HPLC法测定小儿氨酚黄那敏片中对乙酰氨基酚和马来酸氯苯那敏的含量

目的：建立HPLC法同时测定小儿氨酚黄那敏片中对乙酰氨基酚和马来酸氯苯那敏含量。方法：采用HypersilC18（150mm×4．6mm,5μm）色谱柱,甲醇-0．05mol·L^-1磷酸二氢钾溶液-三乙胺（10：90：0．02）（用磷酸调pH=3．4）为流动相,检测波长为216nm,柱温为30℃,流速为1．0ml·min^-1,进样量为20μl。结果：对乙酰氨基酚、马来酸氯苯那敏分别在40．08-240．48μg·ml^-1（r=0．9992）和0．37～2．21μg·ml^-1（r=0．9971）浓度范围内呈现出良好的线性关系;方法平均回收率分别为99．75％和98．95％;RSD分别为0．23％和0．36％。结论：该方法简便、快速,两组分分离度好,其他成分无干扰,测定结果准确可靠,可作为该制剂质量控制的有效方法。     

高效液相色谱法测定酚氨咖敏片中马来酸氯苯那敏含量均匀度

目的：探讨高效液相色谱法（HPLC）测定酚氨咖敏片中马来酸氯苯那敏含量均匀度的方法。方法：采用HPLC,Alltima C18（4．6min×250mm,5μm）;1％醋酸溶液（用二乙胺调节pH值至3．7）-甲醇（62：38）为流动相;检测波长260nm。结果：进样量在0．12-0．80μg与峰面积的线性关系良好（r=-0．9999）;平均回收率为99．75％,99．90％,99．68％;RSD为0．42％,0．25％,0．70％（n=3）,精密度、重复性良好。结论：所建方法准确、简便、快速,适用于酚氨咖敏片中马来酸氯苯那敏含量均匀度的测定。     

马来酸氟吡汀胶囊与进口产品溶出曲线相似性的比较

目的比较自制马来酸氟吡汀胶囊与进口马来酸氟吡汀胶囊的溶出度。方法参考进口药品注册标准,分别测定自制马来酸氟吡汀胶囊和进口马来酸氟吡汀胶囊在不同条件下的溶出曲线,采用相似因子(f2)进行溶出曲线相似性比较。结果各条件下的相似因子(f2)均可到达60以上。结论自制马来酸氟吡汀胶囊与进口产品的溶出曲线具有良好的相似性。     

马来酸桂哌齐特治疗急性脑梗死的临床疗效观察

目的探讨马来酸桂哌齐特治疗急性脑梗死的疗效。方法将80例缺血性脑血管病患者随机分为治疗组和对照组,各40例,治疗组用马来酸桂哌齐特治疗．对照组用丹参注射液治疗,观察临床疗效。结果治疗组总有效率77．5％,明硅优于对照组的57．5％（P〈0．05）,明显减轻患者神经功能缺损症状。结论马来酸桂哌齐特是一种治疗急性腑梗死的有效药物。     

马来酸桂哌齐特治疗外伤性蛛网膜下腔出血的疗效评价

目的:评价马来酸桂哌齐特与硫酸镁联合应用治疗外伤性蛛网膜下腔出血(tSAH)的疗效。方法:160例tSAH患者随机分为对照组和治疗组Ⅰ、Ⅱ、Ⅲ,各40例。对照组给予止血、脱水、激素及促神经功能恢复药等常规治疗;除常规治疗外,治疗组Ⅰ给予马来酸桂哌齐特、治疗组Ⅱ给予硫酸镁、治疗组Ⅲ联合应用马来酸桂哌齐特和硫酸镁,均12h1次,连用14d。分别于入院时及治疗后3、7、14d行经颅多普勒(TCD)检查,观察脑血管痉挛(CVS)的发生情况及预后。结果:在CVS发生、大脑中动脉血流速率的变化、治疗后3个月及6个月的预后方面,治疗组Ⅲ与对照组、治疗组Ⅰ、治疗组Ⅱ比较差异均有统计学意义(P<0.01)。结论:马来酸桂哌齐特与硫酸镁联合应用不仅能降低CVS的发生率,而且能减轻CVS的严重程度,明显改善患者的预后。     

静脉滴注硫酸奈替米星致过敏性喉水肿1例

某例患者,女,25岁,因发热、尿频、尿痛在我院门诊就诊,检查尿常规提示：WBC3＋,诊断为“尿路感染”。用0．9％氯化钠250mL加硫酸奈替米星0．2g（商品名：益天星,0．2g·支,批号：070622,江苏四环生物服务有限公司）。当患者输注约10min后,患者感咽喉堵塞感,刺激性咳嗽,声音嘶哑,出现全身无力,胸闷,头晕,立刻停止输液,平卧,     

纤维蛋白原在2型糖尿病动脉粥样硬化发生中的作用研究

目的探讨纤维蛋白原(FIB)在２型糖尿病动脉粥样硬化发生中的作用。方法以FIB为危险因素,以糖尿病动脉粥样硬化为病例组,以没有动脉粥样硬化的糖尿病为对照组,进行关联研究。结果病例组年龄、病程、血浆胆固醇(TC) 、低密度脂蛋白胆固醇 (LDL-C)、纤维蛋白原(FIB)及收缩压（SBP）高于对照组,有显著差异(P<0.05) 。年龄、FIB、 LDL-C是2型糖尿病颈动脉粥样硬化的危险因素,其中 FIB对糖尿病颈动脉粥样硬化形成的贡献较年龄、LDL-C为强。而体重指数(BMI)和病程对FIB增高有影响,呈正相关。结论年龄、FIB、 LDL-C是２型糖尿病颈动脉粥样硬化的危险因素。BMI和病程对FIB增高有影响,呈正相关。     

反相离子对色谱法同时测定复方岩白菜素片中岩白菜素和马来酸氯苯那敏的含量

目的建立反相离子对色谱法测定复方岩白菜素片中岩白菜素和马来酸氯苯那敏含量的方法。方法采用反相离子对色谱法,色谱柱为Agilent zorbax C8;以0．05mol·L^-1磷酸二氢钠（含4mmol·L^-1庚烷磺酸钠,用磷酸调节pH至3．0）-乙腈（7：3,v／v）为流动相;流速为1．0mL·min^-1,检测波长：208nm;柱温：26℃。结果岩白菜素在浓度为0．125～0．375mg·mL^-1时呈线性关系,平均回收率为99．88％,RSD为0．44％;马来酸氯苯那敏在浓度为0．002～0．006mg·mL^-1时呈线性关系,平均回收率为99．29％,RSD为0．51%。结论该法简便、可靠、准确,适合于复方岩白菜素片中岩白菜素和马来酸氯苯那敏含量的测定。     

Identification of sensitizing diethyleneglycol maleate in a two-component polyester cement

Unsaturated polyester (UP) cement caused allergic contact dermatitis in car repair work. The resin was a condensate of polyols and maleic anhydride with reactive solvent, auxiliary substances, and inorganic reinforcement substances. To identify the causative chemicals, the cement was tested on a sensitized patient. For analysis, samples of the resin were eluted with acetone and eluted with hexane to precipitate inorganic material and large polyester molecules. The eluate was evaporated. The remainder, dissolved in acetone, was separated into fractions on silica plates by thin layer chromatography (TLC). On the developed (hexane/chloroform, 15/85) plates, 20 bands were obtained under UV-light at 254 nm. Samples of the bands were scraped and used for patch testing. The scraping at a retention factor (Rf) of 0.24 caused a skin reaction. The bands at this retention were removed from six plates, combined, eluted with acetone and purified again by TLC. The purified fraction mixed in petrolatum in the dilution series was used for conclusive patch testing on the patient. An allergic reaction was induced at down to 0.003% wt/wt. According to MS and IR analyses, the isolated compound was diethyleneglycol maleate (DEGM, MW204). In addition to the resin part, the sanding dust also contained this monomer.     

Mild mitochondrial inhibition in vivo enhances glutamate-induced neuronal damage through calpain but not caspase activation: role of ionotropic glutamate receptors

Glutamate neurotoxicity is exacerbated when energy metabolism is impaired. In vitro studies show that neuronal death in these conditions is related to mitochondrial dysfunction, ATP depletion, and the loss of calcium homeostasis. We have recently observed that, in vivo, enhancement of glutamate toxicity elicited by previous mitochondrial inhibition does not involve severe ATP depletion, suggesting the involvement of other processes. Factors such as the activation of different proteases may determine the extent and type of cell death. Protease activation might be triggered by internal or external factors, such as mitochondrial damage or the activation of a particular glutamate receptor subtype. In the present study we aimed to investigate whether moderate inhibition of mitochondrial metabolism facilitates glutamate toxicity through caspase-3 or calpain activation, as well as the contribution of NMDA and non-NMDA glutamate ionotropic receptors to this activation. Rats were pre-treated with a subtoxic dose of 3-NP and 4 h later intrastriatally injected with glutamate. Results show that neither of these treatments alone (3-NP or Glu) or in combination (3-NP+Glu) activated caspase-3. Conversely, calpain activity is induced after glutamate injection both in intact and 3-NP pre-treated rats. Inhibition of calpain activity by MDL-28170 significantly prevented striatal damage. NMDA and non-NMDA receptors contributed equally to calpain activation and to the induction of neuronal death. Results suggest that enhancement of glutamate toxicity due to inhibition of mitochondrial metabolism in vivo, does not recruit caspase-dependent apoptosis but favors calpain activation through the stimulation of both subtypes of glutamate ionotropic receptors.