Dysplasia of gastric stump mucosa in 47 cases was studies.Nuclear DNA contents were measured with an automatic imagie analysis system.The results showed that the mean values of the nuclear DNA contents,area,perimeter,maximum diameter,minimum diameter increased with the increase of severity of dysplasia in gastric stump mucosa(Plt;0.01);where as nuclear form factor decreased with the increase of severity of dysplasia in gastric stump mucosa(Plt;0.05).Severe dysplasia is similar to that of gastric stump cancer in the DNA ploidy histogram.Our results indicate biological behaviour of gastric stump mucosa dysplasia.This study suggests that DNA contents analysis may be used as an important reference for grading,screening,and treating dysplasia of gastric stump mucosa.
目的 探讨H2受体拮抗剂和质子泵抑制剂（PPI）缓解急性胃黏膜损伤的时效性研究。 方法 对2008年1月－2010年1月在急诊科就诊的98例急性乙醇中毒后胃黏膜损伤患者，随机分为对照组50例，治疗组48例。常规给予休息、保暖，补液，维持水、电解质、酸碱平衡，维持循环功能等治疗基础上，对照组给予H2受体拮抗剂治疗，治疗组给予PPI治疗。通过观察急性胃黏膜损伤患者上消化道症状及体征，记录不同饮酒及饮酒量，并根据患者就诊时间及不同饮酒组治疗后上消化道症状完全缓解时间进行比较。 结果 治疗组上消化道症状缓解所需时间与对照组比较差异有统计学意义（P＜0.001），不同饮酒组上消化道症状缓解时间上差异有统计学意义（P=0.000）。 结论 PPI在缓解急性乙醇中毒所致胃黏膜损伤的时效上更明显，具有临床价值。
目的 探讨不同病因导致的应激性胃黏膜损伤时胃黏膜环氧化酶(cyclooxygenase,COX)-2表达强度的变化及二者的关系。 方法 通过建立急性甲胺磷中毒及急性心肌梗死动物模型,采用胃黏膜溃疡指数评定是否发生胃黏膜损伤,采用免疫组化方法测定胃黏膜COX-2的表达强度变化。 结果 ①成功建立大鼠急性甲胺磷中毒及急性心肌梗死动物模型；②在急性甲胺磷中毒及急性心肌梗死这两种应激状态下胃黏膜发生了损伤；③不同病因所致应激性胃黏膜损伤时胃黏膜COX-2表达增加。 结论 临床危重疾病可产生应激状态胃黏膜损伤,胃黏膜溃疡指数增加。不同病因所致的应激性胃黏膜损伤时胃黏膜COX-2表达增加,可能为一种保护机制。
ObjectiveTo summarize the research progress of gastric intestinal metaplasia (GIM). MethodsThe literatures about the research progress of the GIM were reviewed. ResultsThe most important histological feature of GIM was the presence of goblet cells, which was associated with the risk factors of Helicobacter pylori, gastric ulcer, reflux of bile acid, old age, overweight, and so on. Eradication of Helicobacter pylori, individual drug intervention, and regular endoscopic surveillance were considered to be effective prevention and treatment measures. GIM was recognized as the precancerous lesion of gastric cancer, however, the pathogenesis of GIM in gastric carcinogenesis had not been recognized so far. ConclusionsIt has a relationship between GIM and gastric cancer. The mechanism of GIM, the pathogenesis of GIM in gastric cancer, individual therapy measures, and the formulation of endoscopic surveillance strategy, however, still need further multicenter and large clinical study.
Gastric cancer is common as one kind of digestive tract malignant tumor, and Helicobacter pylori (Hp) infection is the most important cause of gastric cancer. With the wide application of quadruple therapy, the incidence of Hp-related gastric cancer has been significantly decreased. In addition to the involvement of gastric microbes in the regulation of normal gastric physiological function, the imbalance of gastric microbes is also involved in the pathogenesis of gastritis and gastric cancer. The imbalance of gastric microbes also plays an important role in the development of gastric cancer after eradication of Hp, and the mechanism has also been preliminary studied. Based on this, this article reviews the research progress of gastric microbes in gastric cancer, in order to further understand the pathogenic mechanism of gastric cancer and provide reference for seeking safer and more effective treatment for gastric cancer.