选用猪、兔、鸡、小鼠和豚鼠5种试验动物分别制备猪肺炎支原体高免阳性血清,并测定了其对猪肺炎支原体的代谢抑制效价.再从兔高免血清中纯化特异性抗体,比较抗体纯化前后的代谢抑制效价是否发生变化.结果表明,5种试验动物高免血清对猪肺炎支原体的代谢抑制价分别为0、104、103、105、102,纯化后的抗体仍可抑制猪肺炎支原体的生长,代谢抑制价没有明显变化.由此可见,不同动物来源的高免血清对猪肺炎支原体的代谢抑制价不同,代谢抑制作用的主要作用物质为特异性抗体;首次证明病原靶动物——猪的高免抗血清对猪肺炎支原体没有代谢抑制作用,其他支原体是否也表现为对靶动物(或人)抗血清的耐受性还有待进一步研究.

Objective:In a previous study,we found that low doses of cyclooxygenase-2(COX-2) selective inhibitors could induce the proliferation of esophageal squamous cell carcinoma(ESCC) cells,which can be attributed to the activation of a 5-lipoxygenase(5-LOX) shunt by slight COX-2 inhibition.The objective of the present study was to determine whether highly effective COX-2 siRNA inhibition can avoid this shunt.Methods:TE-1 and Eca109(ESCC) cells were divided into blank control,liposome transfection,random sequence siRNA,and COX-2 siRNA groups.Cell proliferation was assessed using Cell Counting Kit-8 assay.Protein and mRNA expressions were determined using Western blot analysis and RT-PCR,respectively.Prostaglandin E2 and leukotriene B4(LTB_4) levels were measured by enzyme-linked immunosorbent assay.A flow cytometer was used for cell cycle measurement.Results:Compared with the blank controls, COX-2 siRNA-transfected TE-1 and Ecal09 cells showed 79%and 73%inhibition of COX-2 expression,respectively,as well as 45.86% and 48.99%inhibition of cell proliferation,respectively(PO.05).The expression of 5-LOX remained unchanged(P>0.05),and prostaglandin E2 and LTB_4 levels were highly in accordance with alterations in COX-2 and 5-LOX expressions,respectively.The percentages of cells in G_1 stage increased significantly.Bcl-2 expression decreased,whereas the expressions of caspase-9 and Bax increased in the two ESCC cells after COX-2 siRNA transfection(P<0.05).Conclusions:Highly effective inhibition of COX-2 expression may prevent the activation of 5-LOX and the following up-regulation of LTB_4,which is a cell proliferation factor.These suggest that only high-dose COX-2 selective inhibitors with significant COX-2 inhibitory effects can achieve anti-cancer effects in ESCCs.

Objective To investigate the effect of NS-398,a selected cyclooxygenase-2(COX-2) inhibitor and licofelone,a dual COX-2/5-lipoxygenase(5-LOX) inhibitor on the proliferation of TE-1,an esophageal squamous cell carcinoma(ESCC) cell line,and explore the potential limitation of sole COX-2 inhibition on the negative regulation of ESCC cell proliferation.Methods TE-1 cells were divided into drug treatment group,DMSO control group and blank control group.Cells were treated by licofelone or NS-398 in 4 concentrations,including 25 μmol/L,50 μmol/L,75 μmol/L and 100 μmol/L.Cell proliferation was assessed by Cell Counting Kit-8 assay.The expression of COX-2 and 5-LOX were determined by both RT-PCR(mRNA) and Western blot(protein),respectively.The concentrations of prostaglandin E2(PGE2) and leukotriene B_4(LTB_4) were measured by ELISA.Flow cytometer was used for the cell cycle measurement.Results Cell proliferation inhibition was found in both time and concentration-dependent manners in licofelone treated TE-1 cells,but not in those treated by NS-398.Time and concentration-dependent inhibition of COX-2 mRNA,protein and PGE2 expression were found in TE-1 cells treated with either licofelone or NS-398,while downregulation of 5-LOX mRNA,protein and LTB4 expression were found only in cells treated with licofelone.The level of LTB4 showed an upregulation tendency in cells treated with NS-398,but a significant difference was found only under the concentration of 100 μmol/L.After 24 h treatment with 100 μmol/L of licofelone and 50 μmol/L of NS-398,the percentages of TE-1 cells in G_0/G_1-phase were 67.1% and 63.8%,respectively,which were significantly higer than those in control group(P0.05).Conclusion Selected COX-2 inhibitor alone may induce ESCC cell proliferation in several specific concentrations,which may be due to the activation of 5-LOX shunt.A dual COX-2/5-LOX inhibitor should be more effective for the inhibition of esophageal squamous cell carcinoma proliferation.

Cyclooxygenase(COX),lipoxygenase(LOX)and Cytochrome P450(CYP450)pathways are the key metabolic pathways of arachidonic acid(AA)metabolism.It has been well documented that the expression of COX or LOX is related to the carcinogenic process of variety tumors,including esophageal cancer.Since AA is the sole metabolizing substrate of both COX and LOX pathways,the comparative shunts of them should not be ignored in the related anticancer strategies.Meanwhile,there are also raising concerns about the carcinogenic roles of CYP450 gene polymorphism and AA in food supplement.

报告1例老年人因巨大动物肌腱存留食管中下段引起胸痛及呕吐,在夹物钳及网篮取出失败后,将异物送入胃腔以圈套器良好固定后取出。老年人咀嚼功能下降,咽部感受性降低,易致食管异物。食管异物最常见于食管上段,其好发部位与食管生理性狭窄有关,其他部位的食管异物应特别注意有无周围占位压迫致食管狭窄。对非食管静脉曲张者,除非异物巨大,否则约80%可经内镜取出,但异物外形不规则或有尖刺、停留部位在主动脉弓邻近,内镜取出有困难时,需开胸手术。

牙侵蚀指非细菌因素引起的、由于化学或离子化过程导致的牙矿质减少,胃食管反流病(GERD)是其主要病因之一。GERD患者食管动力异常、唾液分泌速率和缓冲能力下降均可促进牙侵蚀的发生和发展。控制酸性饮料摄入、中和口腔酸度以及使用唾液成分替代物有利于防止牙表面pH过低引起的牙釉质去矿化,而氟化物则有利于促进再矿化。在恢复受侵蚀牙齿的美观方面,全瓷贴面被广泛应用。牙侵蚀的诊治需要口腔科和消化科的共同参与。口腔科医生可发现不典型的GERD患者,而消化科医生诊断GERD也应常规排除牙侵蚀的存在。