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| 1 | 胃癌及癌前病变hTERT的表达与细胞免疫功能显示文摘目的观察在胃癌及癌前病变组织中端粒酶催化亚单位hTERT的表达与患者细胞免疫功能,探讨hTERT及细胞免疫功能对胃癌诊断、治疗、预后的临床意义。方法用原位杂交方法对116例内镜胃粘膜活检标本的端粒酶催化亚单位hTERT、进行检测,包括慢性浅表性胃炎(CSG)30例,慢性萎缩性胃炎(CAG)27例、腺瘤型息肉8例、胃溃疡9例,胃癌(GC)42例,并按肿瘤部位、大体类型、有无淋巴结转移及分化程度分组,同时,用流式细胞技术(FCM)检测了30例慢性浅表性胃炎、27例慢性萎缩性胃炎、42例胃癌的外周血T淋巴细胞亚群及自然杀伤(NK)细胞,并与正常对照(NC)相比较。结果 CSG的hTERT阳性率为0%(0/30),癌前病变为36%(13/44),GC为86%(36/42)。胃癌组织hTERT阳性率与肿瘤部位、大体类型、有无淋巴结转移及分化程度无显著可关性,CSG组CD3^+,CD4^+较NC已有明显下降(P<0.05),CAG组T细胞功能(CD3^+,CD4^+,CD4^+/CD8^+)及NK各值较NC及CSG组均明显降低(P<0.05~0.01),GC组T细胞及NK细胞各值较CAG组显著异常(P<0.05-0.01),并随着胃癌进展,CD3^+,CD4^+,CD4^+/CD8^+各值进一步降低。结论端粒酶活化可能是胃粘膜癌变的关键步骤,胃粘膜活检标本hTERT的表达是胃癌癌变过程中重要的生物学标志物,胃癌和癌前病变患者细胞免疫功能低下,对胃癌的发生发展有重要意义。 | 姚希贤 尹雷 张杰英 白文元 李英敏 孙中成 | 2001 | 世界华人消化杂志2001，9，5： | 32 |
| 2 | The expression of hTERT mRNA and cellular immunity in gastric cancer and precancerosis显示文摘AIM:To observe the expression of Human telomerasereverse transcriptase (hTERT) in gastric carcinomas andprecancerosis lesions, to evaluate the immune state ofsuch patients, and to then study the clinical significanceof hTERT and immune state for the diagnosis, treat-ment and prognosis of gastric cancer METHODS: In situ hybridization was used to detect theexpression of hTERT mRNA in 116 endoscopic of gas-tric mucosa. Analyzed tissue samples were as follows:30 cases of chronic superficial gastritis (CSG), 44 ofprecancerosis lesions (including 27 of chronic atrophicgastritis, 8 of adenomatous polyp and 9 of gastric ulcer)and 42 of gastric cancer (GC). In addition, the T lym-phocyte subsets (CD3+, CD4+, CD8+, CD4+/CD8+ ) andnatural killer cells (NK) in peripheral blood were deter-mined by flow cytometric analysis (FCM) in 30 cases ofCSG, 27 of precancorosis (chronic atrophic gastritis,CAG), and 42 of GC. The data were compared with thoseof normal control (NC).RESULTS:The detected positive rate of hTERT varied asfollows: 86 % (36/42) in GC, 36 % (16/44) inprecancerosis lesions and 0 % (0/30) in CSG. The ex-pression of hTERT mRNA was not associated with pa-tient gender, tumor location, macroscopic type, lymphnode metastasis, or degree of differentiation, It wasfound that the CD3+, CD4+ of the CSG group were lowerthan that of NC (P<0.05). Meanwhile, the T lympho-cyte subsets (CD3+,CD4+, CD4+/CD8+ ratio) and NK cellsof CAG were remarkably lower than that of NC and CSGgroups (P<0.05-0.01). Values ofT cells and NK cells ofthe GC group were significantly abnormal when com-pared with the CAG group (P<0.05-0.01). Furthermore,with tumor progression, the function of T cells wasweakened gradually.CONCLUSION: The expression of telomerase may be acrucial step in gastric carcinogenesis and increasedhTERT mRNA may serve as a novel marker for diagno-sis of GC. The immune state of patients with GC andprecancerosis was somewhat depressed, which indi-cates the importance of cellular immunological assaysin cancer patients. | Xi-Xian Yao Lei Yin Department of Digestive Medicine,the 2nd Hospital of Hebei Medical University,Shijiazhuang 050000,Hebei Province,China Zhong-Cheng Sun The Traditional Chinese Medical College of Hebei Medical University,Shijiazhuang 050081,Hebei Province,China | 2002 | World Journal of Gastroenterology2002，8，4： | 32 |
| 3 | 胃溃疡大鼠胃泌素、生长抑素和GD细胞的变化显示文摘目的:研究胃溃疡对大鼠G细胞分泌胃泌素(D细胞分泌生长抑素)和对G(D)细胞变化的影响.方法:建立冰乙酸性大鼠胃溃疡模型,采用大体、光镜、透射电镜观察胃窦黏膜组织学表现和胃窦黏膜细胞超微结构表现,采用放射免疫法检测血清和胃窦组织中的胃泌素、生长抑素含量,采用免疫组化法及定量分析检测G(D)细胞形态、数目、面积、和G/D细胞数目、面积比值,采用免疫电镜及定量分析观察与检测G(D)细胞及G(D)细胞中的胃泌素(生长抑素)分泌颗粒.结果:免疫电镜观察到了G(D)细胞和IG(D)细胞中的胃泌素(生长抑素)分泌颗粒.大鼠胃溃疡后,G细胞内胃泌素分泌量增加,D细胞内生长抑素分泌量减少,G细胞数目增加、面积减少,D细胞数目减少、面积减少,G/D细胞数目比值和G/D细胞面积比值增加,并且血清、胃窦组织中胃泌素含量增加,生长抑素含量减少.结论:大鼠胃溃疡可引起G、D细胞的变化,引起G、D细胞分泌胃泌素、生长抑素的变化,和引起胃泌素、生长抑素含量的变化. | 孙凤蓬 宋于刚 覃汉荣 | 2004 | 世界华人消化杂志2004，12，2： | 16 |
| 4 | Current gene therapy for stomach carcinoma显示文摘Gastric cancer is common in China [1-42],and its early diagnosis and treatment in advanced stage are difficult [31-50].In recent years ,gene study in cancer is a hotspot ,and great progress has been achieved [41-80] .Cancer gene therapy has shifted from the imagination into the laboratory and clinical trials. | Chang-Tai Xu~1 Lian-Tian Huang~1 Bo-Rong Pan~2 1 Editorial Department,the Journal of Fourth Military Medical University2 Oncology Center,Xijing Hospital,Fourth Military Medical University,169 Changle Xilu,Xi’an 710032,Shaanxi Province,China | 2001 | World Journal of Gastroenterology2001，7，6： | 16 |
| 5 | Mechanisms for regulation of gastrin and somatostatin release from isolated rat stomach during gastric distention显示文摘AIM: To investigate the intragastric mechanisms forregulation of gastric neuroendocrine functions during gastricdistention in isolated vascularly perfused rat stomach.METHODS: Isolated vascularly perfused rat stomach wasprepared, then the gastric lumen was distended with either5,10 or 15 ml pH7 isotonic saline during a period of 20 min.During the distention, the axonal blocker tetrodotoxin (TTX),the cholinergic antagonist atropine, or the putativesomatostatin-antagonist cyclo [7-aminoheptanoyl-Phe-D-Trp-Lys-Thr(Bzl)] were applied by vascular perfusion. Thereleases of gastrin and somatostatin were then examinedby radioimmunoassay.RESULTS: The graded gastricdistention caused a significantvolume-dependent decrease in gastrin secretion [-183±75 (5ml), -385±86 (10 ml) and -440±85 (15 ml) pg/20 min] and asignificant increase of somatostatin secretion [260±102 (5 ml),608±148 (10 ml) and 943±316 (15 ml) pg/20 min]. In responseto 10 ml distention, the infusion of either axonal blocker TTX(10-6 M) or cholinergic blocker atropine (10-7 M) had a similaraffect. They both attenuated the decrease of gastrin releaseby approximately 50 %, and attenuated the increase ofsomatostatin release by approximately 40 %. The infusion ofsomatostatin-antagonist cyclo [7-aminoheptanoyl-Phe-D-Trp-Lys-Thr (Bzl)] (10-6M) attenuated the decrease of gastrin releaseby about 60 %. Furthermore, combined infusion of thesomatostatin-antagonist and atropine completely abolisheddistention-induced inhibition of gastrin release.CONCLUSION: The present data suggest that distention ofisolated rat stomach stimulates somatostatin release viacholinergic and non-cholinergic TTX-insensitive pathways. Bothsomatostatin and intrinsic cholinergic pathways are responsiblefor distention-induced inhibition of gastrin release. | Yong-Yu Li Department of Pathophysiology,Medical College of Tongji University,Shanghai 200331,China | 2003 | World Journal of Gastroenterology2003，9，1： | 6 |
| 6 | Significance of Experiments on the Relationship of Spleen Deficiency Syndrome with Gastrin and Somatostatin Changes显示文摘Objective: To explore the relationship among gastrin, somatostatin and pathogenesis of spleen deficiency syndrome (SDS). Methods: The changes of gastrin and somatostatin in body fluid and tissues were measured by radioimmunoassay. G cells (gastrin cells) and D cells (somatostatin cells) of gastroduodenal mucosa were analyzed with polyclonal antibody to gastrin and somatostatin, immunohistochemical technique and Quantimet 500 image analysis system. Sijunzi decoction (四君子汤, SJZD) was chosen for counter confirmation of syndrome. Results: The levels of gastrin in plasma, gastric juice, intestinal juice, gastric antrum, duodenum and hypothalamus of experimental SDS were significantly lowered and somatostatin markedly higher than the control group, which was improved and even better than spontaneous recovery group after prevention and treatment with SJZD ( P <0.05). The count of G cells and D cells reduced ( P <0.05), the area of D cells declined ( P <0.05), but mean grey of G cells elevated ( P <0.05) and ratio of the count and area on G/D also increased ( P <0.05) in experimental SDS, which was improved and even better than spontaneous recovery group after prevention and treatment with SJZD ( P <0.05). Conclusion: The study confirmed that disturbance of relationship between gastrin and somatostatin would lead to gastrointestinal disorder, which was one of important causes for pathogenesis of SDS. | 姚永莉 徐波 宋于刚 张万岱 | 2002 | Chinese Journal of Integrative Medicine2002，8，1： | 3 |
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