The long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) has been demonstrated to participate in the deterioration of many types of cancer. However, the underlying mechanisms of SNHG1-mediating functions in osteosarcoma (OS) have yet to be elucidated. In the present study, our results showed that SNHG1 was upregulated in OS tissues and cell lines, and high SNHG1 expression predicts poor overall survival of OS patients. Knockdown of SNHG1 inhibited cell growth and metastasis of OS in vitro and in vivo. Furthermore, our data demonstrated that there was reciprocal repression between SNHG1 and miR-326 which act as a tumor suppressor in OS cells, and exhibiting a strong negative relationship between SNHG1 and miR-326 expression in OS tissues. Additionally, we identified that SNHG1 increased human nin one binding protein (NOB1), an oncogene, through sponging miR-326 as competing endogenous RNA (ceRNA), finally prompting cell growth, migration and invasion in OS. Collectively, these findings not only uncovered that the SNHG1/miR-326/NOB1 signaling axis has a key role in OS progression but also suggested the potential application of SNHG1 and miR-326 as biomarkers in the OS diagnosis and treatment.

Background: Delay or failure of bone union is a significant clinical challenge all over the world, and it has been reported that bone marrow mesenchymal stem cells (BMSCs) offer a promising approach to accelerate bone fracture healing. Se can modulate the proliferation and differentiation of BMSCs. Se-treatment enhances the osteoblastic differentiation of BMSCs and inhibiting the differentiation and formation of mature osteoclasts. The purpose of this study was to assess the effects of porous Se@SiO₂ nanocomposite on bone regeneration and the underlying biological mechanisms. Methods: We oxidized Se^2-, to develop Se quantum dots, then we used the Se quantum dots to form a solid Se@SiO₂ nanocomposite which was then coated with polyvinylpyrrolidone (PVP) and etched in hot water to synthesize porous Se@SiO₂ nanocomposite. We used XRD pattern to assess the phase structure of the solid Se@SiO₂ nanocomposite. The morphology of porous Se@SiO₂ nanocomposite were evaluated by scanning electron microscope (SEM) and the biocompatibility of porous Se@SiO₂ nanocomposite were investigated by cell counting kit-8 (CCK-8) assays. Then, a release assay was also performed. We used a Transwell assay to determine cell mobility in response to the porous Se@SiO₂ nanocomposite. For in vitro experiments, BMSCs were divided into four groups to detect reactive oxygen species (ROS) generation, cell apoptosis, alkaline phosphatase activity, calcium deposition, gene activation and protein expression. For in vivo experiments, femur fracture model of rats was constructed to assess the osteogenic effects of porous Se@SiO₂ nanocomposite. Results: In vitro, intervention with porous Se@SiO₂ nanocomposite can promote migration and osteogenic differentiation of BMSCs, and protect BMSCs against H₂O₂-induced inhibition of osteogenic differentiation. In vivo, we demonstrated that the porous Se@SiO₂ nanocomposite accelerated bone fracture healing using a rat femur fracture model. Conclusion: Porous Se@SiO₂ nanocomposite promotes migration and osteogenesis differentiation of rat BMSCs and accelerates bone fracture healing, and porous Se@SiO₂ nanocomposite may provide clinic benefit for bone tissue engineering.

Objective: The purpose of this study was to retrospectively evaluate the use of locked plating (LP) and retrograde nailing (RN) for treating extra-articular distal femoral fractures. Materials and Methods: From January 2004 to March 2009, 36 patients with extra-articular distal femoral fractures were surgically treated at our Trauma Center. The patients were divided into two groups according to the treatment method, with 19 patients being treated by LP (LP group) and 17 patients via RN (RN group). Results: The demographics of age (p = 0.460) and gender (p = 0.481) in both LP and RN groups were similar. No differences were found with respect to postoperative malreduction, deep infection, hardware failure, operating time, knee pain, HSS score and range of knee movement. The mean intraoperative blood loss was significantly higher in the RN group (298 ± 65.2 ml, range 200–410) than in the LP group (200 ± 48.9 ml, range 130–300) (p < 0.01). However, a higher rate of union disturbance was observed in the LP group (36.8%) compared to the RN group (5.9%) (p = 0.044). Conclusions: The overall union disturbance rate in the LP group was higher than in the RN group. However, further analysis revealed that clinical outcome may largely depend on surgical technique rather than on the choice of implant. Therefore, correct rules (the same for every procedure) should be strictly adhered to, especially in the application of LP.

Bone metabolism depends on the balance between osteoclast-driven bone resorption and osteoblast-mediated bone formation. Diseases like osteoporosis are characterized by increased bone destruction due to partially enhanced osteoclastogenesis. Here, we report that the post-translational SUMO modification is critical for regulating osteoclastogenesis. The expression of the SUMO-specific protease SENP3 is downregulated in osteoclast precursors during osteoclast differentiation. Mice with SENP3 deficiency in bone marrow-derived monocytes (BMDMs) exhibit more severe bone loss due to over-activation of osteoclasts after ovariectomy. Deleting SENP3 in BMDMs promotes osteoclast differentiation. Mechanistically, loss of SENP3 increases interferon regulatory factor 8 (IRF8) SUMO3 modification at the K310 amino acid site, which upregulates expression of the nuclear factor of activated T cell c1 (NFATc1) and osteoclastogenesis. In summary, IRF8 de-SUMO modification mediated by SENP3 suppresses osteoclast differentiation and suggests strategies to treat bone loss diseases.

Accumulating evidence supports an association between an unhealthy mental state and low back pain (LBP). However, the degree of the association between mental health and chronic low back pain (CLBP) in the general population is poorly understood. The objective of this study was to analyze the incidence of CLBP in Chinese college students and to examine the association between students’ unhealthy mental states and the prevalence of CLBP. This is a cross-sectional study. A total of 10,000 questionnaires were distributed in the second semester of the 2017–2018 academic year by the School of Medicine, Shanghai JiaoTong University. Eligible participants were students aged ≥ 18 years from randomly selected Chinese colleges. Participants completed a questionnaire survey that included items from the Symptom Checklist-90 (SCL-90) and items on demographic factors, LBP prevalence, quality of life at their university, study-related stress and interpersonal relationships. The evaluation of students’ mental states in the survey was divided into two major parts: direct and indirect indicators. A multivariate logistic regression model was mainly used to explore the relationship between CLBP and the students’ mental health. There was a high incidence of CLBP in the college students. Multiple logistic regression analysis indicated that the risk of CLBP increased with increasing scores on the SCL-90, and a clinically unhealthy mental state (scores greater than 3) was significantly associated with CLBP (adjusted odds ratios for depression, anxiety, coercion, paranoia, and interpersonal sensitivity were 7.209, 6.593, 3.959, 4.465, and 4.283, respectively; p < 0.001). Participants who had poor living habits or uncomfortable campus lives and those who experienced heavy academic pressure also showed a higher positive association with CLBP compared with the full sample. Unhealthy psychological conditions, which may be attributed to unsatisfying school lives, excessive learning pressure, and uncomfortable interpersonal relationships, represent a risk factor for CLBP in college students.