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| 1 | Primary adenocarcinomas of lower esophagus,esophagogastric junction and gastric cardia:in special reference to China显示文摘Gastric cardia adenocarcinoma (GCA) is an under-studied subject. The pathogenesis, molecular changes in the early stage of carcinogenesis and related risk factors have not been well characterized. There is evidence, however, that GCA differs from cancer of the rest of the stomach in terms of natural history and histopathogenesis. Adenocarcinomas of the lower esophagus, esophagogastric junction (EGJ)and gastric cardia have been given much attention because of their increasing incidences in the past decades, which is in striking contrast with the steady decrease in distal stomach adenocarcinoma. In China, epidemiologically, GCA shares very similar geographic distribution with esophageal squamous cell carcinoma (SCC), especially in Linzhou (formerly Linxian County), Henan Province, North China,the highest incidence area of esophageal SCC in the world.Historically, both GCA and SCC in these areas were referred to as esophageal cancer (EC) by the public because of the common syndrome of dysphagia. In Western countries,Barrett's esophagus is very common and has been considered as an important precancerous lesion of adenocarcinoma at EGJ. Because of the low incidence of Barrett's esophagus in China, it is unlikely to be an important factor in early stage of EGJ adenocarcinoma development.However, Z line up-growth into lower esophagus may be one of the characteristic changes in these areas in early stage of GCA development. Whether intestinal metaplasia (IM) is a premalignant lesion for GCA is still not clear. Higher frequency of IM observed at adjacent GCA tissues in Henan suggests the possibility of IM as a precancerous lesion for GCA in these areas. Molecular information on GCA,especially in early stage, is very limited. The accumulated data about the changes of tumor suppressor gene, such as p53 mutation, and ontogeny, such as C-erbB2, especially the similar alterations in GCA and SCC in the same patient,indicated that there might be some similar risk factors,such as nitrosamine, involved in both GCA and SCC in Henan population. The present observations also suggest that GCA should be considered as a distinct entity. | Li-DongWang ShuZheng Zuo-YuZheng AlanG.Casson | 2003 | World Journal of Gastroenterology2003，9，6： | 66 |
| 2 | Expression of survivin in human gastric carcinoma and gastric carcinoma model of rats显示文摘AIM: To study the expression of survivin, an inhibitor of apoptosis protein, in human gastric carcinomas and gastric carcinoma models of rats.METHODS: With the method of immunohistochemical staining, we studied the expression of survivin in 20 cases of chronic gastritis and 56 cases of gastric carcinomas. We used N-methyl-N′-nitro-N-nitrosoguanidine (MNNG) and high dose sodium-chloride diet to induce rat gastric carcinomas. Survivin expression was studied in glandular stomachs of normal rats, adenocarcinomas and tissues adjacent to the tumor, as well as in rats during the induction period.RESULTS: Survivin was expressed in 27 of 56 (48.2 %)cases of human gastric carcinoma tissues and 1 of 20 (5 %)cases of chronic gastritis. It was found that the expression of survivin had no relation with the elements of age, tumor depth, tumor size, and disease stage, but was significantly related to histological type. The positive rate of survivin expression in cases of intestinal type was significantly higher than that in cases of diffuse type (P<0.05). In animal experiments, survivin expression in glandular stomachs of normal rats, of rats in middle induction period, in adenocarcinomas and tissues adjacent to tumor were 0,40.0 %, 78.3 % and 38.9 %, respectively. Compared with the survivin expression in normal rats, the differences were significant.CONCLUSION: These data imply that survivin plays an important role in the onset of gastric carcinoma and that high survivin expression is an early event of gastric carcinoma. | Xiao-DonclZhu, Geng-JinLin, Li-PingQian Zhong-QingChen | 2003 | World Journal of Gastroenterology2003，9，7： | 39 |
| 3 | Inhibition of human telomerase in MKN-45 cell line by antisense hTR expression vector induces cell apoptosis and growth arrest显示文摘AIM: To investigate the effects of antisense humantelomerase RNA (hTR) on the biologic behavior of humangastric cancer cell line: MKN-45 by gene transfection and itspotential role in the gene therapy of gastric cancer.METHODS: The hTR cDNA fragment was cloned from MKN-45 through RT-PCR and subcloned into eukaryoticexpression vector (pEF6/V5-His-TOPO) in cis-direction ortrans-direction by DNA recombinant methods. Theconstructed sense, antisense and empty vectors weretransfected into MKN-45 cell lines separately by lipofectin-mediated DNA transfection technology. After drugselection, the expression of antisense hTR gene in stabletransfectants and normal MKN-45 cells was detected by RT-PCR, the telomerase activity by TRAP, the apoptoticfeatures by PI and Hoechst 33258 staining, the cell cycledistribution by flow cytometry and the population doublingtime by cell counting. Comparison among the stabletransfectants and normal MKN-45 cells was made.RESULTS: The sense, antisense hTR eukaryotic expressionvectors and empty vector were successfully constructed andproved to be the same as original design by restrictionendonuclease analysis and sequencing. Then, they weresuccessfully transfected into MKN-45 cell lines separatelywith lipofectin. The expression of antisense hTR gene wasonly detected in MKN-45 cells stably transfected withantisense hTR vector (named as MKN-45-ahTR) but not inthe control cells. In MKN-45-ahTR, the telomerase activitywas inhibited by 75 %, the apoptotic rate was increased to25.3 %, the percentage of cells in the G0/G1 phase wasincreased to 65 %, the proliferation index was decreased to35 % and the population doubling time was prolonged to 35.3hours. However, the telomerase activity, the apoptotic rate,the distribution of cell cycle, the proliferation index and thepopulation doubling time were not different among the controlcells.CONCLUSION: Antisense hTR can significantly inhibittelomerase activity and proliferation of MKN-45 cells andinduce cell apoptosis. Antisense gene therapy based onteiomerase inhibition can be a potential therapeuticapproach to the treatment of gastric cancer. | FengRH ZhuZG 等 | 2002 | World Journal of Gastroenterology2002，8，3： | 31 |
| 4 | Effects of p53 on apoptosis and proliferation of hepatocellular cardnoma cells heated with transcatheter arterial chemoembolization显示文摘AIM:To evaluate the effects of p53 on apoptosis and proliferation of hepatocellular carcinoma (HCC) cells treated with transcatheter arterial chemoernbolization (TACE).METHODS: A total of 136 patients with HCC received TACE and other management before surgery were divided into TACE group and non-TACE group.TACE group included 79 patients who had 1-5 courses of TACE before surgery,of them,11 patients had 1-4 courses of chemotherapy (group A),33 patients had 1-5 courses of chemotherapy combined with iodized oil (group B), 23 patients had 1-3 courses of chemotherapy,iodized oil and gelatin sponge (group C),12 patients had 1-3 courses of chemotherapy combined with iodized oil,ethanol and gelatin sponge (group D).Non-TACE group included the remaining 57 patients who had surgery only.The extent of apoptosis was analyzed by transferase mediated dUTP nick end labeling (TUNEL) staining.The expressions of p53, Bcl-2,Bax,Ki-67 and PCNA protein were detected by immunohistochemical method.RESULTS: P53 protein expressions in trabecular and clear cells in HCC specimens were significantly lower than that in pseudoglandar, solid, poorly differentiated or undifferentiated and sclerosis HCC (P<0.05) Expression of p53 protein in HCC cells increased with the increase of pathological grades(P<0.05),and correlated positively with expressions of Ki-67 and PCNA protein,and negatively with Bcl-2 to Bax protein expression rate and AI (P<0.05).Expression of p53 protein was significantly higher in group A than in groups B, C, D and the non-TACE group, and was higher in group B than in groups C and D,and lower in group D than in the non-TACE group (P<0.05).CONCLUSION:Expression of p53 protein can enhance proliferation of HCC cells and suppress apoptosis of HCC cells after TACE. | En-HuaXiao Jing-QingLi Jie-FuHuang | 2004 | World Journal of Gastroenterology2004，10，2： | 26 |
| 5 | 幽门螺杆菌感染与胃癌前病变演化的关系显示文摘目的:了解幽门螺杆菌(Helicobacterpylori,Hp)长期感染是否促进胃黏膜肠上皮化生和异型增生的形成与发展,评价5a随访根除Hp感染对胃癌前病变的作用并探讨其机制.方法:采用前瞻性队列研究方法,对首次胃镜检查诊断为慢性胃炎而不伴有肠上皮化生和异型增生的患者作为入选病例,入选时Hp阳性患者80例,Hp阴性者30例.Hp阳性患者根据自愿原则采用根除Hp治疗或采用对照治疗.全部病例跟踪随访5a.并采用脱氧核糖核酸末端转移酶介导的缺口末端标记(TUNEL)技术及免疫组织化学染色对Hp阳性患者Hp根除前后及Hp阴性者胃黏膜上皮细胞凋亡和增生情况进行原位观察和比较.结果:Hp阳性观察组肠上皮化生的发生率(32.6%)显著高于Hp阴性对照组(12.0%,χ2=4.147,3.893,P<0.05)和Hp根除观察组(12.9%,χ2=3.869,P<0.05).Hp阳性观察组异型增生的发生率(19.6%)显著高于Hp阴性对照组(4.0%,χ2=3.893,P<0.05).Hp根除观察组肠上皮化生和异型增生的发生率与Hp阴性对照组无统计学差异.Hp阳性患者胃黏膜上皮细胞凋亡指数及PCNA指数(12.7%,14.6%)均显著高于Hp阴性患者(2.9%,8.0%,t=7.241,6.368,P<0.01),Hp根除后胃黏膜上皮细胞PCNA指数和凋亡指数(14.3%,12.9%)均显著下降(9.2%,3.6%,t=5.642,7.410,P<0.01),而Hp未根除者上述指标则无显著性变化.结论:Hp感染可能通过刺激胃黏膜上皮细胞凋亡与增生的调节紊乱,使胃黏膜的不稳定性增加,促进胃黏膜肠上皮化生和异型增生的形成与发展,从而增加患胃癌的危险性.根除Hp感染能明显降低肠上皮化生和异型增生的发生率. | 刘海峰 刘为纹 房殿春 王国安 滕小春 | 2002 | 世界华人消化杂志2002，10，8： | 24 |
| 6 | 辽宁省庄河地区胃癌高发现场高危人群综合防治研究显示文摘 | 袁媛 | 2005 | 中国肿瘤2005，14，5： | 18 |
| 7 | Construction of hpaA gene from a clinical isolate of Helicobacter pyloriand identification of fusion protein显示文摘AIM: To clone hpaA gene from a clinical strain of Helicobacter pylori and to construct the expression vector of the gene and to identify immunity of the fusion protein.METHODS: The hpaA gene from a clinical isolate Y06 of H.pylori was amplified by high fidelity PCR. The nucleotide sequence of the target DNA amplification fragment was sequenced after T-A cloning. The recombinant expression vector inserted with hpaA gene was constructed. The expression of HpaA fusion protein in E. coli BL21DE3 induced by IPTG at different dosages was examined by SDS-PAGE.Western blot with commercial antibody against whole cell of H. pylorias well as immunodiffusion assay with selfprepared rabbit antiserum against HpaA fusion protein were applied to determine immunity of the fusion protein. ELISA was used to detect the antibody against HpaA in sera of 125 patients infected with H. pylori and to examine HpaA expression of 109 clinical isolates of H. pylori.RESULTS: In comparison with the reported corresponding sequences, the homologies of nucleotide and putative amino acid sequences of the cloned hpaA gene were from 94.25-97.32 % and 95.38-98.46 %, respectively. The output of HpaA fusion protein in its expression system of pET32ahpaA-BL21DE3 was approximately 40 % of the total bacterial proteins. HpaA fusion protein was able to combine with the commercial antibody against whole cell of H. pyloriand to induce rabbit producing specific antiserum with 1:4immunodiffusion titer after the animal was immunized with the fusion protein. 81.6 % of the serum samples from 125patients infected with H.pylori(102/125) were positive for HpaA antibody and all of the tested isolates of H.pylori(109/109) were detectable for HpaA.CONCLUSION: A prokaryotic expression system with high efficiency of H.pylorihpaA gene was successfully established.The HpaA expressing fusion protein showed satisfactory immunoreactivity and antigenicity. High frequencies of HpaA expression in different H. pyloriclinicalstrains and specific antibody production in H. pyloriinfected patients indicate that HpaA is an excellent and ideal antigen for developing H. pylori vaccine. | Ya-Fei Mao Jie Yan Li-Wei Li Shu-Ping Li Department of Medical Microbiology and Parasitology,College of Medical Sciences,Zhejiang University,Hangzhou 310031,Zhejiang Province,China | 2003 | World Journal of Gastroenterology2003，9，7： | 17 |
| 8 | Apoptosis-inducing effect of recombinant Caspase-3 expressed by constructed eukaryotic vector on gastric cancer cell line SGC7901显示文摘AIM: To investigate the apoptosis-inducing effect of Caspases-3 expressed by constructed eukaryotic vector on gastric cancer cell line SGC7901.METHODS: PCR was employed to amplify the sequences of both small and large subunits of Caspases-3. Its products were separately cloned into the Sma I site of pBluescript KS+ to generate both plasmids pBS/SS and pBS/LS. The small subunit fragment was excised from plasmid pBS/SS with BarrH- I and then inserted into the BarnH I site of plasmid pBS/LS preceding that of the large subunit to yield plasmid pBS/Rev-Caspase-3. Rev-Caspase-3 cDNA was excised with Kpn Ⅰ+Xba I and then subcloned into plasmid pcDNA3.1(+) to construct Rev-Caspase-3 eukaryotic expression vector pcDNA/Rev-Caspase-3, which was used to transiently transfect SGC7901 cell line. Cell count, MTT assay and electron microscopy were used to confirm the antiproliferation and apoptosis-inducing effect of Rev-Caspase-3 expression on gastric cancer cells.RESULTS: Plasmid pBS/Rev-Caspase-3 and eukaryotic expression vector pcDNA/Rev-Caspase-3 were successfully constructed. SGC7901 cells were transiently transfected by either pcDNA/Rev-Caspase-3 or pcDNA3.1 (+) for 24, 48,72, and 96 h respectively. Cell growth was measured by cell count and MTT assay. In cell count assay, the cell numbers were 1.S×106, 1.55×106, 2.0×106, and 3.1×106 in the experimental group and 2.5×106, 3.1×106, 4.0×106, and 5.7×106 in the control group at 24, 48, 72 and 96 h respectively.The growth of SGC7901 cells was suppressed by RevCaspase-3 in a time-dependent manner (P<0.05). The results of MTT assay were similar to that of cell count (P<0.05).The characteristics of apoptosis such as chromatin condensation, crescent formation and margination were seen and more obvious with time in the given-experimental period in the experimental group, but not easily observed in the control group.CONCLUSION: The expression of Rev-Caspase-3 by the constructed eukaryotic vector can significantly induce apoptosis of gastric cancer cell line SGC7901, which may exhibit a potential way in gastric cancer gene therapy. | Yuan-GenFu Yao-JunQu Kai-ChunWu Hui-HongZhai Zhi-GuoLiu Dai-MingFan | 2003 | World Journal of Gastroenterology2003，9，9： | 16 |
| 9 | COX-2在胰腺癌组织中的表达及其与p53的相关性研究显示文摘目的:探讨环氧化酶-2(COX-2)和p53在胰腺癌组织中的表达与生物学行为之间的关系并探讨二者的相关性及可能机制.方法:用免疫组织化学Envision法对51例胰腺导管癌和11例癌旁非肿瘤胰腺组织的COX-2和p53的表达进行检测.结果:51例胰腺导管癌中COX-2和p53蛋白的表达率分别为74.5%和60.8%;二者在11例癌旁非肿瘤胰腺组织中均未发现阳性表达.COX-2的表达与临床分期和淋巴结转移有关(P=0.022,0.036),而与组织学分级关系不大(P=0.152);p53的表达与淋巴结转移有关(P=0.035),而与组织学分级、临床分期关系不大(P=0.131,0.078);COX-2的表达与p53的表达密切相关(r=0.452,P=0.001).二者的表达与患者的性别、年龄、肿瘤的大小、部位均无关.结论:COX-2和p53的协同作用可能在胰腺癌的发生发展过程中起重要作用,可能为胰腺癌的治疗提供了新的靶点. | 刘江伟 李开宗 窦科峰 | 2003 | 世界华人消化杂志2003，11，2： | 14 |
| 10 | cagA and vacA genotype of Helicobacter pylori associated with gastric diseases in Xi'an area显示文摘AIM: To establish stock of clinical Helicobacter pylori (H.pylon) isolates, to perform cagA and vacA typing of these isolates, to evaluate the relationship between genotypes of cagA and vacA and upper gastrointestinal diseases and to assess the association of vacA genotypes with presence of the pathogenicity marker-cagA.METHODS: Clinical H.pylori strains were isolated from the antrum of 259 patients in Clumbia agar. The isolated H.pylori strains were identified by histology, and16SrRNA PCR.CagA genotypes were detected by colony hybridization, the probe was derived from the cloned plasmid PcagA, and digested by EcoRI-HindⅢ and the isolated PcagA DNA fragment was radioactively labelled by the random priming method. vacA genes types (s,m)and subtypes (s1a, s1b,s2) were typed by PCR. Vacuolating toxin was detected with neutral red absorb test. The results were treated statistically by χ2test, ttest, and rank sum test.RESULTS: A total of 192 clinical H. pylori strains were isolated and the stock of Helicobacter pylori was established. The total positive rate of cagA was 87 % in all gastric diseases,and 95 % in gastric cancer group. There was a difference between gastric cancer group and the other groups (P<0.05)except duodenal ulcer group. The expression of type s1 of vacA was more than type s2 (P<0.05), and, the expression of type m1 was equal to type m2. In gastric cancer group,there was a difference between s1a and s1b (P<0.05), and s1a was more than s1b. Vacuolating toxins were more in Xi′an area isolates.CONCLUSION: The cagA+ vacA type s1 clinical isolates are more in Xi′an area, but this can not serve as an index to predict gastric cancer. | WenQiao Jia-LuHu BingXiao, Kai-ChunWu Dao-RongPeng JohnCAtherton HuiXue | 2003 | World Journal of Gastroenterology2003，9，8： | 13 |
| 11 | Construction of prokaryotic expression system of ureB gene from a clinical Helicobacter pylori strain and identification of the recombinant protein immunity显示文摘AIM: To clone ureB gene from a clinical isolate of Helicobacter pyloriand construct a prokaryotic expression system of the gene and identify immunity of the expressed recombinant protein. METHODS: ureBgene from a clinical Hpyloristrain Y06 was amplified by the high fidelity polymerase chain reaction technique. The target DNA fragment amplified from ureB gene was sequenced after T-A cloning. Prokaryotic recombinant expression vector pET32a inserted with ureB gene (pET32a-ureB) was constructed. The expression of recombinant UreB protein (rUreB) in E. coli BL21DE3 induced by isopropylthio-β-D-galactoside (IPTG) at different concentrations was examined by SDS-PAGE. Western blot using commercial antibodies against whole cell of Hpylori and an immunodiffusion assay using a self-prepared rabbit anti-rUreB antibody were applied to determine immunity of the target recombinant protein. ELISA was used to detect the antibody against rUreB in sera of 125 Hpyloriinfected patients and to examine rUreB expression in 109 Hpylori isolates. RESULTS: In comparison with the reported corresponding sequences, the nucleotide sequence homology of the cloned ureB gene was from 96.88-97.82% while the homology of its putative amino acid sequence was as high as 99.65-99.82%. The rUreB output expressed by pET32a-ureB-BL21DE3 was approximate 30% of the total bacterial proteins, rUreB specifically combined with the commercial antibodies against whole cell of Hpylori and strongly induced rabbits to produce antibody with a 1:8 immunodiffusion titer after the animals were immunized with the recombinant protein. Serum samples from all Hpyloriinfected patients were positive for UreB antibody and UreB expression were detectable in all tested Hpyloriisolates. CONCLUSION: A prokaryotic expression system with high expression efficiency of Hpylori ureBgene was successfully established. The expressed rUreB showed qualified immunoreactivity and antigenicity. High frequencies of UreB expression in different Hpyloriisolates and specific antibody against UreBin sera of Hpyloriinfected patients indicatet hat UreB is an excellent antigen candidate for developing H pylori vaccine. | Ya-FeiMao JieYan | 2004 | World Journal of Gastroenterology2004，10，7： | 12 |
| 12 | 根除幽门螺杆菌对胃癌前病变组织中bax蛋白表达的影响显示文摘目的:研究Hp感染及根除治疗对胃癌前病变组织中促凋亡基因Bax蛋白表达的影响,探讨Hp的致病机制及其在胃癌发生中的作用.方法:采用快速尿素酶试验、Warthin-starry银染色检测Hp;采用免疫组织化学SP法检测72例胃癌前病变组织中Bax蛋白的表达情况,以及Hp阳性患者Hp根除前后胃癌前病变Bax蛋白表达的变化.结果:Bax蛋白在肠上皮化生及不典型增生组织中均有不同程度的表达,其阳性表达率为63.9%.Hp阳性胃癌前病变组Bax蛋白阳性表达率(72.3%)显著高于Hp阴性胃癌前病变组(48.0%,χ2=4.191,P<0.05),Hp感染与Bax阳性表达及分级呈正相关(r=0.978,P<0.01).经三联治疗根除Hp后,Bax蛋白阳性表达率(70.3%)较治疗前显著降低(43.2%,χ2=5.506,P<0.05),而Hp仍为阳性者Bax蛋白阳性表达率则无变化.结论:Hp感染可以促进促凋亡基因Bax蛋白的表达,这可能是Hp感染诱导胃黏膜上皮细胞凋亡的主要机制之一,从而导致细胞凋亡和增生的调节紊乱,使胃黏膜上皮不稳定性增加,使其具有较高的癌变易感性.根除Hp感染可纠正Bax基因表达的异常,对预防或减缓胃癌的发生可能具有重要意义.目的:研究Hp感染及根除治疗对胃癌前病变组织中促凋亡基因Bax蛋白表达的影响,探讨Hp的致病机制及其在胃癌发生中的作用.方法:采用快速尿素酶试验、Warthin-starry银染色检测Hp;采用免疫组织化学SP法检测72例胃癌前病变组织中Bax蛋白的表达情况,以及Hp阳性患者Hp根除前后胃癌前病变Bax蛋白表达的变化.结果:Bax蛋白在肠上皮化生及不典型增生组织中均有不同程度的表达,其阳性表达率为63.9%.Hp阳性胃癌前病变组Bax蛋白阳性表达率(72.3%)显著高于Hp阴性胃癌前病变组(48.0%,χ2=4.191,P<0.05),Hp感染与Bax阳性表达及分级呈正相关(r=0.978,P<0.01).经三联治疗根除Hp后,Bax蛋白阳性表达率(70.3%)较治疗前显著降低(43.2%,χ2=5.506,P<0.05),而Hp仍为阳性者Bax蛋白阳性表达率则无变化.结论:Hp感染可以促进促凋亡基因Bax蛋白的表达,这可能是Hp感染诱导胃黏膜上皮细胞凋亡的主要机制之一,从而导致细胞凋亡和增生的调节紊乱,使胃黏膜上皮不稳定性增加,使其具有较高的癌变易感性.根除Hp感染可纠正Bax基因表达的异常,对预防或减缓胃癌的发生可能具有重要意义. | 刘海峰 刘为纹 房殿春 王国安 滕小春 | 2003 | 世界华人消化杂志2003，11，1： | 12 |
| 13 | 胃粘膜上皮异型增生细胞增殖活性及凋亡与幽门螺杆菌感染的关系显示文摘背景与目的:异型增生是胃癌的癌前病变,但其癌变机制目前仍不清楚,本文通过对异型增生自然转归过程中细胞增殖活性和凋亡变化及幽门螺杆菌(Helicobacterpylori,HP)感染状态的研究,探讨二者之间的关系及其对异型增生癌变的影响。方法:取12例正常胃粘膜(对照组)和105例有随访结果的胃粘膜异型增生胃镜活检标本〔其中高度异型增生35例(癌变30例、未癌变5例);低度异型增生70例(癌变18例、未癌变52例)〕。全部标本均采用TUNEL(terminaldeoxynucleotidyltransferasemediatednickendlabeling)法检测凋亡情况;采用免疫组化法检测增殖细胞核抗原(proliferatingcellnuclearantigen,PCNA)表达情况;采用多聚酶链反应(polymerasechainreaction,PCR)检测HP及其CagA(+)株感染状况。结果:异型增生的HP感染率为84.76%,与对照组的83.33%相比差异无统计学意义,但CagA(+)株感染率为85.39%,高于对照组的60.00%。HP(+)和CagA(+)病例的增殖指数分别较HP(-)和CagA(-)为高(P<0.05),异型增生中PCNA的异常与HP及CagA(+)株感染有关(P<0.05)。凋亡/增殖比的变化与Hp的CagA(+)株感染有关(P<0.05)。结论:胃粘膜异型增生的形成及其自然转归过程中,异型增生的细胞动力学异常与HP、CagA(+)株感染有关。 | 陈孝 王孟薇 尤纬蒂 | 2003 | 癌症2003，22，3： | 12 |
| 14 | Effects of Helicobacter pylori infection on gastric epithelial cell kinetics in patients with chronic renal failure显示文摘AIM: To evaluate the effects of Helicobacter pylori infection on gastric epithelial cell kinetics in patients with chronic renal failure (CRF).METHODS: Forty-four patients were enrolled in this study and divided into four groups with respect to their Helicobacter pylori (H pylori) and CRF status. Groups were labeled as follows: 1a: normal renal function, H pylori negative (n = 12), 1b: normal renal function,H pylori positive (n = 11), 2a: CRF, H pylori negative (n = 10), 2b: CRF, H pylori positive (n = 11). Upper gastrointestinal endoscopy was done in all the patients involved in the study. During endoscopical investigation,antral biopsy specimens were taken from each patient.In order to evaluate the cell apoptosis and proliferation in gastric epithelial cells, Bax and proliferating cell nuclear antigen (PCNA) labeling indexes (LI) were assessed with immunohistochemical staining method.RESULTS: For groups 1a, 1b, 2a, and 2b, mean Bax LI was identified as 34.4±13.7, 44.1±16.5, 46.3±20.5,60.7±13.8, respectively and mean PCNA LI was identified as 36.2±17.2, 53.6±25.6, 59.5±25.6, 67.2±22,respectively. When the one-way ANOVA test was applied,statistically significant differences were detected between the groups for both Bax LI (P = 0.004 <0.01) and PCNA LI (P = 0.009 <0.01). When groups were compared further in terms of Bax LI and PCNA LI with Tukey's HSD test for multiple pairwise comparisons, statistically significant difference was observed only between groups 1a and 2b (P = 0.006 <0.01).CONCLUSION: In gastric epithelial cells, expression of both the pre-apoptotic protein Bax and the proliferation marker PCNA increase with H pylori infection. This increase is more evident in patients with uremia. These findings suggest that uremia accelerates apoptosis and proliferation in gastric epithelial cells. | Selim Aydemir Binnaz Handan Ozdemir Gurden Gur Ibrahim Dogan Ugur Yilmaz Sedat Boyacioglu | 2005 | World Journal of Gastroenterology2005，11，45： | 11 |
| 15 | CagA和VacA不能作为幽门螺杆菌相关性疾病的预测因子显示文摘目的:CagA和VacA能否作为幽门螺杆菌(H.pylori)相关性疾病的预测因子尚有争论,本文旨在研究胃癌高发区的福州市不同胃病患者的H.prLori CagA和VacA的检出率,探讨这二者作为H.pylori毒力标志物的可行性。 方法:胃镜或手术及病理证实的慢性胃病患者170例纳入研究,胃窦癌(CC)34例,十二指肠溃疡(DU)39例,胃溃疡(GU)35例,慢性胃炎62例。无症状的健康志愿者36名为对照组,免疫印迹法检测血清中H.pylori抗体。部分患者同时接受^(14)碳-尿素呼气检测。 结果:DU组、GU组和GC组的HP血清学阳性率高于胃炎组(X^2=4.84,P=0.028)和对照组(X^2=25.877,P<0.001),DU组与GU组、GC组之间的差异无显著性意义(X^2=3.306,P=0.191)。DU组的呼气实验阳性率高于GC组(X^2=16.463,P<0.001)、胃炎组(X^2=4.31,P=0.038)和对照组(X^2=33.33,P<0.001),GU组和胃炎组高于对照组(P<0.05);而DU组与GU组之间、GC组和对照组之间的差异均无统计学意义(P=0.144)。根据免疫印迹结果进行分型,各组间CgaA、VacA和Ⅰ型菌(CagA+、VacA+)阳性率无显著性差异(P>0.05)。 结论:尽管H.pylori感染与慢性胃病有关,但血清CagA和VacA抗体对预测H.pylori感染的后果没有意义。 | 王承党 李劲松 陈玉丽 | 2002 | 世界华人消化杂志2002，10，5： | 10 |
| 16 | Construction of expression systems for flaA and flaB genes of Helicobacter pylori and determination of immunoreactivity and antigenicity of recombinant proteins显示文摘AIM: To clone flagellin genes A (flaA) and B (flaB) from a clinical strain of Helicobacter pylori (H pylori) and to construct prokaryotic expression systems of the genes and identify immunity of the fusion proteins.METHODS: The flaA and flaBgenes from a clinical H pylori isolate Y06 were amplified by high fidelity PCR. The nucleotide sequences of target DNA amplification fragments from the two genes were sequenced after T-A cloning. The recombinant expression vector pET32a inserted with flaA and flaB genes was constructed, respectively. The expressions of FlaA and FlaB fusion proteins in E. Coli BL21DE3 induced by isopropylthio-β-D-galactoside (IPTG)at different concentrations were examined by SDS-PAGE.Western blot using commercial antibodies against whole cell of H pylori and immunodiffusion assay using self-prepared rabbit antiserum against FlaA (rFlaA) or FlaB (rFlaB)recombinant proteins were applied to the determination of the fusion proteins immunity. ELISA was used to detect the antibodies against rFlaA and rFlaB in sera of 125 H pylori infected patients and to examine rFlaA and rFlaB expression in 98 clinical isolates of H pylori, respectively.RESULTS: In comparison with the reported corresponding sequences, the nucleotide sequence homologies of the cloned flaA and flaB genes were from 96.28-97.13% and 96.31-97.73%, and their putative amino acid sequence homologies were 99.61-99.80% and 99.41-100% for the two genes, respectively. The output of rFlaA and rFlaB expressed by pET32a-flaA-BL21DE3 and pET32a-flaBBL21DE3 systems was as high as 40-50% of the total bacterial proteins. Both rFlaA and rFlaB were able to combine with the commercial antibodies against whole cell of H pylori and to induce rabbits to produce specific antibodies with the same 1:2 immunodiffusion titers after the animals were immunized with the two recombinant proteins. Ninety-eight and zero point 4 and 92.80% of the serum samples from 125 patients infected with H pylori were positive for rFlaA and rFlaB antibodies, respectively.One hundred percent and 98.98% of the 98 tested isolates of H pylori were detectable for rFlaA and rFlaB epitopes,respectively.CONCLUSION: Two prokaryotic expression systems with high efficiency of H pylori flaA and flaB genes were successfully established. The expressed rFlaA and rFlaB showed satisfactory immunoreactivity and antigenicity. High frequencies of FlaA and FlaB expression in different H pylori clinical strains and the general existence of specific antibodies against FlaA and FlaB in H pylori infected patients strongly indicate that FlaA and FlaB are excellent antigen candidates for developing H pylori vaccine. | JieYan Shao-HuiLiang Ya-FeiMao Li-WeiLi Shu-PingLi | 2003 | World Journal of Gastroenterology2003，9，10： | 10 |
| 17 | Expression of TFF2 and Helicobacter pylori infection in carcinogenesis of gastric mucosa显示文摘AIM: To investigate the expression of TFF2 and Helicobacter pyloriinfection in carcinogenesis of gastric mucosa.METHODS: The expression of TFF2 was immunohistochemically analyzed in paraffin-embedded samples from 119 patients with endoscopic biopsy and subtotal gastrectomy specimens of gastric mucosal lesions, including 16 cases of chronic superficial gastritis (CSG), 20 chronic atrophic gastritis (CAG),35 intestinal metaplasia (IN), 23 gastric epithelial dysplasia (GED) and 25 gastric carcinoma (CA), and Helicobacter pylori infection was detected by Warthin-Starry staining.RESULTS: 1:TFF2 was located in the cytoplasm of gastrk mucous neck cell. The expression of TFF2 was 100 %,100 %, 0, 56.5 % and 0 in CSGs, CAGs, INs, GEDs and CAs, respectively. 2: The value of TFF2 positive cell density in CSG with Helicobacter pyloriinfection was higher than that without Helicobacter pyloriinfection. (52.89±7.27vs46.49±13.04, P>0.05); But the value of TFF2 positive cell density in CAG and GED with Helicobacter pyloriinfection was significantly lower than that without Helicobacter pylori infection (18.17±4.09 vs 37.93±13.80, P<0.01 and 14.44±9.32 vs 24.84±10.22, P<0.05).CONCLUSION: Increase of TFF2 expression in CSG is perhaps associated with the protective mechanism after gastric mucosal injury. Decrease of TFF2 expression in CAG possibly attributes to the decrease in the number of gastric gland cell expressing TFF2. Re-expression of TFF2 in gastric epithelial dysplasia implies that TFF2 possibly contributes to the initiation of gastric carcinoma. The effect of Helicobacter pylori on the expression of TFF2 depends on the status of gastric mucosa. | Guo-Yong Hu Bao-Ping Yu Wei-Guo Dong Mu-Qi Li Jie-Ping Yu He-Sheng Luo Zong-Xue Rang Gastroenterology Department,Renmin Hospital of Wuhan University,Wuhan 430060,Hubei Province,China | 2003 | World Journal of Gastroenterology2003，9，5： | 10 |
| 18 | 胃癌组织Survivin蛋白表达及其与HP感染关系显示文摘目的探讨Survivin蛋白在胃癌中的表达及其与幽门螺杆菌(HP)感染之间的关系。方法应用免疫组化方法检测70例胃癌及癌旁组织标本Survivin蛋白的表达,Warthin-Starry染色法检测胃癌组织中HP感染情况。结果胃癌组织中Survivin阳性表达率74.3%,癌旁组织为41.4%,胃癌组织中Survivin的表达强度明显高于癌旁组织(Z=5.33,P〈0.05)。Survivin蛋白表达与病人性别、Borrmann分型无关(P〉0.05);而其表达强度与胃癌分化程度、浸润深度、临床分期、淋巴结转移有关(Hc=-4.52~14.70,P〈0.05)。Survivin蛋白表达强度与HP感染有关(Z=2.46,P〈0.05)。结论Survivin蛋白的表达与胃癌发生、演进有关;HP感染可增强胃癌Survivin的表达强度。 | 董丽丽 项锋钢 高建青 | 2008 | 齐鲁医学杂志2008，23，6： | 8 |
| 19 | 幽门螺杆菌诱导蒙古沙鼠胃上皮细胞凋亡可能涉及线粒体途径显示文摘目的建立幽门螺杆菌(Hp)感染蒙古沙鼠模型,探讨线粒体途径在Hp诱导胃上皮细胞凋亡中的作用。方法 48只雄性蒙古沙鼠均分为Hp感染组和对照组,每组分别于1、3和6个月3个时相点各处死8只动物,取胃黏膜行组织学检查:用Warthin-Starry银染、PCR和快速尿素酶法检测 Hp;通过H-E染色,光镜下观察胃黏膜病理变化;流式细胞仪测定细胞凋亡、线粒体膜电位及胞内游离 Ca2+含量。结果 Hp感染蒙古沙鼠后,胃黏膜出现慢性胃炎、肠化生及异型增生改变,而对照组胃黏膜基本正常,Hp感染组肠化生及异型增生发生率明显高于对照组(P<0.05)。Hp感染胃上皮细胞1、3、 6个月后的凋亡率分别为(16.71±3.30)%、(5.90±0.82)%、(5.69±0.70)%,而对照组的凋亡率分别为(4.20±0.94)%、(3.17±0.43)%、(4.70±0.55)%。其中Hp感染1个月后胃上皮细胞的凋亡率高于其他各组(P<0.05)。Hp感染胃上皮细胞1、3、6个月后的线粒体膜电位分别为43.10±17.62、 71.19±38.03、80.56±32.90,而对照组分别为84.70±23.50、84.39±37.51、79.54±30.24,其中Hp 感染1个月后胃上皮细胞的线粒体膜电位低于其他各组(P<0.05);Hp感染1、3、6个月后胃上皮细胞内游离Ca2+含量分别为18.60±9.32、5.18±2.06、4.94±3.25,而对照组分别为4.82±3.70、6.86 ±2.34、5.28±3.13,Hp感染1个月后胃上皮细胞内游离Ca2+含量高于其他各组(P<0.05)。结论 Hp诱导蒙古沙鼠胃上皮细胞凋亡主要发生在Hp感染早期;线粒体膜电位的下降和胞内游离Ca2+含量的升高参与了Hp诱发蒙古沙鼠胃上皮细胞凋亡的过程。 | 兰春慧 房殿春 邹全明 | 2006 | 中华消化杂志2006，26，6： | 7 |
| 20 | 辽宁庄河胃癌防治现场报告显示文摘回顾总结辽宁庄河胃癌防治现场二十余年建设与发展历程,探讨癌症高发地区开展防治工作的成功经验及实现可持续发展的运行模式,为政府制定肿瘤防治规划提供科学依据。 | 袁媛 张荫昌 | 2009 | 中国肿瘤2009，18，1： | 7 |
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