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.     

Influence of omeprazole on pharmacokinetics of domperidone given as free base and maleate salt in healthy Chinese patients

Aim： To investigate the influence of omeprazole on the pharmacokinetics of domperidone given as free base and maleate salt. Methods： An open, randomized, 2-period crossover study with a washout period of 7 d was conducted in 10 healthy Chinese, male patients. In each study period, the patients were administered a single oral dose of 10 mg domperidone as free base or maleate salt on d 1, 20 mg omeprazole twice daily on d 2 and 3, and once on d 4. A single dose of 10 mg domperidone as free base or maleate salt was taken at 4 h after administration of omeprazole on d 4. Plasma samples were collected on d 1 and 4 after the administration of domperidone, and the plasma concentrations of domperidone were determined by a sensitive liquid chromatography-tandem mass spectrometry method. Results： For free-base domperidone, pretreatment with omeprazole resulted in a 16% decrease in maximum concentration （Cmax）, compared with administration alone （P〈0.05）. However, for maleate salt, with the exception of an increase in t1/2, no pharmacokinetic parameters were significantly changed. When the free base and maleate salt were administered alone, no differences were found in any parameters between the 2 formulations. In contrast, when they were administered in the presence of omeprazole, the Cmax of domperidone given as free base was lower （25.9%） than that given as maleate salt （P〈0.05）. Conclusion： Pretreatment of omeprazole does not affect the absorption of domperidone maleate, but leads to a moderately decreased rate of absorption of the free base.     

咳特灵胶囊中扑尔敏的一阶导数光谱测定

采用一阶导数光谱法测定咳特灵胶囊中扑尔敏的含量，平均回收率１００．３％，ＲＳＤ０．５６％，方法简便，结果准确。     

一阶导数差示脉冲极谱法的建立及在药物分析中的应用

本文研究了一阶导数差示脉冲极谱法,并将其运用于扑尔敏、氟哌啶醇、维生素B₆及其制剂的定量分析中。方法简便、快速、灵敏、结果准确。     

薄层扫描法测定扑尔伪麻片中有效成分的含量

以硅胶ＧＦ２５４为吸附剂，氯仿－甲醇－氨水（９∶１∶０１）为展开剂，采用双波长薄层扫描法同时测定了扑尔伪麻片中的扑尔敏和盐酸伪麻黄碱的含量。扑尔敏在紫外灯下检视，λＳ＝２５６ｎｍ，λＲ＝２８５ｎｍ；盐酸伪麻黄碱采用茚三酮显色，λＳ＝５１０ｎｍ，λＲ＝７００ｎｍ，两组分的平均回收率分别为９９３５％和９９０７％，ＲＳＤ分别为１０８％和０８１％。     

马来酸桂哌齐特联合阿加曲班治疗急性脑梗死的临床效果

目的研究马来酸桂哌齐特联合阿加曲班治疗急性脑梗死的效果。方法将89例急性脑梗死患者随机分为对照组(45例,阿加曲班)和观察组(44例,阿加曲班+马来酸桂哌齐特)。比较两组的临床效果。结果观察组的治疗总有效率高于对照组(P<0.05)。治疗后,两组的NIHSS评分均降低,ADL评分均升高,且观察组优于对照组(P<0.05)。治疗后,两组的血清NT-proBNP、MCP-1、sICAM-1、TNF-α水平均降低,IL-10水平均升高,且观察组优于对照组(P<0.05)。治疗后,两组的全血黏度(中切)、血小板聚集率和纤维蛋白原水平均降低,且观察组低于对照组(P<0.05)。结论马来酸桂哌齐特联合阿加曲班能提高急性脑梗死患者的疗效,改善其神经功能、血液流变学和血清细胞因子水平。     

青紫汤加减治疗小儿过敏性紫癜22例

目的:观察青紫汤加减治疗小儿过敏性紫癜的临床疗效。方法:选取过敏性紫癜患儿44例,随机分为对照组和治疗组各22例,对照组给予扑尔敏、潘生丁等西药常规治疗,治疗组在对照组治疗的基础上加用青紫汤加减治疗。两组均1周为1个疗程,1个疗程后比较两组疗效。结果:对照组有效率为81.82%,治疗组有效率为95.45%,两组有效率比较差异有统计学意义(P0.05),治疗组优于对照组。结论:青紫汤加减治疗小儿过敏性紫癜疗效显著。