Objective:To investigate the enhancive effect of N,N'-dinitrosopiperazine(DNP) on induced carcinogenesis in nasal and/or nasopharyngeal epithelia among TgN(p53mt-LMP1)/HT transgenic mice to examine the underlying mechanism for the development of nasopharyngeal carcinoma(NPC). Methods:TgN(p53mt-LMP1)/HT transgenic mice and the same strain of C57BL/6J wild-type mice both at the age of 5 months were randomly divided into 2 groups in parallel,respectively,i.e.,TgN(p53mt-LMP1)/HT cancerous lesion-inducing group(TI),TgN(p53mt-LMP1)/HT control group(TC),C57BL/6J cancerous lesion-inducing group(CI),and C57BL/6J control group(CC). TI and CI mice were treated only with DNP for 16 weeks,twice each week,while TC and CC mice were given the same volume of saline as controls. At the end of treatment,animals were sacrificed to collect epithelial tissue samples from nasal cavity and nasopharynx for pathohistological evaluation by haematoxylin and eosin(HE) staining and for determination on the expression of TRAF2,c-Jun,and p16 by immunohistochemistry. Results:Atypical hyperplasia was more significant in the samples of TI than in those of TC,CI,and CC,with the rates of lesions being 90%,10%,0,and 0(P<0.01) respectively,though DNP was used alone in a much shortened inducing period at less dosage and without the use of carcinogenic promoter 12-O-tetradecanoylphorbol-13-acetate as usual. The expressions of tumor necrosis factor(TNF) recep-tor-associated factor 2(TRAF2) and c-Jun in these samples were significantly up-regulated in TI(P<0.01),while the expression of p16 was significantly lower in TI than in the other groups(P<0.01). Conclusion:TgN(p53mt-LMP1)/HT mice hold inherited con-stitutional defect in immune surveillance function,which can be aggravated by environmental carcinogens,such as DNP used even though in a much less strength. The enhanced carcinogenesis-inducing effect of DNP on TgN(p53mt-LMP1)/HT mice should be closely associated with abnormal signaling of activator protein-1(AP-1) pathway,especially up-regulated expres
目的探讨预防鼻内镜下鼻中隔矫正术后鼻中隔血肿的方法及策略。方法回顾性分析我科2012年1月至2016年10月收治的行鼻中隔矫正术的120例患者资料,其中行鼻中隔嵴突局部切除术30例,鼻内镜下鼻中隔黏膜下矫正术90例(术中鼻中隔一侧黏膜破损10例,鼻中隔黏膜完整80例)。对80例鼻中隔黏膜完整患者,鼻中隔矫正后行一侧中隔黏膜切开40例,未行一侧黏膜切开40例,术后均予膨胀海绵填塞。结果行鼻中隔嵴突局部切除、术中鼻中隔一侧黏膜破损、鼻中隔黏膜完整鼻中隔矫正后一侧中隔黏膜切开的患者均未出现鼻中隔血肿。鼻中隔黏膜完整而未行一侧黏膜切开的患者中,出现鼻中隔血肿6例,所有病例均无鼻中隔穿孔。行一侧中隔黏膜切开组鼻中隔血肿发生率明显低于未行一侧黏膜切开组(0 vs 15.0%),差异有统计学意义(P<0.05)。结论对于术后两侧鼻中隔黏膜完整的患者,鼻中隔矫正后行一侧中隔黏膜切开能有效预防鼻中隔术后鼻中隔血肿。
