[目的]分析血清胰岛素样生长因子-1(IGF-1)和血红素加氧酶-1(HO-1)水平与胃癌患者临床病理特征的相关性.[方法]前瞻纳入符合条件的160例胃癌患者,均于入院时检测血清IGF-1、HO-1水平,记录患者临床病理特征,分析血清IGF-1、HO-1水平与胃癌患者临床病理特征的关系.[结果]Ⅲ～Ⅳ期、合并淋巴结转移的胃癌患者血清IGF-1、HO-1水平分别高于Ⅰ～Ⅱ期及未合并淋巴结转移的患者,差异有统计学意义(P＜0.05);不同发病部位、肿瘤直径、肿瘤分化程度、组织类型、病灶侵袭深度的胃癌患者血清IGF-1及HO-1水平比较,差异无统计学意义(P＞0.05);绘制受试者工作曲线(ROC)发现,胃癌患者入院时血清IGF-1、HO-1水平单项评估及联合评估TNM病理分期、淋巴结转移的曲线下面积(AUC)均＞0.80,均有一定评估预测价值.[结论]胃癌患者血清IGF-1、HO-1水平与患者临床病理特征中TNM病理分期、淋巴结转移有密切关系,并可用作评估和预测指标.

1病例介绍 患者,女,28岁,因腹痛20 d余入院.患者于2020年8月初无明显诱因出现腹痛,以剑突下及脐周疼痛明显,呈持续性胀痛,间断性绞痛,伴恶心、呕吐,呕吐物为胃内容物,停止肛门排气、排便,伴有焦虑、间断四肢肌肉疼痛不适,腹痛加重时更明显.就诊于当地医院,急诊查腹部+盆腔CT未见明显异常,立位腹平片提示不完全性肠梗阻,给予禁食、水,胃肠减压、灌肠、抗炎、补液等治疗,患者逐渐排气、排便,腹痛症状逐渐缓解,复查立位腹平片未见明显异常,于8月20日出院.

目的探讨甲基硒酸(methylseleninic acid,MSA)对胃癌MGC-803细胞增殖、侵袭迁移和凋亡的影响及其相关机制.方法将对数生长期的胃癌MGC-803细胞随机分为对照组、不同浓度(5、10、15 μmol/L)MSA组、抑制剂XAV939组和激活剂SKL2001+MSA组.采用MTT法检测MSA干预MGC-803细胞24、48和72 h后的细胞活力;Transwell小室法检测细胞侵袭、迁移能力;流式细胞术检测细胞凋亡率与周期分布;采用免疫印迹法检测β-联蛋白(β-catenin)、糖原合成酶激酶-3β(glycogen synthase kinase 3β,Gsk-3β)、轴抑制蛋白 2(axis inhibition protein 2,Axin2)的表达水平.结果与对照组相比,不同浓度(5、10、15 μmol/L)MSA组MGC-803细胞活力、S期细胞比例、细胞侵袭、迁移数目和β-联蛋白表达水平均降低(P＜0.05);MGC-803细胞凋亡率、G0/G1期细胞比例、Gsk-3β、Axin2蛋白表达量均增高(P＜0.05),且均呈浓度依赖性;与对照组相比,XAV939组MGC-803细胞活力、S期细胞比例、细胞侵袭、迁移数目和β-联蛋白表达水平均显著降低(P＜0.05),MGC-803细胞凋亡率、G0/G1期细胞比例、Gsk-3β、Axin2蛋白表达水平均显著增高(P＜0.05);与MSA组相比,激活剂SKL2001+MSA组MGC-803细胞活力、S期细胞比例、细胞侵袭、迁移数目和β-联蛋白表达水平均增高(P＜0.05),MGC-803细胞凋亡率、G0/G1期细胞比例、Gsk-3β和Axin2蛋白表达水平均降低(P＜0.05).结论MSA可通过Wnt/β-catenin信号通路抑制胃癌细胞增殖、侵袭和迁移,并诱导其凋亡.

目的 探讨蔓荆子黄素对结直肠癌细胞增殖、周期和凋亡的影响及其可能的调控机制.方法(1)体外培养SW480细胞,采用不同浓度(0、10、20、40μmol/L)的蔓荆子黄素处理后,检测细胞活力、细胞周期和凋亡情况,以及细胞周期蛋白(p21、c-myc)、凋亡相关蛋白[B细胞淋巴瘤-2(Bcl-2)蛋白、Bcl-2相关X蛋白(Bax)]表达水平.同时检测经0μmol/L、40μmol/L的蔓荆子黄素处理后的SW480细胞的泛素样修饰物激活酶2(UBA2)蛋白和mRNA表达水平.(2)另取SW480细胞,分别转染阴性对照小干扰RNA(siRNA)(si-NC组)、UBA2 siRNA转染(si-UBA2组);另取SW480细胞,分别转染空载质粒载体(蔓荆子黄素+vector组)和UBA2过表达质粒载体(蔓荆子黄素+UBA2组)6 h后,加入40μmol/L蔓荆子黄素处理24 h.检测各组细胞活力、细胞周期和凋亡情况,以及细胞周期蛋白、凋亡相关蛋白、UBA2蛋白表达水平.结果 (1)与0μmol/L蔓荆子黄素相比,其他浓度蔓荆子黄素干预后,SW480细胞的活力、S期细胞比例下降,细胞凋亡率、G0/G1期细胞比例增加,p21、Bax蛋白相对表达水平上调,c-myc、Bcl-2蛋白相对表达水平下调(均P<0.05).与0μmol/L蔓荆子黄素相比,40μmol/L蔓荆子黄素干预后SW480细胞中的UBA2 mRNA和蛋白表达均下调(均P<0.05).(2)与si-NC组相比,si-UBA2组的细胞活力、S期细胞比例降低,凋亡率、G0/G1期细胞比例增加,c-myc蛋白、Bcl-2蛋白、UBA2蛋白相对表达水平下调,p21蛋白和Bax蛋白相对表达水平上调(均P<0.05).而转染UBA2过表达质粒载体后给予蔓荆子黄素干预,蔓荆子黄素+UBA2组SW480细胞中上述指标均逆转(均P<0.05).结论 蔓荆子黄素可以抑制结直肠癌细胞的增殖,阻滞细胞周期,并促进细胞凋亡,其作用机制可能与下调UBA2有关.

目的 探讨Pokemon、TIP30和人宫颈癌基因-1(HCCR-1)在直肠癌组织中的表达及预后的关系.方法 纳入100例2016年6月至2018年6月本院收治的直肠癌患者,收集术中切取的100份直肠癌组织及癌旁组织.采用免疫组织化学方法检测Pokemon、TIP30及HCCR-1蛋白的表达水平.比较Pokemon、TIP30及HCCR-1不同表达水平患者临床资料的差异.对患者进行随访2年,采用多元Logistic回归分析影响直肠癌患者预后生存的危险因素,绘制Kaplan-Meier生存曲线,研究Pokemon、TIP30及HCCR-1蛋白表达情况对直肠癌患者预后生存的影响.结果 直肠癌组织中Pokemon、HCCR-1蛋白表达水平显著高于癌旁组织,而TIP30蛋白表达水平显著低于癌旁组织,差异有统计学意义(P<0.05);年龄、性别、局部浸润程度与直肠癌患者组织Pokemon、TIP30及HCCR-1蛋白表达无相关(P>0.05),但Dukes分期、淋巴结转移与Pokemon、HCCR-1蛋白表达呈正相关,而组织分化程度与TIP30蛋白表达呈负相关(P<0.05);100例直肠癌患者2年生存率为43.00％(43/100).Dukes分期、淋巴结转移、分化程度、Pokemon高表达、TIP30低表达及HCCR-1高表达为影响直肠癌患者预后生存的独立危险因素(P<0.05).Pokemon、HCCR-1蛋白低表达组平均生存时间显著长于高表达组,TIP30蛋白高表达组平均生存时间显著长于低表达组,差异有统计学意义(P<0.05).结论 Pokemon、HCCR-1、TIP30与在直肠癌患者组织中密切相关,可作为预测直肠癌患者预后的分子标志物和肿瘤治疗的潜在靶点.

目的 探讨环状RNA叉头框蛋白O3(circFOXO3)靶向微小RNA(miRNA)-122-5 p对结直肠癌细胞恶性生物学行为的影响.方法 (1)选取38例结直肠癌患者结直肠癌组织、癌旁组织,采用实时定量PCR法检测结直肠癌组织、癌旁组织中circFOXO3、miRNA-122-5p的表达水平,并分析结直肠癌组织中circFOXO3与miRNA-122-5p表达水平的相关性.(2)取人结直肠癌细胞HCT116分为6组并给予相应干预,包括si-NC组(转染si-NC)、si-circFOXO3组(转染si-circFOXO3)、miRNA-NC组(转染miRNA-122-5p-NC)、miRNA-122-5p组(转染miRNA-122-5 p模拟物)、si-circFOXO3+抗miRNA-NC组(共转染si-circFOXO3与抗miRNA-122-5 p-NC)、si-circFOXO3+抗miRNA-122-5p组(共转染si-circFOXO3与抗miRNA-122-5p).分别采用细胞计数法、平板克隆形成实验、Transwell小室实验检测人结直肠癌细胞HCT116的增殖、克隆形成、迁移及侵袭能力,采用蛋白质印迹法检测基质金属蛋白酶(MMP)-2、MMP-9蛋白表达水平.(3)通过生物信息学数据库starBase预测circFOXO3的靶基因,通过双荧光素酶报告基因实验检测circFOXO3与miRNA-122-5 p的靶向关系.结果(1)与癌旁组织相比,结直肠癌组织中的circFOXO3表达水平升高,miRNA-122-5p表达水平降低,结直肠癌组织中的circFOXO3与miRNA-122-5p表达水平呈负相关(均P<0.05).(2)与si-NC组比较,si-circFOXO3组的miRNA-122-5p表达水平升高,细胞活力降低,克隆形成数、迁移及侵袭细胞数减少,MMP-2、MMP-9蛋白表达水平降低(均P<0.05).与miRNA-NC组比较,miRNA-122-5p组的细胞活力降低,克隆形成数、迁移及侵袭细胞数均减少,MMP-2、MMP-9蛋白表达水平降低(均P<0.05).与si-circFOXO3+抗miRNA-NC组比较,si-circFOXO3+抗miRNA-122-5p组的细胞活力升高,克隆形成数、迁移及侵袭细胞数均增多,MMP-2、MMP-9蛋白表达水平升高(均P<0.05).(3)circFOXO3与miRNA-122-5p存在结合位点,转染miRNA-122-5p模拟物可明显降低野生型载体WT-circFOXO3的荧光素酶活性(P<0.05),而对突变型载体MUT-circFOXO3的荧光素酶活性无明显影响(P>0.05).结论 干扰circFOXO3的表达可通过靶向调控miRNA-122-5 p从而抑制结直肠癌细胞增殖、克隆形成、迁移及侵袭能力.

目的:分析嗜酸性胃肠炎的临床特及诊治方法,建设误诊误治.方法:回顾性分析我院收治的15例误诊为其他疾病的嗜酸性胃肠炎的临床资料,并复习相关文献.结果15例给予药物治疗(醋酸泼尼松40mg),患者临床症状消失,大便成形,血常规示嗜酸性粒细胞正常.结论:嗜酸性肠炎临床表现多样,缺乏特异性,故缺乏经验的首诊医生容易漏诊.

目的:探讨circ_0000515调控结肠癌细胞增殖和凋亡的分子机制.方法:选取41例结肠癌病人癌组织及癌旁组织标本,用实时荧光定量PCR(RT-qPCR)检测circ_0000515和miR-1258的表达水平;结肠癌细胞SW620分为si-circ_0000515组、si-NC组、miR-1258组、miR-NC组、si-circ_0000515+anti-miR-NC组、si-circ_0000515+anti-miR-1258组.四甲基偶氮唑盐比色法(MTT)检测SW620细胞活性;流式细胞术检测SW620细胞凋亡;双荧光素酶报告实验检测circ_0000515和miR-1258的靶向关系.结果:与癌旁组织比较,结肠癌组织中circ_0000515表达水平升高,miR-1258表达水平降低(P<0.01).抑制circ_0000515表达或过表达miR-1258,SW620细胞活性降低,SW620细胞的凋亡率升高(P<0.01).circ_0000515靶向调控miR-1258;干扰miR-1258表达逆转了抑制circ_0000515表达对结肠癌SW620细胞增殖和凋亡的作用.结论:抑制circ_0000515表达通过靶向上调miR-1258抑制结肠癌细胞增殖,促进凋亡.

目的:比较用埃索美拉唑与奥美拉唑对存在幽门螺杆菌(Hp)感染的十二指肠溃疡患者进行治疗的临床效果.方法:将2017年1月至2019年1月期间保定市第82集团军医院消化内科收治的100例存在Hp感染的十二指肠溃疡患者按照治疗方法的不同分为埃索美拉唑组(n=50)与奥美拉唑组(n=50).对两组患者进行常规治疗的同时,分别加用埃索美拉唑与奥美拉唑对埃索美拉唑组患者与奥美拉唑组患者进行治疗,然后比较两组患者的临床疗效、Hp的根除率及其不良反应的发生率.结果:埃索美拉唑组患者治疗的总有效率高于奥美拉唑组患者,治疗后其Hp的根除率高于奥美拉唑组患者,P<0.05.用药期间,两组患者不良反应的发生率相比,P>0.05.结论:对存在Hp感染的十二指肠溃疡患者进行常规治疗的同时,加用埃索美拉唑对其进行治疗的效果优于加用奥美拉唑对其进行治疗的效果,能更有效地改善其临床症状,提高其Hp的根除率.

目的 观察胃癌组织赖氨酸特异性脱甲基酶2B(KDM2B)的表达情况及与预后的相关性.方法 采用回顾性研究方法,选取2018年6月至2019年6月河北保定市解放军第八十二集团军医院收治的118例胃癌患者,采集患者的胃癌组织标本,采用免疫组织化学法对胃癌组织中的KDM2 B表达情况进行检测,分析其与患者临床指标及预后的相关性.结果 KDM2B在胃癌组织中表达占57.63％(68/118),与对照组胃黏膜的10.00％(5/50)比较,差异具有统计学意义(P<0.05).多因素Cox回归分析显示,患者组织学分型、淋巴结状态、TNM分期以及人表皮生长因子受体2(HER2)表达情况与KDM2B阳性表达密切相关;KDM2B阳性表达组5年生存率为22.06％(18/68),显著低于KDM2B阴性表达组的52.0％(26/50),差异具有统计学意义(P<0.05);KDM2B阳性表达组中位生存期为16个月,低于KDM2B阴性表达组的56个月,差异具有统计学意义(P<0.05).结论 KDM2B在胃癌形成及发展中有着重要的参与作用,其表达与患者预后密切相关,应给予临床关注.

慢传输型便秘(solw transit constipation, STC)属于功能性便秘中较为顽固的一种,由结肠传输功能障碍、肠内容物传输缓慢等原因所引起,主要表现为排便次数减少、大便干硬、排便费力,具有病程长、治疗效果欠佳的特点.尤其老年患者,其病程相对较长,并多长期应用缓泻剂,增加了发生结肠黑便病的风险,且极易诱发各种脑血管意外[1].我科采用结肠水疗仪并联合口服双歧三联活菌胶囊对老年慢传输型便秘患者进行治疗,取得满意效果,现报道如下.

Objective To investigate the expression and significance of human cervical canceroncogene (HCCR-1) protein in colon carcinoma,colon adenoma and normal colon mucosa.Methods Immunohistochemistry and real-time fluorescent quantitative polymerase chain reaction (FQ-PCR) were used to detect the location and expression of HCCR-1 in the 80 colon adenoma samples,30 colon carcinoma,20 normal colon mucosa.Results The positive expression rate of HCCR-1 protein in normal colorectal mucosa,colorectal adenoma and colorectal carcinoma tissues were 10.00％,62.50％,100.00％,respectively,with significant differences among them(P =0.001).The positive expression rate of HCCR-1 protein in tubular adenoma,mixed pattern of adenoma and villous adenoma were 46.70％,66.70％,80.00％,respectively,with significant differences among them(P =0.015).FQ-PCR showed that the HCCR-1 mRNA expression in normal colorectal mucosa,tubular adenoma,mixed pattem of adenoma,villous adenoma and colorectal carcinoma tissues were 0.609 2 ± 0.326 1,4.034 6 ± 1.188 4,12.353 4 ± 2.828 0,22.563 7 ± 78.952 0,43.202 9 ± 7.675 4.Conclusion HCCR-1 is correlated with canceration of colorectal adenoma and the development of colorectal carcinoma.

Objective To explore the expression of calcium channel activated protein 43 (Cap43) in normal colorectal mucosa,colorectal adenoma and colorectal carcinoma,and to analyze the relationships among different histological types of colorectal adenomas and colorectal carcinoma.Methods Immunohistochemistry was used to exzamine the location and expression of Cap43 in the colorectal tissues,colorectal carcinoma tissues and colorectal carcinoma tissues.Real-time fluorescent quantitative polymerase chain reaction (FQ-PCR) was used to detect Cap43 mRNA expression.Results The positive expression rate of Cap43 in normal colorectal mucosa,colorectal colorectal adenoma and and carcinoma tissues was 31.7％,63.8％ and 91.7％ respectively,with significant differences among them (P =0.000).The positive expression rate of Cap43 in tubular adenoma,mixed pattern of adenoma,and villous adenoma was 52.5％,60.0％ and 90.0％ respectively,also with significant differences among them (P =0.016).The Cap43 mRNA expression of the colorectal carcinoma,villous adenoma,the mixed pattern of adenoma,tubular adenoma,and normal colorectal mucosa was 19.552 ± 6.338,13.018 ± 2.417,7.323 ± 2.131,3.660 ± 1.309,and 1.119 ± 0.871 respectively (F =25.943,P =0.028).Conclusion Cap43 is correlated with canceration of colorectal adenoma and the development of colorectal carcinoma.Detecting the expression of Cap43 can evaluate the progression of colorectal adenoma and the development of colorectal carcinoma.Cap43 may be the molecular biological indicator for predicting canceration of colorectal adenoma.

Objective To investigate the expression and significance of Ezrin protein in normal colon mucosa, colorectal adenoma and colorectal carcinoma.Methods Eighty colorectal adenoma samples of different pathological types were removed by endoscope in gastroenterology endoscopy center of PLA 252nd Hospital from January 2013 to December 2014, including 30 cases of tubular adenoma, 30 cases of tubulovillous adenoma, and 20 cases of villous adenoma.30 cases of colorectal carcinoma specimens and 30 cases of pericarcinous tissue specimens that were surgically removed in PLA 252nd Hospital were also obtained.The immunohistochemistry was used to detect the expression of Ezrin protein in the sections of tissues, and polymerase chain reaction (PCR) was used to detect the expression level of Ezrin mRNA.Results The positive expression rate of Ezrin protein in normal mucosa group, colorectal adenoma group and colorectal carcinoma group was 6.7%, 52.5% amd 86.7%, respectively with the difference being statistically significant among them (P=0.000).The positive expression rate of Ezrin in tubular adenoma group, tubulovillous adenoma group and villous adenoma group was 33.3%, 60.0% and 70.0% respectively, with the difference being significant among them (P=0.023).The Ezrin mRNA expression in the colorectal carcinoma, villous adenoma, the mixed pattern of adenoma, tubular adenoma and normal colorectal mucosa was 16.466±3.233, 9.778±0.820, 5.966±0.571, 3.043±1.053 and 0.688±0.351 respectively (F=73.628,P=0.017).SNK multiple comparisons displayed that the differences about any two groups of the total mean showed statistical significance.Conclusion The expression of Ezrin may promote proliferation and malignant transformation of colorectal adenoma.

Objective To explore the expression of minichromosome maintenance protein 2 (MCM2) in normal colorectal mucosa, colorectal adenomas and colorectal carcinoma, and to analyze the relationships among different histological types of colorectal adenomas and colorectal carcinoma.Methods Immunohistochemistry was used to exzamine the location and expression of MCM2 in the colorectal tissues, colorectal adenoma tissues and colorectal carcinoma tissues.Real-time fluorescent quantitative polymerase chain reaction (FQ-PCR) was used to detect MCM2 mRNA and connexin-32 mRNA expression.Results (1) Immunohistochemistry: The positive expression rate of MCM2 protein in normal colorectal mucosa, colorectal adenoma and colorectal carcinoma tissues was 16.7%, 55.0% and 80.0% respectively, with significant differences among them (P=0.031).The positive expression rate of MCM2 in tubular adenoma, mixed pattern of adenoma and villous adenoma was 40.0%, 65.0% and 75.0% respectively, also with significant differences among them (P=0.022).(2) FQ-PCR: The MCM2 mRNA expression in the normal colorectal mucosa, tubular adenoma, the mixed pattern of adenoma, villous adenoma, and colorectal carcinoma was 1.187±0.923, 4.126±1.339, 9.577±0.838, 22.150±4.077 and 48.020±4.811, respectively.The expression of MCM2 gradually increased in colorectal carcinoma, villous adenoma, the mixed pattern of adenoma, tubular adenoma, and normal colorectal mucosa (F=55.512,P=0.029).SNK multiple comparisons displayed that the differences about any two groups of the total mean showed statistical significance.Conclusion MCM2 is correlated with canceration of colorectal adenoma and the development of colorectal carcinoma.Detecting the expression of MCM2 can evaluate the progression of colorectal adenoma and the development of colorectal carcinoma.They may be the molecular biological indicators for predicting canceration of colorectal adenoma.

Objective To explore the expression of protease activated receptor 3 (PAR3) and protease activated receptor 4 (PAR4) in the progression from colorectal polyps to cancer.Methods In this study,five groups of specimens were researched:primary colorectal cancer group (n =30),matched normal colorectal tissues group (taken 5 cm away from the tumour) (n =30),tubular adenoma group (n =30),villous adenoma group (n =20),and adenoma mixed group (n =30).The protein and mRNA levels of PAR3 and PAR4 were detected by immunohistochemistry and real-time fluorescent quantitative polymerase chain reaction (FQ-PCR) respectively.Results The positive expression rate of PAR3 protein in normal colorectal mucosa,colorectal adenoma and colorectal carcinoma tissues was 73.3％,50.0％and 6.7％ respectively,with significant differences among them (P =0.009).The positive expression rate of PAR4 protein in these groups was 6.7％,35.0％ and 70.0％ respectively.FQ-PCR showed that the expression of PAR3 mRNA in normal colorectal mucosa,tubular adenoma,mixed pattern of adenoma,villous adenoma and colorectal carcinoma was 0.787 ± 0.040,0.453 ± 0.023,0.410 ± 0.050,0.368 ±0.032 and 0.259 ± 0.017,P =0.0l 1;and that of PAR4 mRNA in these groups was 0.370 ± 0.301,10.384 ± 1.474,20.892 ± 4.485,36.311 ± 7.953,52.083 ± 12.550 (F =43.342,P =0.009,respectively).Conclusion These results suggested PAR3 and PAR4 may play a role in the development of colorectal cancer.

Objective To explore the expression of human runt-related transcription factor 3 (RUNX3) in the progression from colorectal polyps to cancer.Methods In this study, five groups of specimens were researched: primary colorectal cancer group (n=30), matched normal colorectal tissues group (5 cm away from the tumour, n=30), tubular adenoma group (n=30), villous adenoma group (n=20), and adenoma mixed group (n=30).The protein and mRNA levels of RUNX3 were detected by immunohistochemistry and real-time fluorescent quantitative polymerase chain reaction (FQ-PCR) respectively.Results The positive expression rate of RUNX3 protein in normal colorectal mucosa, colorectal adenoma and colorectal carcinoma tissues was 96.7%, 73.8% and 46.7% respectively, with significant differentces among them (P=0.015).FQ-PCR showed that the expression of RUNX3 mRNA in normal colorectal mucosa, tubular adenoma, mixed pattern of adenoma, villous adenoma and colorectal carcinoma was 33.930 7±8.570 9, 16.459 1±3.383 7, 7.901 2±2.081 6, 3.714 6±1.710 9, and 0.871 5±0.523 1 respectively, F=47.859, P=0.021.Conclusion These results suggested RUNX3 may play a role in the development of colorectal cancer.

Objective To explore the expression of connexin 32 in normal colorectal mucosa,colorectal adenomas and colorectal carcinoma,and to analyze its relationships with different histological types of colorectal adenomas and colorectal carcinoma.Methods Immunohistochemistry was used to exzamine the location and expression of connnexin 32 in the colorectal tissues,colorectal carcinoma tissues and colorectal carcinoma tissues.Real-time fluorescent quantitative polymerase chain reaction (FQ-PCR) was used to detect connexin 32 mRNA expression.Results There was a significant correla tion between up-regulated expression of connexin 32 and unfavorable variables,including nodal metastasis,Dukes stage and differentiation degree (P =0.032).There was no obvious difference in age and sex (P =0.061).The positive expression rate of connexin 32 protein in normal colorectal mucosa,colorectal adenoma and colorectal carcinoma tissues was 66.7％,36.2％ and 5.0％ respectively,with significant differences among them (P =0.000).The positive expression rate of connexin 32 protein in tubular adeno ma,mixed pattern of adenoma and villous adenoma was 47.5％,35.0％ and 15.0％ respectively,with significant differences among them (P =0.047).FQ-PCR showed that the expression of connexin 32 gradually decreased in normal colorectal mucosa,tubular adenoma,mixed pattern of adenoma,villous ade noma and colorectal carcinoma (P =0.006).Conclusion Connexin 32 is correlated with canceration of colorectal adenoma and the development of colorectal carcinoma.Detecting the expression of connexin 32 can evaluate the progression of colorectal adenoma and the development of colorectal carcinoma.

Objective The aim of this study is to detect the expression levels of Tat interacting protein 30 (TIP30) in colorectal carcinoma,colorectal adenomas,normal colorectal mucosa,and analyze the relationships among different histological types of colorectal adenomas and colorectal carcinoma.Methods We collected 60 colorectal carcinoma tissues,40 normal colorectal mucosa tissues,80 colorectal adenomas.Immunohistochemistry and fluorescence quantitative polymerase chain reaction (PCR) were used to detect the expression of TIP30 in the tissues.Results The results of the immunohistochemistry were that the positive expression rates of TIP30 in normal colorectal mucosa,colorectal adenoma and colorectal carcinoma tissues were 95.0％,67.5％,30.0％,respectively,with significant differences among them (P =0.000).The positive expression rates of TIP30 in tubular adenoma,mixed pattern of adenoma,villous adenoma were 86.7％,66.7％,40.0％,respectively,also with significant differences among them (P =0.003).There was a significant correlation between reduced expression of TIP30 and unfavorable variables,including nodal metastasis (P =0.024),Dukes stage (P =0.008),differentiation degree (P =0.015).There was no obvious difference in age (P =0.815) and sex (P =0.955).Fluorescence quantitative PCR showed characterized amplification about TIP30.The expression of TIP30 mRNA in normal colorectal mucosa,tubular adenoma,mixed pattern of adenoma,villous adenoma and colorectal carcinoma were 25.135 ±1.474,18.701 ±1.596,12.412 ±1.677,6.579 ±0.795,2.137 ±0.535,respectively,F =250.931,P =0.015.Conclusion TIP30 may participate in the inhibition of the occurrence and development of colorectal adenoma and colorectal carcinoma.

目的 分析胃异位胰腺的超声内镜特点及内镜下黏膜剥离术(endoscopic submucosal dissection,ESD)治疗,以提高对该病的诊治水平.方法 对10例超声内镜诊断为胃异位胰腺的患者资料进行回顾性分析,总结胃异位胰腺的临床特点,评估超声内镜与病理诊断的符合情况,并行ESD治疗.结果 10例患者均经ESD完整切除肿瘤,术后均无出血及穿孔发生.术后病理证实10例均为异位胰腺,与超声内镜符合率100％.肿瘤完整切除率100％.术后随访6～36个月,患者均未见复发.结论 胃镜及超声内镜是诊断胃异位胰腺的重要手段,行ESD治疗效果确切,较为安全.