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| 1 | Diabetes and gastric cancer: The potential links显示文摘This article reviews the epidemiological evidence linking diabetes and gastric cancer and discusses some of the potential mechanisms,confounders and biases in the evaluation of such an association.Findings from four meta-analyses published from 2011 to 2013 suggest a positive link,which may be more remarkable in females and in the Asian populations.Putative mechanisms may involve shared risk factors,hyperglycemia,Helicobacter pylori(H.pylori)infection,high salt intake,medications and comorbidities.Diabetes may increase the risk of gastric cancer through shared risk factors including obesity,insulin resistance,hyperinsulinemia and smoking.Hyperglycemia,even before the clinical diagnosis of diabetes,may predict gastric cancer in some epidemiological studies,which is supported by in vitro,and in vivo studies.Patients with diabetes may also have a higher risk of gastric cancer through the higher infection rate,lower eradication rate and higher reinfection rate of H.pylori.High salt intake can act synergistically with H.pylori infection in the induction of gastric cancer.Whether a higher risk of gastric cancer in patients with diabetes may be ascribed to a higher intake of salt due to the loss of taste sensation awaits further investigation.The use of medications such as insulin,metformin,sulfonylureas,aspirin,statins and antibiotics may also influence the risk of gastric cancer,but most of them have not been extensively studied.Comorbidities may affect the development of gastric cancer through the use of medications and changes in lifestyle,dietary intake,and the metabolism of drugs.Finally,a potential detection bias related to gastrointestinal symptoms more commonly seen in patients with diabetes and with multiple comorbidities should be pointed out.Taking into account the inconsistent findings and the potential confounders and detection bias in previous epidemiological studies,it is expected that there are still more to be explored for the clarification of the association between diabetes and gastric cancer. | Chin-Hsiao Tseng Farn-Hsuan Tseng | 2014 | World Journal of Gastroenterology2014,20,7: | 13 |
| 2 | 2型糖尿病患者幽门螺旋杆菌感染情况及胃肠病变特点显示文摘目的探讨2型糖尿病患者幽门螺旋杆菌感染情况及胃肠病变特点。方法选择行胃镜检查的453患者的病历资料进行回顾性分析,根据是否合并2型糖尿病分为DM组(213例)及NDM组(240例)。观察两组患者幽门螺旋杆菌感染率及胃镜下胃肠病变检出情况,并进一步分析消化性溃疡临床类型、大小及慢性胃炎临床类型。结果 DM组的幽门螺旋杆菌感染率高于NDM组(P<0.05)。DM组消化性溃疡、反流性食管炎及胃肠息肉检出率均高于NDM组(P<0.05);两组十二指肠球炎检出率无显著差异(P>0.05)。DM组的胃溃疡检出率及溃疡直径≥1.0 cm的患者占比高于NDM组(P<0.05);两组十二指肠溃疡及复合型溃疡检出率无显著差异(P>0.05)。两组慢性浅表性胃炎及萎缩性胃炎检出率无显著差异(P>0.05);DM组慢性浅表性胃炎中合并糜烂性胃炎的比例高于NDM组(P<0.05)。结论 2型糖尿病患者幽门螺旋杆菌感染率、消化性溃疡、反流性食管炎、胃肠息肉及糜烂性胃炎检出率高,且胃溃疡占比例高,消化性溃疡面积较大。 | 宋进展 徐光耀 周海燕 李晶晶 | 2019 | 临床医学研究与实践2019,4,14: | 6 |
| 3 | 肝脏胰岛素基因治疗对链脲霉素糖尿病小鼠肠神经病变的疗效显示文摘目的:检测肝脏胰岛素基因治疗对糖尿病肠神经病变的疗效。方法:经阴茎静脉注射链脲霉素建立糖尿病模型,并随机将小鼠分为正常对照组,糖尿病组和糖尿病基因治疗组。基因治疗组接受肝脏胰岛素基因治疗,其余2组仅接受表达绿色荧光蛋白的空白病毒对照。观察各组小鼠随机血糖、体质量、亚甲基蓝排空率、肠道总长度、亚甲基蓝肠道绝对和相对前进距离,结肠透壁电刺激反应以及结肠神经核染色计数。结果:成功建立糖尿病肠神经病变小鼠模型。具体表现为:8周持续高血糖状态,肠道总长度的延长,亚甲基蓝相对前进距离缩短,结肠平滑肌舒张能力受损以及结肠抑制性神经核减少。而糖尿病基因治疗组小鼠可有效预防或改善上述异常指标,从而阻止肠神经病变的发生。结论:肝脏胰岛素基因治疗可有效预防链脲霉素糖尿病小鼠肠神经病变。 | 游硕 张清 Mallappa Anitha 贾定武 Darin E.0lson Shanthi Srinivasan Peter M.Thule 周智广 | 2011 | 中南大学学报(医学版)2011,36,6: | 1 |
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