Objective To explore the appropriate treatment according to the grading system of adolescent idiopathic cervical kyphosis.Methods A retrospective study was performed in 115 adolescent patients with idiopathic cervical kyphosis.The patients were divided into 4 groups according to the magnitude of kyphosis.The initial Cobb angle of 4 groups were 12.7°±1.4° 25.4°±4.8°,47.2°±4.4° and 62.6°±5.7° respectively.The patients in group I were treated with the collar support for 4-8 weeks.The patients in group Ⅱ were treated with skull traction (3-5 kg) and then fixed by cranio-cervical-thoracic plaster.According to the angles between the tangents of posterior vertebral body at each level on lateral cervical radiograph in extension,the anterior fusion levels of the group Ⅲ and angles and range of osteotomy in the group Ⅳ were decided.In group Ⅳ,the patients were treated by two steps.The anterior release and posterior osteotomy were performed firstly.Then skull traction (1/10 body weight) was maintained in order to correct the deformity for 7-10 days,fusion and anterior fusion with autologous bone graft and internal fixation was completed.Results Post-operative radiograph showed that Cobb angle were -5.5°±2.0°,-8.2°±6.1°,-4.5°±6.6° and -2.9°±7.9° in Ⅰ-Ⅳ group after treatment.The deformed appearance of the patients improved significantly.A improvement neck pain and neurologic function were found in all patients.Post-operative MRI showed that physiological curve of the cervical spine was restored,and the cerebrospinal fluid line was clear in the previous kyphosis area.Conclusion Adolescent idiopathic cervical kyphosis has specific characteristics.Surgical strategy is determined by the severity of deformity.

BACKGROUND:Pathophysiological mechanisms after spinal cord injury are very complex, so there is no compressive and in-depth understanding on it.
OBJECTIVE:To study the effect of dura mater spinalis integrity on cytokine levels in the cerebrospinal fluid of animal models of spinal cord injury.
METHODS:The white rabbit models of spinal cord injury were established using clamp compression method, and then the models were randomly divided into four groups:no dura mater spinalis defect group, dura mater spinalis defect group, dura mater spinalis defect composite with membrane repairing group and dura mater spinalis defect composite with autologous fascia repair group. Enzyme-linked immunosorbent assay was
performed to detect the changes of levels of cytokines (interleukin-6, interleukin-10 and tumor necrosis factorα) in the cerebrospinal fluid at 30 minutes, 1, 3, 6, 12 and 36 hours after surgery.
RESULTS AND CONCLUSION:The levels of interleukin-6, interleukin-10 and tumor necrosis factorαin the
cerebrospinal fluid of the dura mater spinalis defect group, dura mater spinalis defect composite with membrane repairing group and dura mater spinalis defect composite with autologous fascia repair group were significantly lower than those of the no dura mater spinalis defect group at 6 hours after surgery (P<0.05). There were no significant differences in the levels of interleukin-6, interleukin-10 and tumor necrosis factorαat other time points between groups (P>0.05). The results indicate that maintaining the integrity of dura mater spinalis of the spinal cord injury model can affect the levels of interleukin-6, interleukin-10 and tumor necrosis factorαin the
cerebrospinal fluid, thus inhibiting the inflammatory response.

Objective To investigate the effect of carrimycin on the biological function of pancreatic cancer cells. Methods Pancreatic cancer cell lines MIA PaCa-2, BxPC-3, Panc-1, and PATU 8988 were treated with carrimycin at concentrations of 0 (control group), 2, 4, 8, and 16 μmol/L for 24, 48, and 72 hours. MTT assay was used to measure cell viability; EdU cell proliferation assay was used to observe the effect of carrimycin on DNA replication of pancreatic cancer cells; colony formation assay was used to observe the effect of carrimycin on the proliferation of pancreatic cancer cells; flow cytometry was used to analyze the effect of carrimycin on the cell cycle of pancreatic cancer cells; wound healing assay was used to analyze the effect of carrimycin on the migration of pancreatic cancer cells; Western blot was used to measure the expression levels of the markers such as epithelial-mesenchymal transition (EMT) and cell cycle-dependent protein kinase inhibitor 1A (P21); immunofluorescence assay were used to measure the expression levels of EMT-related markers. An analysis of variance was used for comparison between multiple groups, and the least significant difference t -test was used for further comparison between two groups. Results Compared with the control group, carrimycin significantly inhibited the proliferative activity of MIA PaCa-2, BxPC-3, Panc-1, and PATU 8988 cells in a concentration- and time-dependent manner (all P < 0.01); carrimycin at concentrations of 4, 8, and 16 μmol/L significantly reduced DNA replication in MIA PaCa-2 cells ( t =2.378, 4.984, and 18.970, all P < 0.05) and BxPC-3 cells ( t =4.879, 6.089, and 9.521, all P < 0.01); after treatment with carrimycin at concentrations of 4, 8, and 16 μmol/L, colony formation ability significantly decreased with the increase in drug concentration in MIA PaCa-2 cells ( t =5.889, 11.240, and 15.840, all P < 0.001) and BxPC-3 cells ( t =6.717, 15.800, and 18.850, all P < 0.001). After treatment with carrimycin at concentrations of 4, 8, and 16 μmol/L, there was a significant increase in the proportion of cells in G1 phase in MIA PaCa-2 cells ( t =9.071, 12.280, and 19.360, all P < 0.0001) and BxPC-3 cells ( t =3.061, 4.962, and 8.868, all P < 0.05), and there was a significant reduction in the proportion of cells in S phase in MIA PaCa-2 cells ( t =2.316, 4.165, and 5.562, all P < 0.05) and BxPC-3 cells ( t =2.424, 3.264, and 5.744, all P < 0.05). Western blot further demonstrated that compared with the control group, the expression level of the cell cycle-related protein P21 gradually increased with the increase in the concentration of carrimycin in MIA PaCa-2 cells ( t =5.437, 6.453, and 8.799, all P < 0.001) and BxPC-3 cells ( t =25.130, 44.750, and 52.960, all P < 0.000 1). Wound healing assay showed that after treatment for 12, 24, and 48 hours, carrimycin at concentrations of 0, 4, 8, and 16 μmol/L significantly reduced the lateral migration of MIA PaCa-2 cells (all P < 0.05) and BxPC-3 cells (all P < 0.05). Western blot showed that compared with the control group, carrimycin treatment at concentrations of 4, 8, and 16 μmol/L significantly upregulated the expression of the epithelial marker E-cadherin in MIA PaCa-2 cells ( t =2.388, 4.899, and 5.819, all P < 0.05) and BxPC-3 cells ( t =2.533, 5.836, and 6.774, all P < 0.05) and significantly downregulated the expression of the interstitial marker Snail in MIA PaCa-2 cells ( t =12.440, 14.830, and 16.800, all P < 0.000 1) and BxPC-3 cells ( t=5.039, 5.893, and 7.725, all P < 0.01), and it also significantly downregulated the expression of the interstitial marker Vimentin in MIA PaCa-2 cells ( t =3.105, 7.752, and 11.200, all P < 0.05) and BxPC-3 cells ( t =2.555, 4.883, and 9.153, all P < 0.05). Conclusion Carrimycin can effectively inhibit the proliferation, migration, and EMT process of pancreatic cancer cells, thereby exerting an antitumor biological activity.