Analysis of risk factors for C5 nerve root paralysis after posterior cervical decompression.

BACKGROUND: C5 nerve root paralysis is a nonnegligible complication after posterior cervical spine surgery (PCSS). The cause of its occurrence remains controversial. The purpose of this study was to analyse the incidence of and risk factors for C5 nerve root paralysis after posterior cervical decompression. METHODS: We retrospectively analysed the clinical data of 640 patients who underwent PCSS in the Department of Orthopaedics, Affiliated Hospital of Qingdao University from September 2013 to September 2019. According to the status of C5 nerve root paralysis after surgery, all patients were divided into paralysis and normal groups. Univariate and multivariate analyses were used to determine the independent risk factors for C5 nerve root paralysis. A receiver operating characteristic (ROC) curve was used to demonstrate the discrimination of all independent risk factors. RESULTS: Multivariate logistic regression analysis revealed that male sex, preoperative cervical spine curvature, posterior longitudinal ligament ossification, and preoperative C4/5 spinal cord hyperintensity were independent risk factors for paralysis, whereas the width of the intervertebral foramina was an independent protective factor for paralysis. The area under the curve (AUC) values of the T2 signal change at C4-C5, sex, cervical foramina width, curvature and posterior longitudinal ligament ossification were 0.706, 0.633, 0.617, 0.637, and 0.569, respectively. CONCLUSIONS: Male patients with C4-C5 intervertebral foramina stenosis, preoperative C4-C5 spinal cord T2 high signal, combined with OPLL, and higher preoperative cervical spine curvature are more likely to develop C5 nerve root paralysis after surgery. Among the above five risk factors, T2 hyperintensity change in C4-C5 exhibits the highest correlation with C5 paralysis and strong diagnostic power. It seems necessary to inform patients who have had cervical spine T2 hyperintensity before surgery of C5 nerve root paralysis after surgery, especially those with altered spinal cord T2 signals in the C4-C5 segment.

The clinical significance and function of miR-146 in the promotion of epidural fibrosis.

Epidural fibrosis is the main cause of failed back surgery syndrome. To investigate the role of miR-146 in the diagnosis and development of epidural fibrosis. Lumbar disc tissues were collected from 72 lumbar disc herniation patients (45 developed epidural fibrosis and 27 did not). The expression of miR-146 in collected tissues and isolated epidural fibroblasts was detected by RT-qPCR. The relative levels of pro-inflammatory cytokines were analyzed by ELISA. The effect of miR-146 on the proliferation of fibroblasts was evaluated by MTT assay. miR-146 was significantly upregulated in epidural fibrosis patients compared with control patients. The expression of miR-146 was closely associated with the location, lower limb symptom and duration of disease of epidural fibrosis patients, and was positively correlated with the relative levels of pro-inflammatory cytokines. Moreover, miR-146 could discriminate epidural fibrosis patients from control patients. In isolated epidural fibroblasts, the overexpression of miR-146 dramatically enhanced its proliferation and the inflammatory response. miR-146 serves as a diagnostic biomarker for the early detection of epidural fibrosis. The upregulation of miR-146 enhanced the fibroblasts proliferation and inflammatory response in epidural fibrosis. This study provides a novel potential therapeutic target for epidural fibrosis.

How to improve the safety of bicortical pedicle screw insertion in the thoracolumbar vertebrae: analysis base on three-dimensional CT reconstruction of patients in the prone position.

BACKGROUND: Through the comparison of three-dimensional CT reconstruction between the supine position and the prone position, the relative position of thoracolumbar great vessels and vertebral body was studied, and the shortest safe distance between them was measured to improve the safety of bicortical pedicle screw insertion and reduce the risk of vascular injury. METHODS: Forty adults were selected to participate the research. Three-dimensional reconstruction of thoracolumbar (T9-L3) CT was performed in the prone position and the supine position. The relative distance between the Aorta/Inferior Vena Cava (IVC) and vertebral body was obtained as AVD/VVD respectively. The relative angle of the Aorta/ IVC and the vertebral body was calculated as ∠AOY/∠VOY. Self-controlled experiments were carried out in the prone and the supine positions, and the data obtained were analyzed using SPSS 22.0 statistical software. RESULTS: The AVD of the prone position and the supine position was the shortest at T12 (3.18 ± 0.68 mm), but the difference was not statistically significant. The aorta of the T9-L3 segment was shifted from the anterolateral to the anteromedial. The ∠AOY of the other groups differed significantly between the prone and supine positions in all vertebrae except T12 and L1 (P < 0.05), and the aorta in the prone position was more anteromedial than that of supine position. With regard to VVD/∠VOY, there was no significant difference between the prone and supine positions (P ≥ 0.05), and the minimum VVD of L3 segment is greater than 5.4 mm. The IVC has no obvious mobility and is fixed in the range of 20 ° ~ 30 ° near the midline. CONCLUSION: When using bicortical anchoring of pedicle screws, it is safe to ensure that the protruding tips of the screw is less than 3 mm. Due to the mobility of the aorta in different postures and individual differences in anatomy, the prone position CT can help doctors to make better preoperative plans and decisions.

Downregulation of miR-136 promotes the progression of osteosarcoma and is associated with the prognosis of patients with osteosarcoma.

Osteosarcoma (OS) is the most common bone tumor in children and young adults, and is an aggressive tumor with poor prognosis. MicroRNAs (miRNAs) are aberrantly expressed in various types of cancer, and contribute to cancer tumorigenesis and progression. In the present study, the potential prognostic value and biological function of miRNA-136 (miR-136) in OS was investigated. Reverse transcription-quantitative polymerase chain reaction analysis was used to evaluate the expression of miR-136 in OS tissues and cell lines. Kaplan-Meier survival analysis and Cox regression analysis were conducted to investigate the prognostic significance of miR-136. Various in vitro cell based assays were used to evaluate the effects of miR-136 on the biological behavior of OS cells. A luciferase assay was performed to determine the key miR-136 targets associated with OS. The expression of miR-136 was significantly downregulated in osteosarcoma tissues and cells compared with the normal controls (all P<0.05). Decreased miR-136 expression was significantly associated with Enneking staging (P=0.030) and distant metastasis (P=0.016). Decreased miR-136 expression in patients was associated with shorter overall survival compared with patients with increased expression levels (log-rank test; P<0.05). The expression of miR-136 was indicated as an independent prognostic factor for the patients (hazard ratio=0.496; 95% confidence interval=0.250-0.987; P=0.046). MTT, transwell and Matrigel assays demonstrated that upregulation of miR-136 decreased proliferation, migration and invasion of OS cells. Bioinformatics and luciferase assays demonstrated that migration and invasion enhancer 1 (MIEN1) is a direct target of miR-136. Together, the results suggested that miR-136 functions as a tumor suppressor gene to regulate proliferation, migration and invasion of OS cells. MIEN1 was a potential target of miR-136. Additionally, miR-136 may serve as a prognostic biomarker for OS.

Astragalus polysaccharides decrease proliferation, migration, and invasion but increase apoptosis of human osteosarcoma cells by up-regulation of microRNA-133a.

Osteosarcoma (OS) has a high incidence, malignity, and frequency of recurrence and metastasis. In this study, we aimed to explore the potential anti-cancer effects of Astragalus polysaccharides (APS) on human OS MG63 cells as well as underlying mechanisms. Viability of MG63 cells was assessed by CCK-8 assay to determine the adequate concentration of APS. Then, effects of APS on MG63 cell proliferation, cell cycle distribution, apoptosis, and migration and invasion were analyzed by BrdU incorporation, PI staining, flow cytometry, and transwell assays, respectively. The expression levels of proteins involved in these physiological processes were assessed by western blot analysis. Afterwards, miR-133a level in APS-treated cells was determined by qRT-PCR, and whether APS affected MG63 cells through regulation of miR-133a was determined. Finally, the activation of c-Jun N-terminal protein kinase (JNK) pathway was detected. We found that APS treatment suppressed the viability, proliferation, migration, and invasion of MG63 cells, as well as induced cell apoptosis. Moreover, APS enhanced the expression of miR-133a in MG63 cells. Knockdown of miR-133a reversed the APS treatment-induced MG63 cell proliferation, migration and invasion inhibition, as well as cell apoptosis. Furthermore, APS inactivated JNK pathway in MG63 cells. Knockdown of miR-133a reversed the APS treatment-induced inactivation of JNK pathway in MG63 cells. To conclude, APS repressed proliferation, migration, and invasion while induced apoptosis of OS MG63 cells by up-regulating miR-133a and then inactivating JNK pathway.

Applied anatomy of the calcaneocuboid articular surface for internal fixation of calcaneal fractures.

BACKGROUND: Many types of steel plates are used for internal fixation of calcaneal fractures through extensive lateral approach. The fixation screw at the anterior calcaneal process must be placed into the dense compression trabeculae located directly under the calcaneocuboid articular surface to achieve a stable fixation. METHODS: The transverse diameter and inner tilt angle of the calcaneocuboid articular surface were measured and the inner structures near the calcaneocuboid articular surface were observed in forty adult calcaneus bone specimens to provide an anatomical basis for internal fixation of calcaneal fractures. RESULTS: The transverse diameter was 22.67 ± 2.14 mm and the inner tilt angle was 60.4 ± 7.1°. CONCLUSION: Screws should be implanted under the calcaneocuboid articular surface and the length and direction of the screw should be selected according to the transverse diameter of the calcaneal articular surface and the inner tilt angle, respectively.

Astragalus polysaccharides decrease proliferation, migration, and invasion but increase apoptosis of human osteosarcoma cells by up-regulation of microRNA-133a

Osteosarcoma (OS) has a high incidence, malignity, and frequency of recurrence and metastasis. In this study, we aimed to explore the potential anti-cancer effects of Astragalus polysaccharides (APS) on human OS MG63 cells as well as underlying mechanisms. Viability of MG63 cells was assessed by CCK-8 assay to determine the adequate concentration of APS. Then, effects of APS on MG63 cell proliferation, cell cycle distribution, apoptosis, and migration and invasion were analyzed by BrdU incorporation, PI staining, flow cytometry, and transwell assays, respectively. The expression levels of proteins involved in these physiological processes were assessed by western blot analysis. Afterwards, miR-133a level in APS-treated cells was determined by qRT-PCR, and whether APS affected MG63 cells through regulation of miR-133a was determined. Finally, the activation of c-Jun N-terminal protein kinase (JNK) pathway was detected. We found that APS treatment suppressed the viability, proliferation, migration, and invasion of MG63 cells, as well as induced cell apoptosis. Moreover, APS enhanced the expression of miR-133a in MG63 cells. Knockdown of miR-133a reversed the APS treatment-induced MG63 cell proliferation, migration and invasion inhibition, as well as cell apoptosis. Furthermore, APS inactivated JNK pathway in MG63 cells. Knockdown of miR-133a reversed the APS treatment-induced inactivation of JNK pathway in MG63 cells. To conclude, APS repressed proliferation, migration, and invasion while induced apoptosis of OS MG63 cells by up-regulating miR-133a and then inactivating JNK pathway.