AIM To study the effect of Helicobacter pylori ( H. pylori ) infection on gastric epithelial proliferation in the progression from normal mucosa to gastric carcinoma. METHODS Gastric biopsy specimens from nor...AIM To study the effect of Helicobacter pylori ( H. pylori ) infection on gastric epithelial proliferation in the progression from normal mucosa to gastric carcinoma. METHODS Gastric biopsy specimens from normal controls ( n =11), superficial gastritis ( n =32), atrophic gastritis with intestinal metaplasia ( n =83), dysplasia ( n =25) and gastric carcinoma ( n =10) were studied by immunohistochemical staining of proliferating cell nuclear antigen (PCNA). RESULTS The gastric epithelial proliferation, expressed as PCNA labeling index (LI)%, was progressively increased in successive stages from normal mucosa to gastric carcinoma regardless of H. pylori status. There was significant difference in PCNA LI% among all groups ( P <0 01). The analysis pursuing the effect of H. pylori infection on gastric epithelial proliferation in the progression from normal mucosa to gastric carcinoma showed that in superficial gastritis and mild atrophic gastritis groups, PCNA LI% in H. pylori positive patients were 13 14±1 6 and 19 68±2 22 respectively, significantly higher than 6 95±0 78 and 11 34±1 89 in H. pylori negative patients ( P <0 01); but there was no such difference in other groups ( P >0 05). CONCLUSION H. pylori infection causes increased gastric epithelial proliferation in the stages of superficial and mild atrophic gastritis and may play a part in triggering gastric carcinogenesis.展开更多
AIM To establish an experimental model of stress ulcer produced by explosive noise, and to probe into its mechanism and protection. METHODS The country standard Wistar white rats were randomly divided into control ...AIM To establish an experimental model of stress ulcer produced by explosive noise, and to probe into its mechanism and protection. METHODS The country standard Wistar white rats were randomly divided into control group ( n =8), which were neither stimulated nor protected, and stimulating group (divided into subgroups A, B and C, including 8 rats each which were decapitated to draw blood for test immediately, 12 hours and 24 hours after stimulation) and prevention group (divided into subgroups A, B and C, having 8 rats each, subgroup A was given cimetidine, B anisodamine and C both drugs). Firing noises of submachine guns were used as inflicting factor. The rats were fasted for 24 hours and stimulated by firing noise for 12 hours. The change of ulcer index, gastric mucosal and related serum hormones were observed. RESULTS Stress ulcer was significant in the stimulating group, and its ulcer index (8 6±0 6) was remarkably higher than that in both the control group and prevention group (0 3±0 1, P <0 01). Its serum gastrin (Gas ng/L , 294±163 vs 63±40, P <0 01) and endothelin (ET ng/L , 181±57 vs 135±42, P <0 01) were apparently higher than those in the control group, and its serum nitric oxide (NO) level was conspicuously lower than that in the control group ( ng/L , 0 2±0 1 vs 0 8±0 5, P <0 05), while the serum gastrin level ( ng/L , 556±225) in prevention group was distinctly higher than that in both the control ( P <0 01) and stimulating group ( P <0 05). There were no significant differences in the changes of ET and NO between the control and the stimulating groups. CONCLUSION Stress ulcer model of rats can be successfully established by the stimulation of explosive noise. Gas, ET and NO are related to the formation of stress ulcer, and play an important role in its mechanism. Hepatic function affected by noise is observed in this experiment.展开更多
文摘AIM To study the effect of Helicobacter pylori ( H. pylori ) infection on gastric epithelial proliferation in the progression from normal mucosa to gastric carcinoma. METHODS Gastric biopsy specimens from normal controls ( n =11), superficial gastritis ( n =32), atrophic gastritis with intestinal metaplasia ( n =83), dysplasia ( n =25) and gastric carcinoma ( n =10) were studied by immunohistochemical staining of proliferating cell nuclear antigen (PCNA). RESULTS The gastric epithelial proliferation, expressed as PCNA labeling index (LI)%, was progressively increased in successive stages from normal mucosa to gastric carcinoma regardless of H. pylori status. There was significant difference in PCNA LI% among all groups ( P <0 01). The analysis pursuing the effect of H. pylori infection on gastric epithelial proliferation in the progression from normal mucosa to gastric carcinoma showed that in superficial gastritis and mild atrophic gastritis groups, PCNA LI% in H. pylori positive patients were 13 14±1 6 and 19 68±2 22 respectively, significantly higher than 6 95±0 78 and 11 34±1 89 in H. pylori negative patients ( P <0 01); but there was no such difference in other groups ( P >0 05). CONCLUSION H. pylori infection causes increased gastric epithelial proliferation in the stages of superficial and mild atrophic gastritis and may play a part in triggering gastric carcinogenesis.
文摘AIM To establish an experimental model of stress ulcer produced by explosive noise, and to probe into its mechanism and protection. METHODS The country standard Wistar white rats were randomly divided into control group ( n =8), which were neither stimulated nor protected, and stimulating group (divided into subgroups A, B and C, including 8 rats each which were decapitated to draw blood for test immediately, 12 hours and 24 hours after stimulation) and prevention group (divided into subgroups A, B and C, having 8 rats each, subgroup A was given cimetidine, B anisodamine and C both drugs). Firing noises of submachine guns were used as inflicting factor. The rats were fasted for 24 hours and stimulated by firing noise for 12 hours. The change of ulcer index, gastric mucosal and related serum hormones were observed. RESULTS Stress ulcer was significant in the stimulating group, and its ulcer index (8 6±0 6) was remarkably higher than that in both the control group and prevention group (0 3±0 1, P <0 01). Its serum gastrin (Gas ng/L , 294±163 vs 63±40, P <0 01) and endothelin (ET ng/L , 181±57 vs 135±42, P <0 01) were apparently higher than those in the control group, and its serum nitric oxide (NO) level was conspicuously lower than that in the control group ( ng/L , 0 2±0 1 vs 0 8±0 5, P <0 05), while the serum gastrin level ( ng/L , 556±225) in prevention group was distinctly higher than that in both the control ( P <0 01) and stimulating group ( P <0 05). There were no significant differences in the changes of ET and NO between the control and the stimulating groups. CONCLUSION Stress ulcer model of rats can be successfully established by the stimulation of explosive noise. Gas, ET and NO are related to the formation of stress ulcer, and play an important role in its mechanism. Hepatic function affected by noise is observed in this experiment.
