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
目的本文从流行病学角度研究西安地区幽门螺杆菌细胞毒素相关蛋白 A(CagA)阳性 Hp 菌株感染与胃十二指肠溃疡发病的关系.方法采用病例对照研究方法,病例组与对照组的配比比例为1:2.病例组为本院消化科自1997-10/1998-10连续住院的患者,...目的本文从流行病学角度研究西安地区幽门螺杆菌细胞毒素相关蛋白 A(CagA)阳性 Hp 菌株感染与胃十二指肠溃疡发病的关系.方法采用病例对照研究方法,病例组与对照组的配比比例为1:2.病例组为本院消化科自1997-10/1998-10连续住院的患者,经内镜检查及病理检查证实为活动期胃溃疡和(或)十二指肠溃疡.对照组分为两组,对照1组为同期住院的本科及其他科住院的非胃十二指肠疾病患者,对照2组为同期普查健康人群.病例组与对照组的配比因素为性别、民族、年龄(相差5岁以内).采用问卷调查,内容涉及与胃十二指肠溃疡发病可能有关的32个因素,对所有因素进行量化,应用 SAS 软件进行处理.CagA 阳性 Hp 感染的检测结果分析采用 x^2检验.对所调查因素首先进行1:1及1:2单因素条件 Logistic 回归分析,有显著性意义的因素,计算近似相对危险度(odds ratio,OR)及其95%的可信区间(confidence interval,CI).两因素协同作用采用分层分析方法.对单因素分析时作用较大及调查结果较准确的因素,用多因素条件 Logistic 回归分析.血清中抗 CagA 抗体的检测采用斑点金免疫渗滤法(DIGFA).结果①在胃溃疡组与对照1组及对照2组的配对研究中,胃溃疡组的 CagA 阳性 Hp 感染率显著高于两个对照组,OR 分别为5.0与6.5,P 分别<0.05及<0.01.②在十二指肠溃疡组与对照1组及对照2组的配对研究中,十二指肠溃疡组的CagA 阳性 Hp 感染率显著高于两个对照组,OR 分别为9.33与11.00,P 分别<0.05及<0.01.③1:1及1:2单因素及多因素 Logistic 回归分析表明,Caga 阳性 Hp 感染、吸烟、饮酒、食酸辣食物、生活不规律、精神因素等因素与胃十二指肠溃疡发病呈正相关,而按时进餐与胃十二指肠溃疡发病呈负相关.cagA 阳性 Hp 感染与胃溃疡及十二指肠溃疡的发生具有密切的相关性(OR=16.61-84.49).④双因素分层分析中,吸烟、饮酒、生活不规律、精神因素、食酸辣食物等因素与 CagA 阳性Hp 感染之间作用相互独立,但在胃十二指肠溃疡病的发生中具有协同作用.结论消化性溃疡的发生是众多因素共同作用的结果,CagA 阳性 Hp 菌株感染是引起胃溃疡及十二指肠溃疡多因素病因学中一个非常重要的、危险的因素.重视 CagA 阳性 Hp 菌株的研究,对预防和治疗消化性溃疡具有重要的临床意义和社会意义.展开更多
目的观察幽门螺杆菌(Hp)感染诱导胃粘膜上皮细胞凋亡与Bax 蛋白表达的关系,探讨 Hp 诱导胃粘膜上皮细胞凋亡的机制。方法采用脱氧核糖核酸末端转移酶介导的缺口末端标记(TUNEL)技术原位观察和比较73例慢性胃炎患者胃粘膜上皮细胞凋亡情...目的观察幽门螺杆菌(Hp)感染诱导胃粘膜上皮细胞凋亡与Bax 蛋白表达的关系,探讨 Hp 诱导胃粘膜上皮细胞凋亡的机制。方法采用脱氧核糖核酸末端转移酶介导的缺口末端标记(TUNEL)技术原位观察和比较73例慢性胃炎患者胃粘膜上皮细胞凋亡情况,对其中50例 Hp 阳性患者 Hp 根除前后胃粘膜上皮细胞凋亡的变化进行检测;并采用免疫组织化学染色检测 Bax 蛋白表达变化。结果 Hp 阳性患者胃粘膜上皮细胞凋亡指数为12.8%,明显高于 Hp 阴性者(3.6%)(t=6.64,P<0.01);Hp 根除后胃粘膜上皮细胞凋亡指数(4.4%)较治疗前明显降低(12.5%,t=5.39,P<0.01),而持续阳性者凋亡指数无明显降低,Hp阳性患者胃粘膜上皮细胞 Bax 蛋白表达率为62.3%,显著高于Hp 阴性者(35.0%,x^2=4.36,P<O.05);Bax 蛋白表达阳性的 Hp 阳性患者在 Hp 根除后 Bax 阳性细胞密度显著减少(t=3.18,P<0.01),而 Hp 未被根除者 Bax 阳性细胞密度无明显变化。结论 Hp 感染可诱导胃粘膜上皮细胞凋亡,这可能是 Hp 参与胃癌发生的重要机制之一;Hp 感染可促进 Bax 蛋白表达增加,这可能是 Hp 感染诱导胃粘膜上皮细胞凋亡的机制之一。展开更多
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.
文摘目的观察幽门螺杆菌(Hp)感染诱导胃粘膜上皮细胞凋亡与Bax 蛋白表达的关系,探讨 Hp 诱导胃粘膜上皮细胞凋亡的机制。方法采用脱氧核糖核酸末端转移酶介导的缺口末端标记(TUNEL)技术原位观察和比较73例慢性胃炎患者胃粘膜上皮细胞凋亡情况,对其中50例 Hp 阳性患者 Hp 根除前后胃粘膜上皮细胞凋亡的变化进行检测;并采用免疫组织化学染色检测 Bax 蛋白表达变化。结果 Hp 阳性患者胃粘膜上皮细胞凋亡指数为12.8%,明显高于 Hp 阴性者(3.6%)(t=6.64,P<0.01);Hp 根除后胃粘膜上皮细胞凋亡指数(4.4%)较治疗前明显降低(12.5%,t=5.39,P<0.01),而持续阳性者凋亡指数无明显降低,Hp阳性患者胃粘膜上皮细胞 Bax 蛋白表达率为62.3%,显著高于Hp 阴性者(35.0%,x^2=4.36,P<O.05);Bax 蛋白表达阳性的 Hp 阳性患者在 Hp 根除后 Bax 阳性细胞密度显著减少(t=3.18,P<0.01),而 Hp 未被根除者 Bax 阳性细胞密度无明显变化。结论 Hp 感染可诱导胃粘膜上皮细胞凋亡,这可能是 Hp 参与胃癌发生的重要机制之一;Hp 感染可促进 Bax 蛋白表达增加,这可能是 Hp 感染诱导胃粘膜上皮细胞凋亡的机制之一。
