Résumé
ObjectiveLymphatic epithelial cells (LECs) are important links involved in lymphatic metastasis in the microenvironment of cholangiocarcinoma. This study aims to detect the modulation of inflammatory factors and chemokines secreted by LECs after stimulation of cholangiocarcinoma cells, and observe the effects of highly expressed factors on lymphangiogenesis.MethodsThe culture medium of cholangiocarcinoma (RBE, HCCC9810), LECs stimulated by cholangiocarcinoma cell culture medium (CCM), and normal LECs were prepared. Inflammatory factors and chemokines in the culture medium were detected using protein chip. The experiments are divided into the following groups, including a blank control group, CCM group, CCM coupled with Anti-ENA-78 group, Anti-ENA-78 group, ENA-78 group, ENA-78 coupled with SB2252002, and SB225002 group. The relationship between the content of factor and time was investigated using ELISA, while the relation between target factors and lymphangiogenesis obtained by cell proliferation and tubule formation assay.ResultsWe found ENA-78, IP-10, GCP-2, MCP-2, MCP-3, MIP-3a, HCC-1, and Lymphotactin expression increased in LECs supernatant after CCM stimulation. However, I-TAC, MIP-1d, IL-10, MIG, PDGF-BB, and CXCL16 factors showed down-regulation. The secretion of ENA-78 in CCM was relatively low. By ELISA, we found that the ENA-78 protein in RBE-LECs and HCCC9810-LECs gradually increased over time, and reached the plateau phase at the point of 48h. The lymphatic tube forming ability of LECs cultured in CCM was significantly increased compared with that of the control group, and this ability could be partially weakened by ENA-78 neutralizing antibodies. In the exogenous ENA-78 protein group, the lymphatic tube formation ability was as well significantly increased compared with that in the control group, and this ability could be effectively blocked by the IL-8B inhibitor.ConclusionThe increased secretion ENA-78 of lymphatic epithelial cells induced by cholangiocarcinoma may play a role in promoting lymphangiogenesis through the IL-8B receptor.
Résumé
ObjectiveLymphatic epithelial cells (LECs) are important links involved in lymphatic metastasis in the microenvironment of cholangiocarcinoma. This study aims to detect the modulation of inflammatory factors and chemokines secreted by LECs after stimulation of cholangiocarcinoma cells, and observe the effects of highly expressed factors on lymphangiogenesis.MethodsThe culture medium of cholangiocarcinoma (RBE, HCCC9810), LECs stimulated by cholangiocarcinoma cell culture medium (CCM), and normal LECs were prepared. Inflammatory factors and chemokines in the culture medium were detected using protein chip. The experiments are divided into the following groups, including a blank control group, CCM group, CCM coupled with Anti-ENA-78 group, Anti-ENA-78 group, ENA-78 group, ENA-78 coupled with SB2252002, and SB225002 group. The relationship between the content of factor and time was investigated using ELISA, while the relation between target factors and lymphangiogenesis obtained by cell proliferation and tubule formation assay.ResultsWe found ENA-78, IP-10, GCP-2, MCP-2, MCP-3, MIP-3a, HCC-1, and Lymphotactin expression increased in LECs supernatant after CCM stimulation. However, I-TAC, MIP-1d, IL-10, MIG, PDGF-BB, and CXCL16 factors showed down-regulation. The secretion of ENA-78 in CCM was relatively low. By ELISA, we found that the ENA-78 protein in RBE-LECs and HCCC9810-LECs gradually increased over time, and reached the plateau phase at the point of 48h. The lymphatic tube forming ability of LECs cultured in CCM was significantly increased compared with that of the control group, and this ability could be partially weakened by ENA-78 neutralizing antibodies. In the exogenous ENA-78 protein group, the lymphatic tube formation ability was as well significantly increased compared with that in the control group, and this ability could be effectively blocked by the IL-8B inhibitor.ConclusionThe increased secretion ENA-78 of lymphatic epithelial cells induced by cholangiocarcinoma may play a role in promoting lymphangiogenesis through the IL-8B receptor.
Résumé
Objective Few reports are seen comparing esophageal stent placement (ESP) and the endoscopic incision method (EIM) in the treatment refractory esophageal anastomotic strictures (EAS) following esophageal carcinoma resection (ECR). This study was to evaluate the effect ESP versus that of EIM in the treatment of refractory EAS after ECR. Methods We retrospectively analyzed the clinical data on 50 cases of post-ECR refractory EAS treated by ESP (n = 32) or EIM (n = 18) in our Center of Digestive Medicine between January 2012 and December 2018. We recorded and compared the pre- and post-operative dysphagia scores, post-operative complications and follow-up results between the two groups of patients. Results Compared with the EIM group, the patients of the ESP group had a remarkably lower dysphagia score post-operatively (1.4±0.5 vs 1.0±0.0, P<0.01), a smaller diameter of the dilated esophagus ([19.9±1.8] vs [11.0±1.9] mm, P<0.01), higher incidence rates mild and severe chest pain (P=0.022), and a higher rate of relief of esophageal stricture at 12 months after surgery (P<0.05). Conclusion EIM can rapidly relieve the symptoms of esophageal anastomotic stricture, while ESP may achieve a longer duration of relief. Both of the procedures are safe for patients with refractory esophageal anastomotic stricture.
Résumé
Based on studying the manifestation of untranslatability of traditional Chinese medicine (TCM) technical terms, and through analysis on the enriched cultural content and special linguistic characteristics, the author summarized the factors that caused the untranslatability, and suggested some projects for compensation and reformation, including transliteration, word-formation, free translation and literal translation. Although the existence of untranslatability of TCM technical terms is affirmable, on account of the uninterrupted international cultural communications, the untranslatability of TCM terms will not be lasting invariable.