腹安汤治疗腹泻型肠易激综合征40例疗效观察及机制探讨

目的:探讨腹安汤治疗腹泻型肠易激综合征的临床疗效及对血浆血管活性肠肽(VIP)、P物质(SP)的影响。方法:将80例患者随机分为治疗组和对照组,每组40例,治疗组用腹安汤,对照组用匹维溴胺,对比两组的临床疗效和治疗前后血浆VIP、SP水平。另选20例体检健康者作正常对照。结果:治疗组总有效率92.5%,对照组总有效率77.5%,两组总有效率比较,差异有统计学意义(P<0.05);血浆VIP、SP水平在治疗组用药前后比较,有显著性差异(P<0.05),在治疗组用药后与对照组比较,有显著性差异(P<0.05)。结论:腹安汤治疗腹泻型肠易激综合征疗效明显,值得临床推广应用。其作用机制之一可能是通过调节血浆中VIP、SP的分泌而达到治疗效果。     

三七总皂苷调控PI3K/AKT信号通路预防糖尿病大血管病变的机制

目的从PI3K/AKT信号通路研究三七总皂苷(panax notoginseng saponins,PNS)预防糖尿病大血管病变的机制。方法雄性SD大鼠分为对照组、模型组和治疗组,模型组和治疗组大鼠高脂饲料喂养6周后给予链脲佐菌素单次腹腔注射(30 mg·kg^-1体质量)建立2型糖尿病模型,成模后治疗组给予PNS灌胃干预(100mg·kg^-1体质量)。血糖仪检测大鼠空腹尾静脉血糖(FBG),ELISA法测定血清空腹胰岛素(FINS)和糖化血红蛋白(GHbA1c)水平,苏木素-伊红(HE)染色观察腹主动脉病理形态改变,荧光定量PCR检测腹主动脉标记物MMP2、MMP9、CD34、VEGF及PI3K、AKT mRNA相对表达,Western Blot法观察PI3K和AKT蛋白表达情况。结果模型组和治疗组大鼠在STZ注射造模后,FBG均显著高于对照组(P<0.01和P<0.01),两组间差异无统计学意义(P>0.05)。模型组和治疗组血清INS均显著高于对照组(P<0.01和P<0.01),治疗组INS显著低于模型组(P<0.05)。HE染色显示,与对照组比较,模型组动脉壁变薄,平滑肌细胞增多,排列紊乱,内膜不光滑;治疗组较模型组明显改善。模型组MMP2、MMP9表达较对照组显著上调(P<0.05和P<0.01),治疗组MMP9较模型组显著下调(P<0.01)。模型组CD34、VEGF表达较对照组显著上调(P<0.05和P<0.01),治疗组CD34较模型组显著下调(P<0.05)。模型组大鼠PI3K表达较对照组显著上调(P<0.05),治疗组PI3K表达较模型组显著下调(P<0.05)。模型组PI3K蛋白、p-AKT蛋白表达均显著高于对照组(P<0.01和P<0.01),治疗组PI3K、p-AKT均显著低于对照组(P<0.01和P<0.05),模型组p-AKT/AKT显著高于对照组(P<0.05),治疗组p-AKT/AKT较模型组有显著降低趋势,且与对照组差异无统计学意义。结论PNS可能通过下调PI3K/AKT信号通路预防糖尿病大血管病变。     

大鼠正常血糖脑缺血及高血糖脑缺血时p38MAPK的表达

目的探讨p38MAPK与脑缺血及高血糖脑缺血损害的关系。方法实验大鼠随机分为3组:(1)高血糖脑缺血组(简称高血糖组,20只),于脑缺血术前30min尾静脉注射25%葡萄糖(4g/kg);(2)正常血糖脑缺血组(简称正常血糖组,20只),于脑缺血术前30min尾静脉注射等量18%D-甘露醇;(3)手术非缺血性对照组(10只)。采用双侧颈动脉结扎和放血法在高血糖组和正常血糖组制造全脑缺血模型,通过免疫组织化学技术与Western blot免疫印迹技术对比检测缺血30min,再灌注1、3、6h各时间点脑组织p38MAPK表达。结果对照组海马CAI区、CAIII区,未见p38MAPK阳性神经元;免疫组化在CAI区和CAIII区,在缺血30min,再灌注13、、6 h不同时间点高血糖组阳性细胞数与正常血糖组比较差异无统计学意义(P>0.05);Western blot检测可见正常血糖组和高血糖组脑缺血30min,再灌注1、36、h时激活的p38MAPK蛋白明显增加,高血糖组灰度比值(分别为7.25±1.91、8.64±2.41、9.58±2.98、12.00±3.01)与正常血糖组(分别为6.68±1.51、7.92±1.75、8.34±2.00、9.02±2.27)比较,p38MAPK差异无统计学意义(P>0.05)。结论脑缺血再灌注时p38MAPK被激活,参与缺血性损伤的发生,但高血糖并不能明显增加p38MAPK的总量,故在高血糖加重脑缺血性损伤中p38MAPK可能不发挥主要作用。     

麻仁软胶囊对便秘型 IBS 大鼠模型肠黏膜 5 - HT 含量的影响

目的研究麻仁软胶囊对便秘型肠易激综合征（IBS）模型大鼠5-HT含量的影响,探讨麻仁软胶囊治疗便秘型IBS的作用机制。方法将大鼠分为中药组、西药组、模型组、正常组4组,采用冰水灌胃慢性刺激方法将前3组复制为大鼠便秘型IBS模型,观察各组大鼠粪便的数量及性状,于第14天造模成功后中药组灌中药,西药组灌西药,模型组及正常组予以正常饮食。于第28天将各组大鼠进行解剖取其部分结肠,将其做成石蜡切片,在HE染色下和SABC免疫组化染色下镜下观察各组肠组织变化及肠黏膜上5-HT的含量。结果IBS模型大鼠5-HT表达增高,出现IBS临床症状;经麻仁软胶囊干预后,大鼠5-HT表达降低。结论麻仁软胶囊可增高大鼠肠道敏感性,其作用机制与降低大鼠结肠5-HT表达、增高肠道敏感性有关。     

Associations between Abnormal Eating Styles and Irritable Bowel Syndrome: A Cross-Sectional Study among Medical School Students

(1) Background: Few studies have investigated the association between eating styles and IBS. This study aimed to explore the association between abnormal eating styles and irritable bowel syndrome (IBS). (2) Methods: This cross-sectional study investigated students in China Medical University and Shenyang Medical College. Eating styles were evaluated by the Dutch Eating Behavior Questionnaire (DEBQ), and IBS was diagnosed according to Rome III criteria. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). (3) Results: A total of 335 students were diagnosed with IBS. Students with the total scores in tertile 2 and 3 had 1.29 times and 2.75 times higher risk of IBS than students with the total scores in tertile 1, respectively. Simultaneously, the risk of IBS in the tertile 3 of external eating, emotional eating, and restraint eating trends was 3.87 times, 2.71 times, and 3.82 times higher than that of tertile 1, respectively. (4) Conclusions: this study showed that a high score in both total eating styles and each eating style was associated with the odds of having IBS and suggested that the psychological factors behind eating styles may play a critical role in controlling the IBS.     

高血糖对中重型颅脑损伤患者预后的影响

目的了解高血糖与颅脑损伤严重程度之间的关系以及控制血糖对颅脑损伤预后的影响。方法我们前瞻性地研究了146例中重型颅脑损伤患者(格拉斯哥昏迷评分GCS3~12分)的血糖,并将血糖高于11.1mmol/L的患者随机分为两组,一组接受强化胰岛素治疗,将血糖控制在6.11mmol/L以下,另一组不接受胰岛治疗,以明确血糖水平同损伤严重程度之间的关系以及控制血糖对预后的影响。结果重型颅脑损伤患者的血糖水平明显高于中型颅脑损伤患者,并且颅内压水平同血糖水平显著相关。同血糖水平高于11.1mmol/L的患者相比,血糖控制在6.11mmol/L以下的患者预后明显改善。结论早期高血糖是颅脑损伤后应激反应的一个组成部分,是预测损伤严重度的一个重要指标,控制血糖可改善颅脑损伤患者的预后。     

Stratification of Gallstones in the Gallbladder

A clinical approach to the diagnosis of congenital cardiac malformations is described which the authors have found effective in exposing the important signs and their significance. Each available diagnostic method is evaluated separately before all data are correlated.

Clinical diagnosis based on history, physical examination, roentgenography and electrocardiography was 94 per cent accurate in a series of cases seen in office consultation and 90 per cent accurate in a series of hospital cases reviewed. The significance of the various signs and symptoms that are routinely searched for in the physical examination is discussed.

The salient points in the clinical diagnosis of the common entities are presented.