How I do it: dual operation channels percutaneous endoscopic far-lateral transforaminal lumbar interbody fusion.

BACKGROUND: The current surgical procedure of interbody fusion in the lumbar spine has several limitations including low efficiency, potential endplate damage, overdose radiation exposure, and failure of fusion. METHODS: Through the endoscopic operating channel, we efficiently removed the superior and inferior articular processes and decompressed the ligamentum flavum. Another operating channel was established under endoscopic monitoring to excise the annulus fibrosus, remove the cartilaginous endplate using open instruments, perform interbody bone grafting, and place a non-expandable polyetheretherketone open surgical fusion cage. CONCLUSION: Lumbar interbody fusion was performed successfully using a far-lateral transforaminal approach combined with dual operation channels of percutaneous endoscopic-assisted technique.

Infectious bursal disease virus replication is inhibited by avain T cell chemoattractant chemokine CCL19.

Chemokine CCL19, together with its receptor CCR7, is one of the most important factors recruiting immune cells into target organ during virus infection. Our previous study has shown that CCL19 played a vital role in the process of T cell trafficking into bursae during bursal disease virus (IBDV) infection. In this study, we hypothesized that CCL19 could exert direct influences on IBDV replication other than recruiting immune cells. A eukaryotic expression vector of pEGFP-N1/CCL19 was successfully constructed and identified by PCR, double enzymes digestion, and sequencing. Different concentrations of pEGFP-N1/CCL19 plasmids were transfected into DF1 cells and CCL19 protein was highly expressed. Then, DF1 cells were infected with IBDV B87 strain post-transfection. Based on PCR and Western blot results, CCL19 could obviously decrease the gene levels of VP1 and VP2 and the protein levels of VP2 and VP3. When CCL19 was knocked down, the gene levels of VP1 and VP2 were significantly upregulated. Moreover, indirect immunostaining revealed that the IBDV content was largely decreased after CCL19 overexpression. Additionally, CCL19 inhibitory effects might rely on activation of the JNK signal pathway. Taken together, chemokine CCL19 directly blocks IBDV replication in DF1 cells, indicating that CCL19 could play crucial functions other than recruiting T cells during the pathogenesis of IBDV.