[Objective] To discuss the mechanism and relative problems of lumbar traction. [Method] Relevant articles and retrospect clinical data in the author's hospital were reviewed. Review relevant articles and retrospect clinical data of our hospital. [ Result ] Traction force : 40 kg + 15% ～ 20% of body weight, fineness rate reached 83.5% in 1606 patients being treated. According to course of disease, fineness rate was 90. 1% in the group of less than 3 years, 68.2% in the group of more than 3 years. [ Conclusion] Lumbosacral nerve root leave the peak of the protruding nucleus and establish a new harmonious "root-disc" relationship after traction. The pressure and tension to the nerve root reduces or disappears, meanwhile, the pain of low back and leg is alleviated or eradicated. Appropriate traction weight and correct traction body posture are key factors of good therapeutic effect.

Sesamin, a lipid-soluble lignin originally isolated from sesame seeds, which induces cancer cell apoptosis and autophagy. In the present study, has been reported that sesamin induces apoptosis via several pathways in human lung cancer cells. However, whether mitophagy is involved in sesamin induced lung cancer cell apotosis remains unclear. This study, the anticancer activity of sesamin in lung cancer was studied by reactive oxygen species (ROS) and mitophagy. A549 cells were treated with sesamin, and cell viability, migration ability, and cell cycle were assessed using the CCK8 assay, scratch-wound test, and flow cytometry, respectively. ROS levels, mitochondrial membrane potential, and apoptosis were examined by flow cytometric detection of DCFH-DA fluorescence and by using JC-1 and TUNEL assays. The results indicated that sesamin treatment inhibited the cell viability and migration ability of A549 cells and induced G0/G1 phase arrest. Furthermore, sesamin induced an increase in ROS levels, a reduction in mitochondrial membrane potential, and apoptosis accompanied by an increase in cleaved caspase-3 and cleaved caspase-9. Additionally, sesamin triggered mitophagy and increased the expression of PINK1 and translocation of Parkin from the cytoplasm to the mitochondria. However, the antioxidant N-acetyl-L-cysteine clearly reduced the oxidative stress and mitophagy induced by sesamin. Furthermore, we found that cyclosporine A (an inhibitor of mitophagy) decreased the inhibitory effect of sesamin on A549 cell viability. Collectively, our data indicate that sesamin exerts lethal effects on lung cancer cells through the induction of ROS-mediated mitophagy and mitochondrial apoptosis.

Sesamin, a lipid-soluble lignin originally isolated from sesame seeds, which induces cancer cell apoptosis and autophagy. In the present study, has been reported that sesamin induces apoptosis via several pathways in human lung cancer cells. However, whether mitophagy is involved in sesamin induced lung cancer cell apotosis remains unclear. This study, the anticancer activity of sesamin in lung cancer was studied by reactive oxygen species (ROS) and mitophagy. A549 cells were treated with sesamin, and cell viability, migration ability, and cell cycle were assessed using the CCK8 assay, scratch-wound test, and flow cytometry, respectively. ROS levels, mitochondrial membrane potential, and apoptosis were examined by flow cytometric detection of DCFH-DA fluorescence and by using JC-1 and TUNEL assays. The results indicated that sesamin treatment inhibited the cell viability and migration ability of A549 cells and induced G0/G1 phase arrest. Furthermore, sesamin induced an increase in ROS levels, a reduction in mitochondrial membrane potential, and apoptosis accompanied by an increase in cleaved caspase-3 and cleaved caspase-9. Additionally, sesamin triggered mitophagy and increased the expression of PINK1 and translocation of Parkin from the cytoplasm to the mitochondria. However, the antioxidant N-acetyl-L-cysteine clearly reduced the oxidative stress and mitophagy induced by sesamin. Furthermore, we found that cyclosporine A (an inhibitor of mitophagy) decreased the inhibitory effect of sesamin on A549 cell viability. Collectively, our data indicate that sesamin exerts lethal effects on lung cancer cells through the induction of ROS-mediated mitophagy and mitochondrial apoptosis.

Objective: To investigate the expression of Artemin in chondrosarcoma and its effect on proliferation and migration of endothelial cells, and to explore the mechanism. Methods: A total of 40 chondrosarcoma tissue samples (low degree (Ⅰ), 20 cases; high degree (Ⅱ,Ⅲ), 20 cases) surgically resected from patients, who were treated in Lianyungang HospitalAffiliated to Nanjing University of Chinese Medicine from May, 2015 to April, 2019, were collected for this study. Another 20 cases of normal cartilage tissue specimen from patients with amputations due to car accidents were served as control. The expressions of Artemin, vascular endothelial growth factor (VEGF), Ki-67 and CD31+ vascular density in tumor tissues were detected by immunohistochemistry.After being treated with 10 ng/ml Artemin, the changes of VEGF, stromal cell derived factor-1 (SDF-1), matric metalloproteinase 2 (MMP2) and MMP9 in the supernatant of SW1353 cell culture were detected by enzyme-linked immunosorbent assay (ELISA), and the effects of Artemin-treated chondrosarcoma cells on the migration and proliferation of ECV304 cells were detected by Transwell migration assay and MTT cell proliferation assay, respectively. Results: The expressions of Artemin and Ki-67 in the tissues of low-level group were significantly higher than those in the control group (all P<0.01); the expressions ofArtemin and Ki-67 in the tissues of high-level group were significantly higher than those in the low-level group (all P<0.01). The expression of Artemin was positively correlated with VEGF level and vascular density in chondrosarcoma tissues (all P<0.01);Artemin promoted the secretion of VEGF by chondrosarcoma cells, but had no significant effect on the secretion of SDF-1, MMP2 and MMP9. Artemin induced the proliferation and migration of ECV304 cells by promoting the secretion of VEGF by chondrosarcoma cells (all P<0.01). Conclusion: Artemin is highly expressed in chondrosarcoma tissues and has a positive correlation with the expression of VEGF and vascular density. Artemin can enhance the angiogenesis induced by chondrosarcoma.