AIM: To carry out a comparative study on ultrastructure and molecular biological changes of chronic gastritis (CG),gastric cancer (GC) aand gastric precancerous lesions.METHODS: By the use of histochemical staining, S...AIM: To carry out a comparative study on ultrastructure and molecular biological changes of chronic gastritis (CG),gastric cancer (GC) aand gastric precancerous lesions.METHODS: By the use of histochemical staining, SEM with EDAX, TEM with EDAX, image analysis technique, RIA and chemiluminescence method, gastric mucosa of 168 patients were synchronously analyzed in morphology, trace elements, DNA, cAMP, SOD, 3H-TdR LCT and serum LPO were also done.RESULTS: The incidence of epithelial nucleoplasmic ratio >1, lobulated nuclei, inter-chromatin aggregation of granules, nucleolar hypertrophy, and the content of DNA,Zn, Cu in nuclei and serum LPO of each group were showed as belows: normal control group (0.0, 0.0, 6.7, 0.0, 12.6±2.7,7.6±0.4, 58.4±0.3, 2.6±0.6), CSG group (5.7, 2.9, 7.4, 2.9,15.2±3.1, 8.1±0.5, 58.9±0.5, 4.2±0.7), CAG group (31.3,29.7, 45.3, 42.2, 16.5±3.1, 8.6±0.4, 59.3±0.5, 4.5±0.6), CA group (100.0, 100.0, 72.2, 50.0, 30.7±8.2, 8.8±0.3, 59.5±0.4,6.8±1.6), ATP++group (61.5, 38.5, 23.1, 38.5, 23.5±8.9,8.3±0.4, 59.1±0.4, 5.1±1.2), IM+++ ATP++group (77.8, 55.5,33.3, 44.4, 25.1±7.2, 8.4±0.5, 59.5±0.4, 6.5±1.1),IM++++ATP++ group (100.0, 100.0, 75.0, 62.5, 28.5±9.1,8.9±0.5, 59.7±0.4, 7.6±0.7), IMⅡb group (100.0, 62.5, 75.0,50.0, 27.3±10.3, 8.6±0.3, 59.5±0.4, 6.1±0.9); whereas the content of Zn, Cu in mitochondria and cAMP, SOD in gastric mucosa, and 3H-TdR LCT of each group were showen as belows: normal control group (9.2±0.5, 58.3±0.3, 15.9±1.5,170.5±6.1, 1079.7±227.4), CSG group (8.6±0.5, 57.8±0.3,14.6±1.8, 163.3±5.6, 867.3±240.5), CAG group (8.3±0.4,57.5±0.3, 13.4±1.8, 161.2±4.3, 800.9±221.8), CA group (8.9±0.4, 57.1±0.3, 10.2±3.9, 152.2±3.8, 325.7±186.8),ATP++ group (9.1±0.4, 57.0±0.3, 12.4±1.8, 161.5±3.8,642.9±174.3), IM+++ ATP++ group (8.6±0.4, 56.9±0.3,12.0±2.3, 152.2±2.5, 326.3±160.3), IM++++ATP++ group (8.5±0.3, 56.8±0.2, 10.4±0.9, 147.4±2.6, 316.1±170.7),IMⅡb group (8.6±0.3, 56.9±0.3, 11.9±1.9, 150.0±2.8,318.9±145.8), there were significant differences between groups (P<0.05-0.01).CONCLUSION: There was a significant difference between CG and GC in their ultrastructure and molecular biology.Only on the condition of changes of internal environment in combination with the harmful effect of external environment, chronic atrophic gastritis can then develop into gastric cancer. Hence it might have similar epithelial cell ultrastructure and molecular biological changes in ATP++, IMⅡb and cancer, hence there were similar patterns of occurrence, development and transformation.Recognition of this trend might help to explore problems of prevention and cure.展开更多
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 gastri...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 3H-TdR Lymphocyte Transfer Test.RESULTS: The content of Zn, Cu, cAMP and 3H-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±L.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.展开更多
文摘AIM: To carry out a comparative study on ultrastructure and molecular biological changes of chronic gastritis (CG),gastric cancer (GC) aand gastric precancerous lesions.METHODS: By the use of histochemical staining, SEM with EDAX, TEM with EDAX, image analysis technique, RIA and chemiluminescence method, gastric mucosa of 168 patients were synchronously analyzed in morphology, trace elements, DNA, cAMP, SOD, 3H-TdR LCT and serum LPO were also done.RESULTS: The incidence of epithelial nucleoplasmic ratio >1, lobulated nuclei, inter-chromatin aggregation of granules, nucleolar hypertrophy, and the content of DNA,Zn, Cu in nuclei and serum LPO of each group were showed as belows: normal control group (0.0, 0.0, 6.7, 0.0, 12.6±2.7,7.6±0.4, 58.4±0.3, 2.6±0.6), CSG group (5.7, 2.9, 7.4, 2.9,15.2±3.1, 8.1±0.5, 58.9±0.5, 4.2±0.7), CAG group (31.3,29.7, 45.3, 42.2, 16.5±3.1, 8.6±0.4, 59.3±0.5, 4.5±0.6), CA group (100.0, 100.0, 72.2, 50.0, 30.7±8.2, 8.8±0.3, 59.5±0.4,6.8±1.6), ATP++group (61.5, 38.5, 23.1, 38.5, 23.5±8.9,8.3±0.4, 59.1±0.4, 5.1±1.2), IM+++ ATP++group (77.8, 55.5,33.3, 44.4, 25.1±7.2, 8.4±0.5, 59.5±0.4, 6.5±1.1),IM++++ATP++ group (100.0, 100.0, 75.0, 62.5, 28.5±9.1,8.9±0.5, 59.7±0.4, 7.6±0.7), IMⅡb group (100.0, 62.5, 75.0,50.0, 27.3±10.3, 8.6±0.3, 59.5±0.4, 6.1±0.9); whereas the content of Zn, Cu in mitochondria and cAMP, SOD in gastric mucosa, and 3H-TdR LCT of each group were showen as belows: normal control group (9.2±0.5, 58.3±0.3, 15.9±1.5,170.5±6.1, 1079.7±227.4), CSG group (8.6±0.5, 57.8±0.3,14.6±1.8, 163.3±5.6, 867.3±240.5), CAG group (8.3±0.4,57.5±0.3, 13.4±1.8, 161.2±4.3, 800.9±221.8), CA group (8.9±0.4, 57.1±0.3, 10.2±3.9, 152.2±3.8, 325.7±186.8),ATP++ group (9.1±0.4, 57.0±0.3, 12.4±1.8, 161.5±3.8,642.9±174.3), IM+++ ATP++ group (8.6±0.4, 56.9±0.3,12.0±2.3, 152.2±2.5, 326.3±160.3), IM++++ATP++ group (8.5±0.3, 56.8±0.2, 10.4±0.9, 147.4±2.6, 316.1±170.7),IMⅡb group (8.6±0.3, 56.9±0.3, 11.9±1.9, 150.0±2.8,318.9±145.8), there were significant differences between groups (P<0.05-0.01).CONCLUSION: There was a significant difference between CG and GC in their ultrastructure and molecular biology.Only on the condition of changes of internal environment in combination with the harmful effect of external environment, chronic atrophic gastritis can then develop into gastric cancer. Hence it might have similar epithelial cell ultrastructure and molecular biological changes in ATP++, IMⅡb and cancer, hence there were similar patterns of occurrence, development and transformation.Recognition of this trend might help to explore problems of prevention and cure.
文摘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 3H-TdR Lymphocyte Transfer Test.RESULTS: The content of Zn, Cu, cAMP and 3H-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±L.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.