Objective To evaluate therapeutic effect of tile shape perineal stapled prolapse resection in treatment of rectal prolapse.Methods The clinical data of 31 patients with rectal prolapse underwent tile shape perineal stapled prolapse resection in the Renmin Hospital of Wuhan University from December 2013 to August 2015 were retrospectively analyzed.All the patients with rectal prolapse were performed the tile shape perineal stapled prolapse resection with general anesthesia and (or) epidural anesthesia.The prolapse was completely pulled out and then axially cut open with a linear stapler in the lithotomy position.Finally,the prolapse was resected stepwise with the curved stapler at the prolapse's uptake.Results There were 8 males and 23 females in the 31 patients.The age was (65.8±3.2)years old.There were 14 patients with Ⅱ degree and 17 patients with Ⅲ degree prolapses.The median course was 5.8 years.The 31 patients were followed up for 0.5-7.0 months.Of 31 cases,the 24 cases were cured and 7 cases were better.It was found out that there was a significant difference between the number of axially cut open with a linear stapler and the weight of specimen (P＜0.05).And there was a significant difference between the number of axially cut open with a linear stapler and the recurrence (P＜0.05) too.When the number of axially cut open with a linear stapler were 4 for Ⅱ degree and 3 for Ⅲ degree,the treatment had been proved to be the highest efficacy.Conclusions Preliminary results of limited cases in this study show that tile shape perineal stapled prolapse resection is safe and effective in treatment of rectal prolapsed.Key of operation is that prolapse is completely pulled out and then axially cut open with a linear stapler at some o'clock for 2-4 points and rectal valves are formed.Prolapsed is resected stepwise with curved stapler at prolapse's uptake.When number of axially cut open with a linear stapler are 4 for Ⅱ degree and 3 for Ⅲ degree,it could achieve the best therapeutic effect.

M cells,with special morphological structure,are a kind of immune cells in the gut,and also a kind of special antigen-transporting cells,and are closely related to the intestinal mucosal immune function.At an early stage of Crohn''s disease(CD),the presence of M cells proliferation and pathological fracture damage of cytology existed.This article will review literatures about M-cell origin,morphological structure,functions,and adherent-invasive Escherchia coli(AIEC)caused CD by M cell-mediated pathway in recent years.

Objective:To investigate the risk factors for bleeding after endoscopic submucosal dissection (ESD) in treatment of gastric gastrointestinal stromal tumor (GIST).Methods:The clinical data of 124 patients with gastric GIST undergoing ESD from February 2011 to May 2017 in Renmin Hospital of Wuhan University were retrospectively analyzed.The risk factors for hemorrhage after ESD for gastric GIST were determined by univariate and multivariate unconditional logistic regression analysis.Results:Of the 124 patients enrolled,postoperative bleeding occurred in 10 cases (8.06％).Results of the univariate logistic regression analysis showed that histories of liver cirrhosis,coronary heart disease,old brain infarcts and atrial fibrillation were significantly associated with bleeding after ESD for gastric GIST (all OR＞ 1,P＜0.05);further multivariate logistic regression analysis revealed that histories of liver cirrhosis,coronary heart disease,old brain infarcts and atrial fibrillation were independent risk factors for bleeding after ESD for gastric GIST (all OR＞1,P＜0.05).Conclusion:The histories of liver cirrhosis,coronary heart disease,old brain infarcts and atrial fibrillation are risk factors for bleeding after ESD for gastric GIST.Therefore,the preoperative assessment should be optimized and the pre-and postoperative management should be enhanced in patients with these risk factors,so as to reduce the incidence of postoperative bleeding.

目的观察小鼠克罗恩病模型外周血单核细胞及结肠组织中白细胞介素(IL) 17、叉头状/翅状螺旋蛋白3(Foxp3)的表达,探讨其在2,4,6-三硝基苯磺酸(TNBS)诱导的克罗恩病小鼠急性炎症中的作用.方法 共40只6～8周龄雌性Bal/c小鼠,采用随机数字表法随机分为两组,20只以TNBS/乙醇溶液灌肠诱导克罗恩病模型(实验组),另外20只小鼠以同等浓度的乙醇氯化钠灌肠(正常对照组).干预1周后行疾病活动指数(DAI),结肠病理组织学评分(TDI)和结肠大体形态损伤指数(CMDI)评价,以实时荧光定量反转录聚合酶链反应(RT-PCR)检测小鼠外周血单核细胞IL-17mRNA、Foxp3 mRNA的表达,采用免疫印迹法检测小鼠结肠组织IL-17蛋白、Foxp3蛋白的表达.结果 与正常对照组相比,实验组的DAI、TDI、CMDI显著升高[DAI(5.41±0.48)比(0.85±0.07),TDI(5.63±0.74)比(0.74±0.08),CMDI(6.88±0.84)比(0.91±0.06),P＜0.01],外周血单核细胞的IL-17 mRNA显著升高[(1.118±0.145)比(1.000±0.000),P＜0.01],与其DAI、TDI及CMDI呈正相关(r =0.875,0.935,0.825,P＜0.01),Foxp3 mRNA显著降低[(0.797±0.271)比(1.000±0.000),P＜0.01],与其DAI、TDI及CMDI呈负相关(r=-0.885,-0.734,r-0.812,P＜0.01),结肠组织IL-17蛋白显著上升[(0.631±0.331)比(0.272±0.112),P＜0.01],与其DAI、TDI及CMDI呈正相关(r =0.765,0.778,0.734,P＜0.01),Foxp3蛋白显著降低[(0.274±0.112)比(0.592±0212),P＜0.01],与DAI、TDI及CMDI呈负相关(r=-0.889,-0.809,-0.851,P＜0.01).结论在TNBS诱导的结肠炎中,Th17/Treg轴的免疫偏倚是导致克罗恩病发生和发展的重要因素.

目的：探讨IL-33对克罗恩病（ CD）小鼠肠组织细胞因子（ IFN-γ、IL-4、IL-10、TGF-β）及转录因子（ T-bet、GATA-3、FOXP3）的影响。方法选择雌性BALB／c小鼠45只，随机分为对照组、TNBS组、IL-33组，每组15只。TNBS组、IL-33组给予TNBS／50％乙醇混合溶液灌肠建立CD模型，对照组仅予生理盐水灌肠。灌肠后TNBS组腹腔注射PBS，IL-33组腹腔注射重组鼠IL-33（rIL-33），对照组腹腔注射PBS。各组于腹腔注射第5天处死，取肠组织行HE染色，观察肠组织病理变化；采用ELISA法检测肠组织上清液IFN-γ、IL-4、IL-10、TGF-β，Western blotting法检测肠组织T-bet、GATA-3、FOXP3蛋白表达。结果与对照组比较，TNBS组肠组织炎症明显；肠组织IFN-γ水平升高，IL-4、IL-10、TGF-β水平降低（P均＜0．05）；T-bet蛋白表达升高，GATA-3、FOXP3蛋白表达降低（P均＜0．05）。与TNBS组比较，IL-33组肠组织炎症相对较轻；IFN-γ水平降低，IL-4、IL-10、TGF-β表达升高（P均＜0．05），T-bet蛋白表达降低，GATA-3、FOXP3蛋白表达升高（P均＜0．05）。结论 IL-33能缓解CD小鼠病情，其机制与抑制Th1细胞分化、诱导Th2和Treg细胞产生有关。

克罗恩病是一种病因尚不清楚的胃肠道疾病,近年来我国克罗恩病的发病率呈上升趋势.白介素-33(IL-33)是近期发现的白介素-1(IL-1)家族中的新成员,其受体是ST2,IL-33/ST2途径在机体多种疾病的发病过程中发挥重要作用,越来越多的研究发现其与克罗恩病的发生也有一定的关系.本文简述了IL-33在克罗恩病中的研究发现.

The immune response plays an important role in the occurrence,development and outcome of various diseases.The T-immunoglobulin and mucin-3(Tim-3) is a newly found surface molecule of immune cell type-1 in recent years.It can alter the normal immune function of body,delay or promote the occurrence of related diseases due to its combination with a widely distributive ligand Galectin-9(Gal-9),influencing the orientation,the differentiation tendency and the secretion function of the immune cells,especially Th1 cell. Here is to make a review of the impact of Tim-3/Gal-9 on autoimmune diseases,transplantation immunity, anti-infection immunity and tumor immunity.

Objective To investigate the effect of immature dentritic cell(imDC) on the Crohn's mice models induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS).Methods The mouse were randomly divided into 4 groups:normal group,TNBS group,immature dentritic cell (imDC)group,mature dentritic cell (mDC) group.The other three gourps were administered 50％ ethanol/TNBS vain anus except control group,Each group was injected saline or cells via tail vein before and after administration of anus enema.Control group and TNBS group were injected saline.imDC group was injected imDC.mDC-group was injected mDC.Then we observe the general situation of murine.After one week,the disease activity index (DAI),tissue damage index (TDI) and colon macroscopic damage index (CMDI) were evaluated,the colon level of interleukin-10 (IL-10),transforming growth factor-β (TGF-β) determined by enzyme-linked immunosorbent assay (ELISA).The level of colon forkhead/winged helix protein 3 (Foxp3) protein was determined by Western blotting.Results The scores of DAI,CMDI,TDI in TNBS group were 5.420 ± 0.326,4.923 ± 0.226,7.200 ± 0.851,incresed significantly compared with control group (P＜0.01).And the colon tissue level of IL-10,TGF-β protein were (6.103 ± 1.140),(21.164 ±3.252) ng/L,the relatively expression of protein was 0.439 2 ±0.045 9,decresed significantly compared with crotrol group (P ＜ 0.01).ImDC can significantly decrease the scores of DAI,CMDI,TDI and increse the colon tissue level of IL-10,TGF-β,Foxp3 protein (P ＜0.05).But the mDC increased the scores of DAI,CMDI,TDI and decrese the colon tissue level of IL-10,TGF-β,Foxp3 protein (P ＜ 0.05).Conclusion We succsefully induce Crohn' s mice models by TNBS.And obseve the imDC can significantly inhabit intestinal inflammation in Crohn' s mice models and the mechanism of immune tolerance induced by imDC might be inhibit T lymphocytes responsiveness by regulatory T cells.