用带有弯曲进样管的程序升温汽化进样器进样CGC法测定注射液中丙二醇含量(英)

本文采用带有弯曲进样管程序升温汽化进样器进样，毛细管气相色谱（CGC）法测定注射液中丙二醇含量，实验结果表明：这种方法不仅比常规CGC中采用的分流方法能得到更为准确和精密的结果（回收率约99％，RSD＜2％），分析周期短（＜7分钟），测定时不需预处理直接进稀释样即可，不存在损伤毛细柱的可能；而且比迄今发表的程序升温汽化进样（PTV）方法也有优越之处。     

程序升温法测定麝香祛痛搽剂中3种有效成分的含量

麝香祛痛搽剂[1] 具有活血祛瘀、舒筋通络、消肿止痛的功效 ,应用广泛 ,疗效明确。我们对其中的主要成分樟脑 (ｃａｍｐｈｏｒ)、薄荷脑 (ｍｅｎｔｈｏｌ)、冰片 (ｂｏｒｎｅｏｌ)进行了含量测定研究。以往文献报道中对樟脑、薄荷脑、冰片的含量测定有许多[2～ 6] 。本实验根据 3种成分的性质 ,以及为排除样品中其它药味的影响 ,用气相色谱法 ,程序升温方式 ,同时测定了上述 3种成分。方法简便、灵敏、准确 ,重现性好 ,可作为该品种质量控制指标。1　仪器与试药岛津ＧＣ7ＡＧ气相色谱仪 ,氢火焰检测器 ,Ｃ -ＲＩＢ数据处理机 ,玻璃柱 3ｍ× …     

程序升温气相色谱法测定肌醇的含量

目的：建立程序升温气相色谱法测定肌醇的含量。方法：将肌醇进行硅烷化处理，正己烷提取后，以程序升温气相色谱法测定肌醇的含量。结果：肌醇的重复性试验ＲｓＤ为２．０％；平均回收率为９９．４％。结果：该方法操作简便，易行，线性关系良好。     

用旋光法测定甘露醇注射液的含量

用旋光法测定甘露醇注射液的含量山东省潍坊市人民医院（２６１０４１）庄衍秀，朱美华，吕素芹，张言镇甘露醇注射液中甘露醇的含量测定常用高碘酸钠法，费时费力，操作繁琐。根据甘露醇水溶液显极微弱的右旋性，但于其水溶液中加入硼砂，则形成甘露醇硼酸钠，从而增大旋...     

用旋光法测定硫酸庆大霉素注射液的含量

硫酸庆大霉素注射液的含量测定药典采用微生物检定法,但因测定条件要求高,检验周期长、不适合对产品中间体质量控制和快速分析的需要。根据硫酸庆大霉素具有旋光性的特点（比旋度为＋107～121°）,笔者采用旋光法测定硫酸庆大霉素注射液的含量,得到了满意的结果,现介绍如下。1仪器和试药WZZ－2型自动指示旋光仪（上海物理光学仪器厂）,硫酸庆大霉素原料,批号98O812,效价62On／mg（邯郸制药厂）,亚硫酸氢钠（AR）,EDTA－ZNa（AR）,五批注射液均由泅水制药厂用上述原料牛产提供。2试验及结果标准曲线的绘制：精密称取硫酸庆…     

程序升温气相色谱法测定樟脑乳膏中主药的含量

目的:建立以程序升温气相色谱法测定樟脑乳膏中主药含量的方法。方法:色谱柱为ATSE-54石英毛细管柱;程序升温中初始温度60℃,维持时间5min,升温速度为10℃·min-1,最终温度180℃,维持时间5min;进样口温度为130℃;氢火焰离子化检测器温度为215℃;进样量为2μL。水浴加热下用甲醇溶解樟脑乳膏,冰浴,过滤后直接进样测定。结果:樟脑检测浓度线性范围为10～120μg·mL-1(r=0.9998),平均回收率为101.41%～103.04%,RSD<0.56%。结论:该方法简单、准确、快速,适用于控制樟脑乳膏中主药的含量。     

程序升温气相色谱法测定肌醇的含量

目的 :建立程序升温气相色谱法测定肌醇的含量。方法 :将肌醇进行硅烷化处理 ,正己烷提取后 ,以程序升温气相色谱法测定肌醇的含量。结果 :肌醇的重复性试验 RSD为 2 .0 % ;平均回收率为 99.4 %。结果 :该方法操作简便 ,易行 ,线性关系良好     

四苯硼钠法测定甲硝唑葡萄糖注射液中甲硝唑的含量

为了消除《中国药典》法测定甲硝唑葡萄糖注射中葡萄糖分解产物5－HMF对测定甲硝唑的含量的影响,采用四苯硼钠法测定甲硝唑葡萄糖注射液中甲硝唑的含量。求得该法的平均回收率98．95,RDS为0．4％,表明该法简便,可靠,能消除5－HMF的干扰,检测无需特殊条件。     

毛细管柱气相色谱法测定注射液中丙二醇的含量

目的：建立气相色谱法测定注射液中的丙二醇。方法：采用毛细管柱气相色谱法,FID检测器,色谱柱为HP-INNOWax毛细管柱（30mx0.32mmx0.25μm）,载气为氮气,运用程序升温的方法测定注射液中丙二醇的含量。结果：得到线性回归方程为Y=0.000859X＋0.009051,相关系数r=0.9992,平均回收率为99.7%（n=9）。结论：方法操作简便、快速,能满足检测注射液中丙二醇含量的要求。     

Ligand-Specific Targeting of Microspheres to Phagocytes by Surface Modification with Poly(L-Lysine)-Grafted Poly(Ethylene Glycol) Conjugate

Purpose. The purpose of this study was to demonstrate specific receptor-mediated targeting of phagocytes by functional surface coatings of microparticles, shielding from nonspecific phagocytosis and allowing ligand-specific interactions via molecular recognition. Methods. Coatings of the comb polymer poly(L-lysine)-g-poly(ethylene glycol) (PLL-g-PEG) were investigated for potential to inhibit 1) nonspecific spreading of human blood-derived macrophages (MOs) and dendritic cells (DCs) on glass and 2) nonspecific phagocytosis of PLL-g-PEG-coated, carboxylated polystyrene (PS) or biodegradable poly(D,L-lactide-co-glycolide) (PLGA) microspheres. Coating was performed by adsorption of positively charged PLL-g-PEG on negatively charged microparticles or plasma-cleaned glass through electrostatic interaction. The feasibility of ligand-specific interactions was tested with a model ligand, RGD, conjugated to PEG chains of PLL-g-PEG to form PLL-g-PEG-RGD and compared with inactive ligand conjugate, PLL-g-PEG-RDG. Results. Coatings with PLL-g-PEG largely impaired the adherence and spreading of MOs and DCs on glass. The repellent character of PLL-g-PEG coatings drastically reduced phagocytosis of coated PS and PLGA microparticles to 10% in presence of serum. With both MOs and DCs, we observed ligand-specific interactions with PLL-g-PEG-RGD coatings on glass and PS and PLGA microspheres. Ligand specificity was abolished when using inactive ligand conjugate PLL-g-PEG-RDG, whereas repellency of coating was maintained. Conclusions. Coatings of PLL-g-PEG-ligand conjugates provide a novel technology for ligand specific targeting of microspheres to MOs and DCs while reducing nonspecific phagocytosis.     

Degradation of O6-Benzylguanine in Aqueous Polyethylene Glycol 400 (PEG 400) Solutions: Concerns with Formaldehyde in PEG 400

The degradation of O⁶-benzylguanine (BG) in aqueous polyethylene glycol (PEG) 400 solution at room temperature had been investigated using chromatographic and spectrometric methods. The degradation of BG in this solvent appeared to arise from a reaction between BG and formaldehyde. The formaldehyde was present as an impurity in PEG 400 and probably formed through air oxidation of PEG 400. The major product of this reaction was believed to be a methylene-bridged compound containing two BG molecules. This was probably produced via an intermediate imine, a schiff base between one BG molecule and formaldehyde. This degradation reaction was the only observable reaction in the 40% PEG/water solvent (pH 8.0) i.e. degradation of the drug via hydrolysis was minimal under these conditions.     

注射用丹参（冻干）联合阿托伐他汀治疗伴出血急性脑梗死的临床研究

目的分析注射用丹参(冻干)联合阿托伐他汀钙片治疗伴出血的急性脑梗死的临床疗效。方法选取2015年1月—2018年1月在青海省心脑血管病专科医院收治的64例伴出血急性脑梗死患者作为研究对象,将所有患者随机分对照组和治疗组,每组各32例。对照组患者口服阿托伐他汀钙片,1片/次,1次/d。治疗组在对照组治疗的基础上静脉滴注注射用丹参(冻干),0.4 g注射用丹参(冻干)加入到100 mL生理盐水中,1次/d。两组患者均连续治疗2周。观察对比两组患者的临床疗效,比较治疗前后两组的NIHSS评分、超敏C反应蛋白(hs-CRP)、血脂水平和再出血情况。结果治疗后,对照组的总有效率为78.1%,显著低于治疗组的96.9%,两组比较差异具有统计学意义(P0.05)。治疗后,两组患者NIHSS评分显著降低,同组治疗前后比较差异具有统计学意义(P0.05);治疗后,治疗组NIHSS评分明显低于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,治疗组血清hs-CRP、总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL-C)水平均显著降低,高密度脂蛋白(HDL-C)水平明显升高,同组治疗前后比较差异具有统计学意义(P0.05);治疗后,治疗组hs-CRP和血脂水平显著优于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,对照组再出血率为15.6%,治疗组再出血率为3.1%,两组比较差异具有统计学意义(P0.05)。结论注射用丹参(冻干)联合阿托伐他汀钙片治疗伴出血的急性脑梗死具有较好的临床疗效,可提升患者生活质量,改善出血情况,具有一定的临床推广应用价值。     

Synergistic effects of chemotherapeutic drugs in lymphoma cells are associated with down-regulation of inhibitor of apoptosis proteins (IAPs), prostate-apoptosis-response-gene 4 (Par-4), death-associated protein (Daxx) and with enforced caspase activation

Cytotoxic drugs mediate apoptotic tumor cell death by influencing key regulator proteins of programmed cell death. In clinical practice cytotoxic drug combinations are desired to potentiate tumor cell kill and to minimize side effects. Nevertheless, the molecular mechanisms underlying synergistic and antagonistic effects on tumor cells are still poorly understood. In order to elucidate these molecular mechanisms we established models of synergistic and antagonistic drug combinations within the same lymphoma cell lines. By combination index method we demonstrated that bendamustine in combination with either doxorubicin or mitoxantrone caused antagonistic effects on disruption of mitochondrial membrane potential as well as on the rate of apoptosis. In contrast the combination of bendamustine with cladribine acted synergistically on these parameters. By using the IC(50) (dosages causing 50% rate of apoptosis) the synergistic effect of the combination of bendamustine and cladribine was associated with an enhanced mitochondrial release of cytochrome c and Smac/DIABLO, by down-regulation of x-linked inhibitor of apoptosis (XIAP), cIAP1, Par-4 and Daxx as well as by a significantly increased activation of caspases-3, -6, -7, -8 and -9. At the same rate of apoptosis (IC(50)), the antagonistic combinations did not increase the release of cytochrome c or Smac/DIABLO, nor down-regulate the expression of XIAP, cIAP1, Par-4 and Daxx, nor increase the activation of caspases. The role of down-regulation of IAPs and of enforced caspase activation for synergism in this model was supported by the observation, that broad spectrum inhibition of caspases re-established expression of XIAP. Our study is the first to outline the molecular alterations caused by synergistic and antagonistic drug combinations within the same lymphoma cell model. The above described mechanisms were already assessable at a point where the effects of synergistic or antagonistic combinations could not yet be discriminated quantitatively by the level of apoptosis rate of the lymphoma cells.