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本文引用的文献

1
Ultrastructure and molecular biological changes of chronic gastritis, gastric cancer and gastric precancerous lesions: a comparative study.慢性胃炎、胃癌及胃癌前病变的超微结构与分子生物学变化:一项对比研究。
World J Gastroenterol. 2003 Apr;9(4):851-7. doi: 10.3748/wjg.v9.i4.851.
2
[Therapeutic effect of weikangfu on gastric precancerous disorder with spleen deficiency syndrome and its effect of gastric mucosal zinc, copper, cyclic adenosine monophosphate, superoxide dismutase, lipid peroxide and 3H-TdR lymphocyte conversion test].胃康复对脾虚证胃癌前期病变的治疗作用及其对胃黏膜锌、铜、环磷酸腺苷、超氧化物歧化酶、脂质过氧化物和3H-TdR淋巴细胞转化试验的影响
Zhongguo Zhong Xi Yi Jie He Za Zhi. 2000 Mar;20(3):176-9.
3
[Effect of Weikangfu granule on ultrastructure of gastric mucosa in patients of precancerosis with spleen deficiency syndrome].[胃康复颗粒对脾虚证胃癌前病变患者胃黏膜超微结构的影响]
Zhongguo Zhong Xi Yi Jie He Za Zhi. 2000 Sep;20(9):667-70.
4
[Histocytopathological study on gastric mucosa of spleen deficiency syndrome].[脾虚证胃黏膜的组织细胞病理学研究]
Zhongguo Zhong Xi Yi Jie He Za Zhi. 1999 Nov;19(11):660-3.
5
[Study on mitochondrial ultrastructure, trace elements and correlative factors of gastric mucosa in patients with spleen deficiency syndrome].脾虚证患者胃黏膜线粒体超微结构、微量元素及相关因素的研究
Zhongguo Zhong Xi Yi Jie He Za Zhi. 1995 Dec;15(12):719-23.

慢性胃炎分子生物学水平分类研究

Study on the classification of chronic gastritis at molecular biological level.

作者信息

Yin Goang-Yao, Zhang Wu-Ning, He Xue-Fen, Chen Yi, Shen Xiao-Jing

机构信息

Wuxi No.3 Peoples Hospital, 230 Eastern Tonghhui Road Wuxi 214041, Jiangsu Province, China.

出版信息

World J Gastroenterol. 2003 Apr;9(4):836-42. doi: 10.3748/wjg.v9.i4.836.

DOI:10.3748/wjg.v9.i4.836
PMID:12679944
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4611461/
Abstract

AIM

To explore the pathophysiologibasis for the fact that patients with digestive tract symptoms do not necessarily have gastric mucosal pathology and those without clinical symptoms do not necessarily have no gastric mucosal pathology.

METHODS

The ultrastructure, trace elements, cAMP, DNA, SOD and LPO in the gastric mucosa and its epithelial cells of 188 patients without organic lesions of heart, lung, liver, gallbladder, pancreas, kidney or intestine and basically histopathological normal persons (F) were detected synchronously by SEM, TEM, EDAX, Image analysis system RIA and (3)H-TdR Lymphocyte Transfer Test.

RESULTS

The content of Zn, Cu, cAMP and (3)H-TdR LCT in gastric mucosa and the content of Zn, Cu, DNA and LPO in gastric mucosa epithelial nuclei of each group were shown as belows: Normal control (4.1+/-1.0, 5.2+/-0.8, 15.9+/-1.5, 1079.7+/-227.4, 7.6+/-0.4, 58.4+/-0.3, 12.6+/-2.7, 2.6+/-0.6); CSG without symptoms group (3.7+/-1.2, 5.1+/-1.8, 15.6+/-0.9, 924.5+/-234.9, 7.8+/-0.3, 58.6+/-0.4, 13.0+/-3.1, 2.9+/-0.4); CAG without symptoms group (3.3+/-1.0, 4.8+/-0.9, 14.9+/-0.7, 887.7+/-243.6, 7.8+/-0.3, 58.7+/-0.3, 14.3+/-2.8, 3.1+/-0.4); F type with symptoms group (3.5+/-1.4, 4.5+/-1.0, 15.7+/-1.4, 932.1+/-2449.3, 7.9+/-0.4, 58.7+/-0.5, 13.5+/-4.6, 2.9+/-0.7); CSG with symptoms group (2.8+/-1.9, 4.0+/-1.5, 14.2+/-1.8, 867.3+/-240.5, 8.1+/-0.5, 58.9+/-0.5, 15.2+/-3.2, 4.2+/-0.7); CAG with symptoms group (2.0+/-1.8, 3.4+/-1.5, 13.4+/-1.8, 800.9+/-221.8, 8.6+/-0.4, 59.3+/-0.5, 16.5+/-3.1, 4.5+/-0.6). The contents of Zn, Cu in mitochonondria and SOD in gastric mucosa of each group were shown as belows: Normal control group (9.2+/-0.5, 58.3+/-0.3, 170.5+/-6.1), CSG without symptoms group (8.9+/-0.5, 58.2+/-0.3, 167.2+/-5.3), CAG without symptoms group (8.8+/-0.4, 57.5+/-0.2, 166.1+/-4.2); F type with symptoms group (8.9+/-0.5, 58.0+/-0.3, 167.9+/-5.7), CSG with symptoms group (8.6+/-0.5, 57.8+/-0.3, 163.3+/-5.6); CAG with symptoms group (8.3+/-0.4, 57.5+/-0.3, 161.2+/-4.3). There were significant differences in these cases, P<0.05-0.001. There were synchronous changes of gastric mucosa epithelial cellular ultrastructure. The "background lesions" (focal atrophic gastritis, focal intestinal metaplasia, micro-ulcer) in nonfocal gastric mucosa of all groups had significant differences (P<0.05-0.001).

CONCLUSION

Disease with symptoms, disease without symptoms, nondisease with symptoms occur on the basis of the quantitative changes of gastric mucosa epithelial cellular ultrastructure and related bioactive substances.

摘要

目的

探讨消化道症状患者不一定存在胃黏膜病变,而无症状者不一定无胃黏膜病变这一现象的病理生理基础。

方法

采用扫描电镜(SEM)、透射电镜(TEM)、能谱仪(EDAX)、图像分析系统、放射免疫分析(RIA)及³H-TdR淋巴细胞转化试验,同步检测188例无心脏、肺、肝、胆、胰、肾及肠道器质性病变且组织病理学基本正常者(F)胃黏膜及其上皮细胞的超微结构、微量元素、环磷酸腺苷(cAMP)、DNA、超氧化物歧化酶(SOD)及脂质过氧化物(LPO)。

结果

各组胃黏膜中锌(Zn)、铜(Cu)、cAMP及³H-TdR淋巴细胞转化试验(LCT)含量,以及胃黏膜上皮细胞核中Zn、Cu、DNA及LPO含量如下:正常对照组(4.1±1.0,5.2±0.8,15.9±1.5,1079.7±227.4,7.6±0.4,58.4±0.3,12.6±2.7,2.6±0.6);无症状慢性浅表性胃炎(CSG)组(3.7±1.2,5.1±1.8,15.6±0.9,924.5±234.9,7.8±0.3,58.6±0.4,13.0±3.1,2.9±0.4);无症状慢性萎缩性胃炎(CAG)组(3.3±1.0,4.8±0.9,14.9±0.7,887.7±243.6,7.8±0.3,58.7±0.3,14.3±2.8,3.1±0.4);有症状F型组(3.5±1.4,4.5±1.0,15.7±1.4,932.1±2449.3,7.9±0.4,58.7±0.5,13.5±4.6,2.9±0.7);有症状CSG组(2.8±1.9,4.0±1.5,14.2±1.8,867.3±240.5,8.1±0.5,58.9±0.5,15.2±3.2,4.2±0.7);有症状CAG组(2.0±1.8,3.4±1.5,13.4±1.8,800.9±221.8,8.6±0.4,59.3±0.5,16.5±3.1,4.5±0.6)。各组胃黏膜线粒体中Zn、Cu含量及SOD含量如下:正常对照组(9.2±0.5,58.3±0.3,170.5±6.1),无症状CSG组(8.9±0.5,58.2±0.3,167.2±5.3),无症状CAG组(8.8±0.4,57.5±0.2,166.1±4.2);有症状F型组(8.9±0.5,58.0±0.3,167.9±5.7),有症状CSG组(8.6±0.5,57.8±0.3,163.3±5.6);有症状CAG组(8.3±0.4,57.5±0.3,161.2±4.3)。这些情况差异有统计学意义,P<0.05 - 0.001。胃黏膜上皮细胞超微结构有同步变化。各组非病灶性胃黏膜中的“背景病变”(局灶性萎缩性胃炎、局灶性肠化生、微小溃疡)差异有统计学意义(P<0.05 - 0.001)。

结论

有症状疾病、无症状疾病、有症状非疾病的发生是基于胃黏膜上皮细胞超微结构及相关生物活性物质的定量变化。