BackgroundAnterior plate fusion is an effective procedure for the treatment of cervical spinal diseases but is accompanied by a high incidence of postoperative dysphagia. A zero profile (Zero-P) spacer is increasingly being used to reduce postoperative dysphagia and other potential complications associated with surgical intervention. Studies comparing the Zero-P spacer and anterior plate have reported conflicting results.MethodologyA meta-analysis was conducted to compare the safety, efficacy, radiological outcomes and complications associated with the use of a Zero-P spacer versus an anterior plate in anterior cervical spine fusion for the treatment of cervical spinal disease. We comprehensively searched PubMed, Embase, the Cochrane Library and other databases and performed a meta-analysis of all randomized controlled trials (RCTs) and prospective or retrospective comparative studies assessing the two techniques.ResultsTen studies enrolling 719 cervical spondylosis patients were included. The pooled data showed significant differences in the operation time [SMD = –0.58 (95% CI = −0.77 to 0.40, p < 0.01)] and blood loss [SMD = −0.40, 95% CI (−0.59 to –0.21), p < 0.01] between the two groups. Compared to the anterior plate group, the Zero-P group exhibited a significantly improved JOA score and reduced NDI and VAS. However, anterior plate fusion had greater postoperative segmental and cervical Cobb’s angles than the Zero-P group at the last follow-up. The fusion rate in the two groups was similar. More importantly, the Zero-P group had a lower incidence of earlier and later postoperative dysphagia.ConclusionsCompared to anterior plate fusion, Zero-P is a safer and effective procedure, with a similar fusion rate and lower incidence of earlier and later postoperative dysphagia. However, the results of this meta-analysis should be accepted with caution due to the limitations of the study. Further evaluation and large-sample RCTs are required to confirm and update the results of this study.

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Human glioblastoma is a malignant and aggressive primary human brain solid tumor characterized by severe hypoxia. Hypoxia can induce autophagy, which may result in chemoresistance and malignant progression of cancer cells. MicroRNAs (miRNAs) have been reported to modulate hypoxia-induced autophagy in various types of cancers. In the present study, we observed that hypoxia-inducible factor (HIF)-1α expression was increased while miR-224-3p expression was decreased under hypoxia in a time-dependent manner in glioma LN229 and astrocytoma U-251MG cell lines, as deteced by western blot analysis and real-time quantitative polymerase chain reaction. In addition, HIF-1α knockout inhibited cell motility and chemosensitivity by negatively regulating the expression of miR-224-3p under a hypoxic condition by Transwell and MTT assay. Moreover, hypoxia increased the relative expression of ATG5 (autophagy-related gene 5) and LC3 II/I with a decreased level of p62. These results were correlated with autophagy in a time-dependent manner, suggesting that hypoxia induced autophagy in glioblastoma and astrocytoma cells. Through bioinformatic prediction and luciferase reporter assay, we confirmed that ATG5 is a target of miR-224-3p and ATG5 expression was negatively regulated by miR-224-3p. Knockdown of ATG5 inhibited cell mobility with increased chemosensitivity of glioblastoma cells under hypoxia. Moreover, overexpression of miR-224-3p also inhibited cell mobility with increased chemosensitivity of glioblastoma cells under hypoxia. However, activation of autophagy was able to counteract these effects of miR-224-3p. Furthermore, in vivo experiments indicated that the miR-224-3p mimic enhanced the chemosensitivity of LN229 cells to temozolomide by immunohistochemistry and TUNEL assay. In summary, our experiments elucidated that the HIF-1α/miR-224-3p/ATG5 axis affects cell mobility and chemosensitivity by regulating hypoxia-induced autophagy in glioblastoma and astrocytoma. Therefore, miR-224-3p could be a novel target against hypoxia-induced autophagy in glioblastoma and astrocytoma.

This was an in vitro and in vivo study to develop a novel artificial cervical vertebra and intervertebral complex (ACVC) joint in a goat model to provide a new method for treating degenerative disc disease in the cervical spine. The objectives of this study were to test the safety, validity, and effectiveness of ACVC by goat model and to provide preclinical data for a clinical trial in humans in future. We designed the ACVC based on the radiological and anatomical data on goat and human cervical spines, established an animal model by implanting the ACVC into goat cervical spines in vitro prior to in vivo implantation through the anterior approach, and evaluated clinical, radiological, biomechanical parameters after implantation. The X-ray radiological data revealed similarities between goat and human intervertebral angles at the levels of C2-3, C3-4, and C4-5, and between goat and human lordosis angles at the levels of C3-4 and C4-5. In the in vivo implantation, the goats successfully endured the entire experimental procedure and recovered well after the surgery. The radiological results showed that there was no dislocation of the ACVC and that the ACVC successfully restored the intervertebral disc height after the surgery. The biomechanical data showed that there was no significant difference in range of motion (ROM) or neural zone (NZ) between the control group and the ACVC group in flexion-extension and lateral bending before or after the fatigue test. The ROM and NZ of the ACVC group were greater than those of the control group for rotation. In conclusion, the goat provides an excellent animal model for the biomechanical study of the cervical spine. The ACVC is able to provide instant stability after surgery and to preserve normal motion in the cervical spine.

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