目的 探討不同病因導致的應激性胃黏膜損傷時胃黏膜環氧化酶(cyclooxygenase,COX)-2表達強度的變化及二者的關系。 方法 通過建立急性甲胺磷中毒及急性心肌梗死動物模型,采用胃黏膜潰瘍指數評定是否發生胃黏膜損傷,采用免疫組化方法測定胃黏膜COX-2的表達強度變化。 結果 ①成功建立大鼠急性甲胺磷中毒及急性心肌梗死動物模型；②在急性甲胺磷中毒及急性心肌梗死這兩種應激狀態下胃黏膜發生了損傷；③不同病因所致應激性胃黏膜損傷時胃黏膜COX-2表達增加。 結論 臨床危重疾病可產生應激狀態胃黏膜損傷,胃黏膜潰瘍指數增加。不同病因所致的應激性胃黏膜損傷時胃黏膜COX-2表達增加,可能為一種保護機制。
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.
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.
目的 探討H2受體拮抗劑和質子泵抑制劑（PPI）緩解急性胃黏膜損傷的時效性研究。 方法 對2008年1月－2010年1月在急診科就診的98例急性乙醇中毒后胃黏膜損傷患者，隨機分為對照組50例，治療組48例。常規給予休息、保暖，補液，維持水、電解質、酸堿平衡，維持循環功能等治療基礎上，對照組給予H2受體拮抗劑治療，治療組給予PPI治療。通過觀察急性胃黏膜損傷患者上消化道癥狀及體征，記錄不同飲酒及飲酒量，并根據患者就診時間及不同飲酒組治療后上消化道癥狀完全緩解時間進行比較。 結果 治療組上消化道癥狀緩解所需時間與對照組比較差異有統計學意義（P＜0.001），不同飲酒組上消化道癥狀緩解時間上差異有統計學意義（P=0.000）。 結論 PPI在緩解急性乙醇中毒所致胃黏膜損傷的時效上更明顯，具有臨床價值。
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.