[Objective]To introduce cervical laminoplasty fixation with Ti-mesh plates in posterior open door decompression and evaluate its clinical outcomes.[Method]A total of 27 cases with cervical spinal stenosis were treated by laminoplasty with mini titanium plates.The mean following-up time were 18 months.[Result]All cases were primary healed,the preoperative symptoms were improved satisfactorily with 88% good to excellent outcome over 6 months following-up.One case without relief of nurological symptoms underwent an additional anterior multilevel corpectomy.The surgical lamina achieved bone fusion without stenosis.[Conclusion]The laminoplasty with Ti-mesh plates restore spinal posterior construction with less loss of range of motion and maintain larminar in open position without stenosis.The surgical procedure is easier to perform with less complication rates.

BACKGROUND:In recent years,studies have shown the effects of tumor necrosis factor-a(TNF-а)on fibroblasts at different organizations in a tissue-specific and dose-dependent manner.OBJECTIVE:TO investigate the biologic effects of TNF-а and its signal transduction pathway-specific kinase inhibitors on mouse embryonic fibroblasts(NIH3T3).METHODS:NIH3T3 cells were cultured in vitro,and then the cells were assigned into 3 groups.Cells in the control group were cultured in DMEM high-glucose medium with 2%serum;those in the TNF-а group were cultured in 100 μg/L TNF-аmedium;those in the TNF-а+Anti-TNFRSF 1 B group were firstly cultured in medium with 50 μg/L Anti-TNFRSF 1 B for 1 hour,and then placed in the medium with 100 μg/L TNF-а.RT-PCR and Western blot methods were used to evaluate mRNA and protein expressions of type Ⅰ collagen and matrix metalloproteinase 3(MMP3)in each group.RESULTS AND CONCLUSION:In this experiment,NlH3T3 cells cultured with a certain concentration of TNF-а,the specificity kinase signal of transduction pathway presented with phosphorylation or protein activation,and the signal pathway was activated,which promoted MMP3 activation,and significantly reduced the expression of type Ⅰ collagen.The effect of TNF-а was certainly inhibited,but not completely eliminated after adding its signal transduction pathway inhibitor Anti-TNFRSF1 B.This further proves the role of TNF-а on NIH3T3 activation.