Assessment of Neck Imbalance in Adolescent Idiopathic Scoliosis Patients: A Cross-Section Study Based on Body Image of 115 Patients with Main or Double Thoracic Curve.

OBJECTIVE: Neck imbalance negatively affects body aesthetics of adolescent idiopathic scoliosis (AIS) patients. The evaluation of neck imbalance is currently limited to radiographic parameters, but lacks visual indicators. Therefore, the purpose of this study was to establish indexes of neck imbalance based on body image and to investigate whether these indexes can truly reflect neck imbalance in AIS patients. METHODS: We performed a cross-sectional study at a single institution between June 2017 and September 2020 and there were 115 subjects involved in this research. All patients were diagnosed with adolescent idiopathic scoliosis, Lenke type I/II. Radiographic parameters measured included cervical axis tilt (CAT), T1 tilt, first rib angle (FRA), clavicle angle (CA), radiographic shoulder height (RSH), proximal thoracic curve (PTC), apical vertebra translation of proximal thoracic (AVT of PT), main thoracic curve (MTC), apical vertebra translation of main thoracic (AVT of MT) and coronal balance (CB/C7PL-CSVL). Neck imbalance indexes were obtained and measured following a standardized manner. Intra-class correlation coefficient (ICC) analysis was performed for neck imbalance indexes to determine their intra-observer and inter-observer reliability, and correlation tests were performed for neck imbalance indexes with the radiographic parameters mentioned above. RESULTS: Strong intraobserver and interobserver reliability were observed in neck imbalance index (NII) 1 (0.91 and 0.88), neck imbalance index 2 (0.85 and 0.81) and NII 3 (0.82 and 0.80), P < 0.05. Significant correlation was found in cervical axis tilt (R = 0.81 for NII 1, R = 0.77 for NII 2 and R = 0.78 for NII 3), T1 tilt (R = 0.43 for NII 1, R = 0.52 for NII 2 and R = 0.48 for NII 3), first rib angle (R = 0.41 for NII 1, R = 0.48 for NII 2 and R = 0.43 for NII 3), proximal thoracic curve (R = 0.36 for NII 2) and apical vertebra translation of proximal thoracic (R = -0.37 for NII 2 and R = -0.35 for NII 3) with neck imbalance indexes. Neck imbalance index 1 showed the highest correlation with cervical axis tilt (R = 0.81, P < 0.01). CONCLUSIONS: Neck imbalance indexes established in our study were in good correlation with cervical axis tilt (CAT), At the meantime, they showed significant correlations with T1 tilt and first rib angle (FRA). Our study provides a practical method for measurement of neck imbalance regarding realistic perspective and makes up for the lack of photographic indexes about neck imbalance.

Corynoline Alleviates Osteoarthritis Development via the Nrf2/NF-κB Pathway.

Purpose: OA is a multifactorial joint disease in which inflammation plays a substantial role in the destruction of joints. Corynoline (COR), a component of Corydalis bungeana Turcz., has anti-inflammatory effects. Materials and Methods: We evaluated the significance and potential mechanisms of COR in OA development. The viabilities of chondrocytic cells upon COR exposure were assessed by CCK-8 assays. Western blot, qPCR, and ELISA were used to assess extracellular matrix (ECM) degeneration and inflammation. The NF-κB pathway was evaluated by western blot and immunofluorescence (IF). Prediction of the interacting proteins of COR was done by molecular docking, while Nrf2 knockdown by siRNAs was performed to ascertain its significance. Micro-CT, H&E, Safranin O-Fast Green (S-O), toluidine blue staining, and immunohistochemical examination were conducted to assess the therapeutic effects of COR on OA in destabilization of medial meniscus (DMM) models. Results: COR inhibited ECM degeneration and proinflammatory factor levels and modulated the NF-κB pathway in IL-1ß-treated chondrocytes. Mechanistically, COR bound Nrf2 to downregulate the NF-κB pathway. Moreover, COR ameliorated the OA process in DMM models. Conclusion: We suggest that COR ameliorates OA progress through the Nrf2/NF-κB axis, indicating COR may have a therapeutic potential for OA.

RNA-binding protein HuR suppresses senescence through Atg7 mediated autophagy activation in diabetic intervertebral disc degeneration.

OBJECTIVES: Diabetes is a risk factor for intervertebral disc degeneration (IVDD). Studies have demonstrated that diabetes may affect IVDD through transcriptional regulation; however, whether post-transcriptional regulation is involved in diabetic IVDD (DB-IVDD) is still unknown. This study was performed to illustrate the role of HuR, an RNA-binding protein, in DB-IVDD development and its mechanism. MATERIALS AND METHODS: The expression of HuR was evaluated in nucleus pulposus (NP) tissues from diabetic IVDD patients and in high glucose-treated NP cells. Senescence and autophagy were assessed in HuR over-expressing and downregulation NP cells. The mRNAs that were regulated by HuR were screened, and immunoprecipitation was applied to confirm the regulation of HuR on targeted mRNAs. RESULTS: The results showed that the expression of HuR was decreased in diabetic NP tissues and high glucose-treated NP cells. Downregulation of HuR may lead to increased senescence in high glucose-treated NP cells, while autophagy activation attenuates senescence in HuR deficient NP cells. Mechanistic study showed that HuR prompted Atg7 mRNA stability via binding to the AU-rich elements. Furthermore, overexpression of Atg7, but not HuR, may ameliorate DB-IVDD in rats in vivo. CONCLUSIONS: In conclusion, HuR may suppress senescence through autophagy activation via stabilizing Atg7 in diabetic NP cells; while Atg7, but not HuR, may serve as a potential therapeutic target for DB-IVDD.

Urolithin A-induced mitophagy suppresses apoptosis and attenuates intervertebral disc degeneration via the AMPK signaling pathway.

Intervertebral disc degeneration (IDD) is a major cause of low back pain (LBP), and effective therapies are still lacking. Previous studies reported that mitochondrial dysfunction contributes to apoptosis, and urolithin A (UA) specifically induces mitophagy. Herein, we aimed to investigate the protective effect of UA-induced mitophagy on tert-butyl hydroperoxide (TBHP)-induced apoptosis in nucleus pulposus (NP) cells in vitro and a rat model of IDD in vivo. Mitochondrial function, apoptosis, and mitophagy were measured in UA-treated NP cells by western blotting and immunofluorescence; the therapeutic effects of UA on IDD were assessed in rats with puncture-induced IDD. The results showed that UA could activate mitophagy in primary NP cells, and UA treatment inhibited TBHP-induced mitochondrial dysfunction and the intrinsic apoptosis pathway. Mechanistically, we revealed that UA promoted mitophagy by activating AMPK signaling in TBHP-induced NP cells. In vivo, UA was shown to effectively alleviate the progression of puncture-induced IDD in rats. Taken together, our results suggest that UA could be a novel and effective therapeutic strategy for IDD.

Survival and prognosis in malignant giant cell tumor of bone: A population-based analysis from 1984 to 2013.

BACKGROUND: Malignant giant cell tumor of bone (MGCTB) is extremely rare. Currently, population-based prognosis studies are lacking. This study aimed to determine the impact of demographics, tumor characteristics, and treatment on prognosis among patients with MGCTB. METHODS: The Surveillance, Epidemiology, and End Results database was used to identify patients with MGCTB from 1984 to 2013. Kaplan-Meier analyses were performed to determine the overall survival (OS). Univariable and multivariable Cox analyses were conducted to identify prognostic factors. RESULTS: There were 250 patients with MGCTB included in our study. The multivariate Cox analysis revealed that age at diagnosis (hazard ratio [HR]: 1.09; 95% confidence interval [CI]: 1.07-1.11; P < 0.001), tumor size (HR: 7.04; 95% CI: 2.38-20.77; P < 0.001), tumor extension (regional vs. localized, HR: 2.64; 95% CI: 1.10-6.34; P = 0.030; distant vs. localized, HR: 6.12; 95% CI: 2.27-16.49; P < 0.001), and radiotherapy (HR: 0.41; 95% CI: 0.18-0.89; P = 0.025) were independent risk factors of OS in patients with MGCTB. Notably, tumor site (HR: 1.98; 95% CI: 0.99-4.00; P = 0.055) exhibited borderline significance. Additionally, we found that patients with tumors measuring >70 mm (P = 0.015), located in the axial skeleton (P < 0.001) and presented with distant metastasis (P < 0.001) tended to receive radiotherapy. Moreover, a nomogram model integrating independent predictors was established to estimate the OS of patients with MGCTB. CONCLUSION: This study provides a population-based assessment of the largest number of patients with MGCTB. We found that older age, larger tumor size, regional or distant metastasis, and lack of radiotherapy was associated with poor OS. Surgical methods were not significantly associated with OS. Furthermore, we built a high-quality nomogram to predict 1-, 3-, and 5-year OS for patients with MGCTB. These findings may assist in the clinical diagnosis and treatment of MGCTB.