轻度脑外伤患者SPECT局部脑血流显像

目的 探讨SPECT脑血流灌注显像在研究轻度脑外伤后临床症状发病机理中的作用。方法对39例无意识丧失、CT检查正常的轻度脑外伤患者进行^99Tc^m-双半胱乙酯(ECD)脑血流灌注断层显像。以双侧小脑平均每像素的均数为参比值，计算各大脑感兴趣区(ROI)放射性计数比值(RAR)。大脑皮质或基底神经节RAR低于70％，颞叶中部低于50％视为异常。结果39例患者中23例(59％)SPECT显示异常，其中3例为弥漫性血流灌注减低，20例为局部血流灌注减低灶，共计74个病灶。伤后3个月内脑血流灌注异常15例，2例为弥漫性血流灌注减低，13例为局灶性血流灌注减低；13例中发现病灶58个。8例受伤3个月后显像异常者，1例为弥漫性血流灌注减低，7例为局灶性血流灌注减低，发现病灶16个。结论 轻度脑外伤后患者主要症状为头痛、头昏、记忆力减退；无意识丧失的脑外伤患者可出现局部脑血流灌注减低，且SPECT检查比CT灵敏。     

局部脑血流显像对硬膜外血肿快速减压后脑损伤机理的实验研究

目的探讨局部脑血流(rCBF)断层显像在硬膜外血肿快速减压后脑损伤的应用价值。方法利用rCBF显像分别对新西兰大白兔硬膜外血肿动物模型压迫前、压迫时及解压后的不同时段进行显像。对不同时相点数据进行三维重建,利用感兴趣区(ROI)技术,生成脑顶叶时间放射性曲线。同时分别测定局部脑游离[Ca2 ]浓度与脑含水量的动态变化。结果硬膜外血肿急性减压后,rCBF显像示脑皮质首先表现为严重的低灌注,快速减压后则表现为急性的超过正常的过度灌注。[Ca2 ]于压迫后明显升高;减压后短暂降低,继之缓慢增加,24h达到高峰。减压后[Ca2 ]与脑组织含水量呈显著正相关关系(r=0469,P<001)。结论rCBF显像对判断硬膜外血肿急性减压后脑组织的再灌注损伤有价值。     

Determination of serum diltiazem concentrations in a pharmacokinetic study using gas chromatography with electron capture detection

An open cross-over randomized clinical trial was performed in nine healthy humans to determine steady-state pharmacokinetics and bioavailability of three oral diltiazem preparations, tablets containing 60 and 90 mg of diltiazem hydrochloride, administered in total daily doses of 180 mg. Serum drug levels were determined by gas chromatography with electron capture detection following a simple extraction procedure. Blood samples were collected before and at several post-dosing intervals after administration of the last dose in steady state, and pharmacokinetic parameters were calculated. The steady-state diltiazem concentrations in sera were determined 48 h after the first dose, and were (mean ±SD): 46.4 ± 28.1, 60.8 ± 36.3 and 36.8 ± 22.6 μg l⁻¹ for Pliva 60, Pliva 90, and Aldizem 90 diltiazem preparations, respectively. The corresponding elimination half-lives were 5.6 ± 2.0, 5.2 ± 1.8 and 6.9 ± 3.2 h; peak concentrations were 88.4 ± 29.5, 153.5 ± 86.5 and 139.2 ± 72.5 μg l⁻¹, and areas under the concentration curves (AUC 12 h) were 477.4 ± 172.5, 989.2 ± 536.3 and 817.9 ± 494.5 μg h l⁻¹ respectively.     

HBx上调HepG2细胞DNA修复酶hMTH1表达的意义

目的: 探讨DNA氧化损伤修复酶hMTH1在HBx致肝细胞癌发生机制中的作用.方法: 应用HPLC/ECD法检测稳定表达HBx的转基因细胞HepG2/HBx及其对照组HepG2与HepG2/pcDNA3.1细胞中的8-OHdG的含量;并以β-actin为内对照, 应用RT-实时PCR定量检测各组细胞中可水解8-OHdG的DNA修复酶hMTH1的表达.结果: 8-OHdG在He pG2/HBx细胞中的含量(fmol 8-OHdG/mg DNA)显著高于对照组HepG2和HepG2/pDNA3.1细胞(36.5±6.25 vs8.52±1.65, 9.12±2.69, 均P<0.05). DNA修复酶hMTH1在HepG2/HBx细胞中的表达较两对照组细胞明显增高(1.213±0.100 vs 0.087±0.026, 0.112±0.052 hMTH1/β-actin mRNA×100, 均P<0.05).结论: H B x 可能通过诱导氧化应激增加HepG2细胞内DNA氧化损伤产物8-OHdG的含量, 从而反应性上调DNA修复酶hMTH1的表达.     

采用均匀设计法优选双半胱乙酯药盒处方

通过均匀设计法优化双半胱乙酯（ECD）药盒的处方。以ECD药盒中A瓶的pH、B瓶的氯化亚锡含量为考察因素,以药盒与^99m TcO₄ ^-标记后得到配合物的放射化学纯度为考察指标,通过效应值曲面图确定优化处方,最后进行验证。试验优化得到回归方程y=0.567+0.103x₁+9.68e^-4x₂-9.86e^-4x₁³-5.48e^-8x₂³。结合效应值曲面可知,当A瓶的pH为6.4、氯化亚锡含量为65μg时,试验结果最佳。验证结果表明,理论预测值与实测值接近,优化处方后的产品明显优于现行产品。实验结果表明,采用均匀设计法得到的结果,可以对ECD药盒的处方进行优化。     

癫痫发作间期脑血流灌注功能与脑组织损伤程度相关性研究

目的探讨癫痫患者抗癫痫药物治疗期间不同疗效状态下,发作间期致痫灶局部血流灌注和脑细胞功能低下与脑组织损伤程度的相关性。方法按随机数字表法随机选择48例癫痫发作间期患者,采用双抗体夹心ELISA法测血清S-10013蛋白的水平,SPECT脑血流显像测定局部脑血流量,并与30例对照者进行比较。采用SPSS11．0软件进行统计学分析,两样本均数之间行t检验,多样本比较采用方差分析,两变量间相关性分析用线性相关分析法进行。结果癫痫发作间期患者血清S-10013蛋白水平（0．572±0．163）μg/L,高于对照组（0．218±0．134）μg/L,差异有统计学意义（t=9．96,P〈0．01）。根据癫痫控制标准,患者中控制20例,显效和有效18例,无效10例;3组s．100t3蛋白水平和局部脑血流（rCBF,％）分别为（0．443±0．083）μg/L和（0．035±0．038）％,（0．585±0．108）μg/L和（0．187±0．075）％,（0．809±0．056）μg/L和（0．337±0．060）％,无效组与其他两组比较,S-10013蛋白水平与rCBF的变化均有统计学意义,其余两组比较差异亦有统计学意义（F=56．740,92．316,P〈0．01）。癫痫患者血清S-100p蛋白水平、rCBF下降百分率呈高度正相关（r=0．887,P〈0．01）。结论SPECT脑血流灌注显像联合检测血清S-100β蛋白水平,可对癫痫致痫灶进行定位,并评价癫痫所致的脑组织损伤。S-100β蛋白水平可作为抗癫痫药物治疗癫痫疗效的监测指标。     

热脱附-ECD气相色谱法测定室内空气中的五种氯苯类化合物

目的:建立用热脱附气相色谱分析方法分析室内空气中5种氯苯类化合物的方法.方法:在合适的仪器条件下,将吸附管置于全自动热解吸仪中直接加热解吸,各待测组分随载气进入毛细管气相色谱仪分离,ECD检测器榆测.结果:样品中的各类化合物都能得到较好的分离,相关系数r在0.9942～0.9989之间.RSD为7.4%～10.4%,各...     

Noralashinol B,a norlignan with cytotoxicity from stem barks of Syringa pinnatifolia

One new norlignan, noralashinol B (1), and one new natural product, proposed noralashinol C (2), were isolated in a continuous phytochemical investigation on the stem barks of Syringa pinnatifolia. Their structures were elucidated based on the analysis of spectroscopic data, including mass spectrometry and 1D and 2D NMR spectroscopies, and the absolute configuration was determined by experimental and calculated electronic circular dichroism. Compound 1 showed a weak cytotoxicity against HepG2 hepatic cancer cells with its IC₅₀ value of 31.7 μM. Furthermore, 1 induced apoptosis of HepG2 cells in a dose-dependent manner at concentrations of 0–80.0 μM.