Autophagy Blockage Enhances Radiosensitivity of Osteosarcoma MG-63 Cells In Vitro.

BACKGROUND: Osteosarcoma is the most prevalent malignant neoplasm in children and young adults with a very high propensity for local invasion and early systemic metastases. Radiotherapy has been widely used in metastatic and recurrent osteosarcoma, particularly with chemoresistance. METHODS: To determine whether autophagy is induced by radiation therapy and contributes to cell death of osteosarcoma, we investigated the influence of autophagy blockage on the radiosensitivity of osteosarcoma MG-63 cells in vitro. Firstly, autophagy in the MG-63 osteosarcoma cells after radiation treatment was determined by quantitative GFP-LC3 analysis and autophagy-related molecules analysis by western blotting. Then the viability and death of cells post-blockage of autophagy was determined by MTT assay and flow cytometry. RESULTS: It was demonstrated that autophagy was involved in MG-63 cells subject to radiation. Significantly up-regulated autophagic vesicles in MG-63 cells were subject to radiation. The transformation of LC-3 I to LC-3 II and the expression of autophagy-associated molecules were promoted in the radiation-treated MG-63 cells. Moreover, autophagy could ameliorate the cell viability post radiation. On the other hand, the chemical blockage of autophagy by 3MA not only could downregulate the level of autophagy, but also could reduce cell viability and accelerate apoptosis in the radiation-treated MG-63 cells. CONCLUSIONS: Autophagy was involved in the radiation treatment of MG-63 osteosarcoma cells, and autophagy blockage enhances the radiosensitivity of the osteosarcoma cell line MG-63 in vitro.

A clinical study of the rotational alignment of the femoral component in total knee arthroplasty.

[Purpose] The reasons for femorotibial rotational malalignment after total knee arthroplasty (TKA) were analyzed to provide evidence for clinical knee joint surgery and to reduce complications. [Subjects and Methods] Ninety knees of 60 patients were selected and randomly divided into two groups (n=30). For one group, rotational alignment of the femoral component was determined by the transepicondylar axis and TKA was performed. For the other group, rotational alignment of the femoral component was conducted through 3° external rotation of the posterior femoral condyles. Knee joint specimens were operated with TKA and various biomechanical indices were measured. [Results] The femoral epicondylar axis was a constant, reliable reference for femoral component rotational alignment. When the femoral component was rotated by 0° versus the epicondylar axis, the peak contact pressure on the patellofemoral joint was optimal. When the femoral component was arranged in parallel with Whiteside's line, the peak contact pressure on the patellofemoral joint varied largely. The patellofemoral contact areas of the two groups were similar. [Conclusion] Axial rotational alignment of the femoral component influenced the contact pressure of patellofemoral joints in TKA more significantly than external rotation of the femoral condyles. It is more reliable to use the femoral epicondylar axis as the reference for the rotational alignment of the femoral component.

Ultrasound-guided fascia iliaca compartment block for pain control in total hip arthroplasty: A systematic review and meta-analysis.

BACKGROUND: Previous studies have investigated the effectiveness and safety of ultrasound-guided fascia iliaca compartment block (UGFICB) compared to quadratus lumborum block (QLB) for pain management in total hip arthroplasty (THA). However, there is currently a lack of a systematic review specifically addressing this issue. Therefore, the purpose of this study was to conduct a comprehensive analysis and comparison of the efficacy and safety of UGFICB versus QLB for pain management in THA. METHODS: An extensive search was conducted in various electronic databases, including PUBMED, EMBASE, Cochrane Library, Web of Science, Scopus, China Biomedical Literature Service System, and China National Knowledge Infrastructure. This search encompassed all relevant studies published from the inception of these databases until June 30, 2023. The selected outcomes for analysis included moving and resting visual analogue scale (VAS) scores at 12 hours and 24 hours post-surgery, as well as opioids consumption at 24 hours post-surgery. The Cochrane risk-of-bias tool was utilized to assess the risk of bias in the trials included in the analysis. Statistical analysis was conducted using RevMan 5.4 software. RESULTS: A total of 8 trials, involving 656 patients, were included in this study. The results of the meta-analysis showed no significant differences between the 2 modalities in terms of moving VAS scores (mean difference [MD] = 0.17, 95% confidence interval [CI] [-0.79, 1.14], P = .72) and resting VAS scores (MD = 0.04, 95% CI [-0.27, 0.36], P = .78) at 12 hours post-surgery, and moving VAS scores (MD = 0.27, 95% CI [-0.46, 1.01], P = .47) and resting VAS scores (MD = -0.05, 95% CI [-0.45, 0.35], P = .80) at 24 hours post-surgery. However, there was significant differences in opioids consumption at 24 hours post-surgery (MD = 8.98, 95% CI [2.04, 15.93], P = .01) between the 2 groups. CONCLUSION: Based on these findings, the study concludes that UGFICB may be more beneficial than QLB for pain management in THA. However, it is important to interpret these results with caution due to certain limitations.

lncRNA SNHG16 promotes the occurrence of osteoarthritis by sponging miR­373­3p.

Osteoarthritis (OA) is a common age­related joint disorder, for which no effective disease­modifying drugs are currently available. Long non­coding RNAs (lncRNAs) are involved in the occurrence of OA. lncRNA small nucleolar RNA host gene 16 (SNHG16) has been reported to regulate inflammation; however, the exact biological function of SNHG16 in OA and its underlying mechanism of action remain unclear. In this study, gene and protein expression levels were detected using reverse transcription­quantitative PCR and western blotting, respectively. Cell apoptosis was analyzed using flow cytometry and ELISA was performed to detect TNF­α levels. The interactions between lncRNA SNHG16 and microRNA (miR)­373­3p were examined using the dual­luciferase reporter assay. lncRNA SNHG16 was upregulated in OA tissue compared with normal joint tissue. The expression levels of collagen II were significantly reduced in OA tissue compared with normal tissue. Similarly, aggrecan expression levels were significantly reduced in IL­1ß­treated CHON­001 cells compared with the controls. In addition, the protein expression levels of MMP13 were significantly increased in OA tissues and IL­1ß­treated CHON­001 cells compared with the controls. SNHG16 knockdown significantly increased the expression levels of aggrecan, and decreased the expression levels of MMP13, cleaved caspase­3 and p21 in IL­1ß­treated CHON­001 cells. In addition, IL­1ß induced CHON­001 cell apoptosis, while SNHG16 knockdown decreased IL­1ß­induced apoptosis. Furthermore, the luciferase activity assay suggested that SNHG16 negatively regulated miR­373­3p in OA. Finally, the results suggested that the proinflammatory effect of IL­1ß on CHON­001 cells was significantly reduced by SNHG16 knockdown. In conclusion, lncRNA SNHG16 knockdown significantly limited the progression of OA by sponging miR­373­3p in vitro, which suggested that SNHG16 may serve as a potential therapeutic target for OA.

LncRNA MIR4435-2HG inhibits the progression of osteoarthritis through miR-510-3p sponging.

Osteoarthritis (OA) is a disorder of diarthrodial joints that can have multiple causes. Long non-coding RNAs (lncRNAs) participate in multiple diseases, including OA. It has recently been reported that the lncRNA microRNA 4435-2HG (MIR4435-2HG) is downregulated in OA tissues; however, the biological role of MIR4435-2HG during OA progression remains unclear. In the present study, interleukin (IL)-1ß was used to establish an in vitro model of OA. Protein expressions of matrix metallopeptidase (MMP) 1, MMP13, collagen II, interleukin (IL)-17A, p65, phosphorylated (p)-p65, IκB and p-IκB in CHON-001 cells were detected by western blotting. Gene expressions of IL-17A, MIR4435-2HG and miR-510-3p in tissues or CHON-001 cells were measured by reverse transcription-quantitative PCR and western blotting, respectively. Cell Counting Kit-8 assay and immunofluorescence staining were used to investigate cell proliferation, and cell apoptosis was detected by flow cytometry. The association between MIR4435-2HG, miR-510-3p and IL-17A was investigated using the dual luciferase report assay. MIR4435-2HG and miR-510-3p overexpression were transfected into CHON-001 cells. The results demonstrated that miR4435-2HG overexpression significantly increased proliferation and inhibited apoptosis of CHON-001 cells. In addition, miR-510-3p was identified as the downstream target of MIR4435-2HG, and miR-510-3p directly targeted IL-17A. The results from the present study suggested that MIR4435-2HG could mediate the progression of OA by inactivating the NF-κB signaling pathway. In addition, miR4435-2HG overexpression inhibited OA progression, suggesting that miR4435-2HG may be considered as a potential therapeutic target in OA.