简介：目的：这研究的目的是在腹的子宫切除以后把吗啡消费与在针的麻醉(SA)(bupivacaine，吗啡和芬太奴)和一般麻醉(GA)(sufentanil)之间的控制病人的痛觉缺失(PCA)作比较。方法：四十个女人随机被分配与bupivacaine收到SA15mg，intrathecal吗啡的0.15mg和有sufentanil的芬太奴或GA的15μg，两个都与PCA结合了。主要结果是有PCA设备的吗啡消费。第二等的结果是在休息并且在标准化规模上的视觉模拟规模，恶心，瘙痒和呼吸消沉上的应力下面的手术后的疼痛。结果措施在6，12，18，24和48h被记录麻醉以后。联合起来的麻醉以后的照顾(PACU)和医院停留的持续时间被记录。结果：在SA组的病人消费了至少twotimes更少吗啡在每次间隔比GA组：在48h，他们使用了19±17对81±31mg(P<0.0001)。在休息的手术后的疼痛在SA组是更低的直到第18小时并且在应力下面直到第48。在GA组有更多的镇静直到第18小时。小差别在瘙痒的发生被观察。恶心在在GA组的第6小时是更强烈的。处于呼吸的率没有差别。PACU停留的持续时间为SA组是更短的(52±9对73±11min，P<0.0001)这是医院停留的持续时间(2.2±0.4对3.3±0.7天，P=0.01)。结论：有芬太奴的15μg的intrathecal吗啡0.15mg减少，这被结束由没有为经历腹的子宫切除的女人增加不利反应的PCA的手术后的疼痛和吗啡消费。

简介：瞄准：在与足够的胆汁的排水在胆汁郁积的病人减少胆管炎在以后决定ciprofloxacin的角色内视镜后退cholangiopancreatography(ERCP)。方法：A使随机化的、控制试用在Rajavithi医院在48个胆汁郁积的病人被执行(ERCP的第三级的工作分派中心：600个案例每年)。所有48个病人在开始任何过程前为30min收到了200mgciprofloxacin静脉注射，然后随机在二个组被划分。在学习的22个病人在ERCP以后组织不断地收到的ciprofloxacin直到48h。胆汁的阻塞的原因，胆汁和血的细菌学(在胆管炎)并且临床的胆管炎被记录。结果：48个病人被注册并且划分了成连续ciprofloxacin治疗组(n=22)并且不连续的ciprofloxacin治疗组(n=26)。在ERCP期间，石头在5个病人在22个病人，在24个病人的恶性病和另外的病理学的损害被发现。谁的22个病人的(4.5%)收到了ciprofloxacin，(6.3%)2在ERCP以后中止了ciprofloxacin的26个病人开发了胆管炎(相对风险=0.71；95%CI=0.14-3.65；P=0.88)。Bacterobilia在27被发现(56.3%)从48个病人。E。关口i和链球菌青绿色的ans是最普通的有机体。结论：在有在足够的胆汁的排水过程以后的胆汁郁积的病人的ciprofloxacin的不断的使用不在减少胆管炎起作用。

简介：AbstractObjective:This study aimed at investigating the expression of nuclear factor kappa B (NF-κB) and mammalian target of rapamycin (mTOR) related signal pathways in liver tissues of intrahepatic cholestasis of pregnancy animal models.Methods:Estrogen (EE)-induced cholestasis and a placental ischemia-reperfusion (IR) model were established in pregnant rats. All pregnant rats were divided into four groups by random number table: EE-IR group (n= 6), EE-sham group (n = 6), control-IR group (n= 6) and control-sham group (n= 6). Liver expression of mTOR, its upstream regulator DNA damage response-1 (REDD1), and downstream factor glucose transporter type-1 (GLUT1), accompanied by NF-κB (p65 is the most important component), its activator toll-like receptor 4 (TLR4), and inhibitor IκBα, were detected by western blot analysis and real-time polymerase chain reaction. The intergroup comparisons were performed with a one-way analysis of variance, the comparisons among groups were analyzed with the nonparametric Kruskal-Wallis test.Results:Giving pregnant rats EE alone reduced the hepatic expression of IκBα (0.72 ± 0.20 vs. 1.01 ± 0.07, P= 0.008). Meanwhile, giving pregnant rats placental IR alone increased liver levels of REDD1 (3.24 ± 0.98 vs. 1.06 ± 0.24, P= 0.025), GLUT1 (2.37 ± 0.82 vs. 1.09 ± 0.10, P= 0.039), TLR4 (2.12 ± 0.29 vs. 1.20 ± 0.28, P= 0.010), and p65 (2.09 ± 0.85 vs. 1.04 ± 0.06, P= 0.023), and decreased hepatic mTOR (0.50 ± 0.07 vs. 1.01 ± 0.03, P= 0.001) and IκBα (0.61 ± 0.08 vs. 1.01 ± 0.07, P= 0.014) expression. Subjecting EE-treated rats to placental IR did not further alter liver levels of GLUT1 (2.02 ± 0.45 vs. 1.79 ± 0.39, P= 0.240), TLR4 (2.10 ± 0.74 vs. 1.60 ± 0.36, P= 0.129), or p65 (2.41 ± 0.83 vs. 1.65 ± 0.46, P= 0.145), whereas it did decrease hepatic mTOR (0.42 ± 0.09 vs. 0.90 ± 0.14, P= 0.008) and IκBα (0.43 ± 0.09 vs. 0.72 ± 0.20, P= 0.004) expression and enhance REDD1 expression (4.46 ± 0.65 vs. 2.05 ± 0.47, P= 0.009). Placental IR stress did impact the hepatic expression of REDD1-mTOR-GLUT1 and TLR4/NF-κB/IκBα in pregnant rats.Conclusion:Placental IR-induced hepatic GLUT1, TLR4, and p65 alternation, which responded efficiently in control rats, were impaired in EE-induced ICP rats.

简介：AbstractObjective:To investigate the possible regulatory mechanism of corticotropin-releasing hormone (CRH), urocortin (UCN), and Wolfram syndrome 1 (WFS1) in 17α-ethynylestradiol (EE)-induced intrahepatic cholestasis pregnant rats and its ischemia reperfusion (IR) model.Methods:Pregnant rats (n=60) were randomly divided into four experimental groups by random number table (Control, EE, IR, and EE-IR groups),and were studied on the 17th, 19th, and 21st gestational days (GD) (n=5 in each group at the indicated time). Growth and development indicators of fetal rats among these four groups were recorded. Enzyme-linked immunosorbent assay was employed to detect CRH, UCN, and WFS1 levels in maternal sera. Western blotting and real-time polymerase chain reaction were used to quantify placental protein and placental mRNA levels of CRH, UCN, and WFS1. Multivariate analysis of variance and least significant difference test were used to establish the group and individual comparisons.Results:A significant difference was found in placenta weight (F=8.10, P<0.05), fetal rat weight (F=40.86, P<0.05), fetal rat length (F=61.61, P<0.05), and fetal rat tail length (F=55.63, P<0.05) among four groups on the 17th ,19th , and 21st GD.What’s more, the overall differences of maternal serum UCN levels among Control, EE, IR, and EE-IR groups were significant (F=2.48, P<0.05). Expression of WFS1 mRNA in the EE-IR group was significantly increased and higher than Control (0.46±0.15 vs. 0.24±0.09, P<0.05), EE (0.46±0.15 vs. 0.17±0.04, P>0.05), and IR (0.46±0.15 vs. 0.22±0.15, P>0.05) groups at 19th GD, indicating that endoplasmic reticulum stress may be activated. However, the expression of CRH (0.42±0.05 vs. 0.58±0.12, P<0.05), UCN (0.43±0.01 vs. 0.47±0.16, P>0.05), and WFS1 (0.57±0.07 vs. 0.74±0.12, P>0.05) protein in the EE-IR group was subsided compared to the IR group at 17th GD.Conclusion:Fetal rat growth restriction was found in the EE-induced intrahepatic cholestasis model. This study revealed that significant changes in the maternal sera level of UCN , placental level of WFS1 mRNA and placental levels of CRH, UCN, and WFS1 protein in chronic versus acute stress in a rat model of pregnancy. This suggests an impaired compensatory vasodilatory effect mediated by these factors at gene transcription and protein translation levels, following acute hypoxia stress in EE-induced intrahepatic cholestasis in pregnant rats.