制细胞侵袭和迁移水平，以及增加PTEN蛋白表达水平(均P0.05)。另外，与hFOB1.19细胞比较，PTEN在骨肉瘤细胞中的蛋白表达水平显著降低(P0.05)。结论：DJ-1可抑制人骨肉瘤细胞增殖，促进细胞凋亡，抑制细胞侵袭和迁移水平，其机制可能与增加PTEN蛋白的表达水平有关。.