Analysis of Ecstasy Tablets Using Capillary Electrophoresis with Capacitively Coupled Contactless Conductivity Detection

A method for the identification of 3,4‐methylenedioxymethamphetamine (MDMA) and meta‐chlorophenylpiperazine (mCPP) was developed employing capillary electrophoresis (CE) with capacitively coupled contactless conductivity detection (C⁴D). Sample extraction, separation, and detection of “Ecstasy” tablets were performed in <10 min without sample derivatization. The separation electrolyte was 20 mm TAPS/Lithium, pH 8.7. Average minimal detectable amounts for MDMA and mCPP were 0.04 mg/tablet, several orders of magnitude lower than the minimum amount encountered in a tablet. Seven different Ecstasy tablets seized in Rio de Janeiro, Brazil, were analyzed by CE‐C⁴D and compared against routine gas chromatography‐mass spectrometry (GC‐MS). The CE method demonstrated sufficient selectivity to discriminate the two target drugs, MDMA and mCPP, from the other drugs present in seizures, namely amphepramone, fenproporex, caffeine, lidocaine, and cocaine. Separation was performed in <90 sec. The advantages of using C⁴D instead of traditional CE‐UV methods for in‐field analysis are also discussed.     

A unified model of settlement and trial expenditures: The Priest–Klein model extended

Settlement and trial expenditures are crucially interrelated. The literature on settlement, however, takes no account of models of trial. In this paper, we develop a unified model of settlement and trial expenditures. We do this by discarding the usual assumption of settlement models that trial costs are constant across cases. Instead, we follow the literature on trial by permitting trial costs to vary with the legal merit of the plaintiff's case. Our approach can be used to extend standard models of settlement such as the well-known Priest–Klein model as well as models based on asymmetric information. As a demonstration, we extend the Priest–Klein model and generally overturn that model's canonical results. In particular, we show that even in a fully symmetric model, predicted win rates at trial can deviate substantially from 50 percent. Furthermore, win rates will vary in response to legal reforms that shift the decision standard.     

苓桂术甘汤含药血清对过氧化氢诱导的乳鼠原代心肌细胞氧化应激损伤及细胞凋亡的影响

目的 观察苓桂术甘汤含药血清对H2O2诱导的心肌细胞氧化应激损伤及细胞凋亡的影响。方法 建立H2O2诱导的心肌细胞氧化应激损伤模型,将心肌细胞随机分为正常对照组、H2O2模型组、空白大鼠血清（20%）组、苓桂术甘汤含药血清（5%、10%、20%）组,用苓桂术甘汤含药血清（5%、10%、20%）,分别预处理心肌细胞12 h后,加入100 μmol/L H2O2继续培养6 h,用MTT法测定心肌细胞存活率,比色法检测乳酸脱氢酶（lactate dehydrogenase,LDH）、超氧化物歧化酶（superoxide dismutase,SOD）、谷胱甘肽过氧化酶（glutathione peroxidase ,GSH- Px）活性及丙二醛（malonic dialdehyde,MDA）水平,用荧光核染色法观察细胞凋亡形态学变化,流式细胞术（Annexin Ⅴ- FITC/PI）检测细胞凋亡率,荧光探针法测定氧自由基水平。结果 与正常组比较,模型组心肌细胞活力明显降低（P<0.05）,氧自由基、LDH活性及MDA水平均显著升高（P<0.05）,SOD及GSH- Px活性均显著降低（P<0.05）,细胞核浓染数目增加,细胞凋亡率明显升高（P<0.05）;与模型组比较,苓桂术甘汤含药血清组心肌细胞活力明显升高（P<0.05）,GSH- Px、SOD活性均显著升高（P<0.05）,LDH活性,氧自由基、MDA水平均显著降低（P<0.05）,心肌细胞核浓染减少,细胞凋亡率明显降低（P<0.05）。结论 苓桂术甘汤能够清除细胞内氧自由基,抑制心肌细胞凋亡,增强细胞活性,对心肌细胞氧化应激损伤具有保护作用。     

糖肾康颗粒对糖尿病肾病气阴两虚、瘀血阻络证患者血清胱抑素C及尿纤维连接蛋白的干预作用

目的 观察Ⅲ～Ⅳ期糖尿病肾病（diabetic nephropathy,DN）气阴两虚、瘀血阻络证患者血清胱抑素C（cystatin C,CysC）、尿纤维连接蛋白（urinary fibronectin,UFn）水平及糖肾康颗粒的干预作用。方法 将60例Ⅲ～Ⅳ期糖尿病肾病气阴两虚、瘀血阻络证患者随机分为治疗组和对照组,各30例,并选取20名健康体检者作为正常组。治疗组与对照组均给予常规降糖、降压治疗,治疗组加用糖肾康颗粒,疗程2个月。治疗前后分别检测治疗组与对照组尿白蛋白/尿肌酐比值（microalbuminuria/urine creatinine,MAU/UCr）、肾小球滤过率估算值（estimated glomerular filtration rate,eGFR）以及CysC、UFn水平,并与正常组比较。结果 治疗组中医证候疗效显著优于对照组（P＜0.01）;在降低MAU/UCr比值和CysC、UFn水平,以及升高eGFR水平方面,治疗组显著优于对照组（P<0.01）。结论 糖肾康颗粒可降低Ⅲ～Ⅳ期DN气阴两虚、瘀血阻络证患者血清CysC、UFn水平,并可减少DN患者尿蛋白排泄,维持肾小球滤过率,在一定程度上具有保护肾功能、延缓疾病进展的作用。     

褐藻多糖硫酸酯治疗慢性肾功能不全临床观察

目的 观察褐藻多糖硫酸酯(海昆肾喜胶囊)治疗慢性肾功能不全(chronic renal insufficiency,CRI)的临床疗效.方法 将42例CRI患者按照性别、年龄、原发疾病、血清肌酐(serum creatinine,SCr)、血尿素氮(blood urea nitrogen,BUN)、肌酐清除率(crea...     

清下解胰方及其拆方对重症急性胰腺炎大鼠血清淀粉酶的影响

目的 观察清下解胰方及其拆方对重症急性胰腺炎(severe acute pancreatitis,SAP)大鼠血清淀粉酶的影响.方法 采用逆胆胰管注射牛黄胆酸钠的方法复制SAP大鼠模型.将大鼠随机分为假手术组、模型组、清下解胰汤全方组及其拆方组(包括通腑清热、活血化瘀、疏肝理气).各中药干预组均于模型复制苏醒后即刻,模...     

丹皮酚对高脂血清诱导的大鼠主动脉内皮细胞损伤的保护作用及其黏附功能的影响

目的观察丹皮酚（Paeonal，Pae）对高脂血清诱导的大鼠单核细胞（mononuclear cell，MC）与大鼠主动脉内皮细胞（rat aortic endothelial cells，RAECs）黏附的影响及对RAECs损伤的保护作用。方法高脂乳剂灌胃大鼠并制备高脂血清；组织块预消化贴壁法培养RAECs；淋巴细胞分离液分离MC；孟加拉玫瑰红活细胞染色法测定MC与RAECs的黏附功能；甲基噻唑基四唑比色法以及台盼蓝死细胞染色法检测Pae对高脂血清诱导的RAECs损伤的保护作用。结果30～70ml／L高脂血清呈剂量依赖性地诱导MC与RAECs的黏附，50ml／L时促进MC与RAECs黏附达最大值；高脂血清与RAECs共育6h即可明显促进黏附作用，24h时达最大诱导效应。Pae在浓度为15～240μmol／L时，呈剂量依赖性地抑制高脂血清诱导的黏附作用；240μmol／L孵育24h时抑制作用最明显；Pae在30，60，120μmol／L浓度时，对高脂血清损伤的大鼠RAECs有明显的保护作用。结论Pae对高脂血清诱导的大鼠MC与RAECs黏附功能有抑制效应，对高脂血清损伤的大鼠RAECs有明显的保护作用。