酚磺乙胺注射液pH下降原因的探讨

目的：探讨酚磺乙胺注射液在贮存期内PH下降的原因，方法：用单因素考察法，找出使酚磺乙胺注射液在贮存期内PH下降的原因，结果：酚磺乙胺注射液在贮存期内PH下降的原因是NaHSO3被氧化后引起的，结论：酚磺乙胺注射液中应选择合适的抗氧剂或加入缓冲齐可以解决酚磺乙胺注射液在贮存期内PH下降的原因。     

兽用诺氟沙星注射液的稳定性研究

用光照和初均速法对兽用诺氟沙星注射液的光稳定性和热稳定性进行了考察，并用美国ＦＤＡ低温考察法和室温留样观察法考察其贮存期。结果表明，本品稳定性好，有效期达２年以上。     

穿琥宁注射液的处方筛选及稳定性实验研究

目的考察辅料和温度对穿琥宁注射液的影响,预测其在室温下的贮存期。方法建立HPLC法测定穿琥宁注射液含量,采用经典恒温加速实验方法考察注射液不同处方的稳定性,筛选最佳处方,并预测其在室温下的贮存期。结果与结论筛选出含0.05?TA-2Na的最佳处方,其室温下的贮存期为3.45年。     

呋喃硫胺注射液的有效期研究

考察了不同厂家的30个批号的呋喃硫胺注射液样品,结果表明,PH值合格率只有43．3％,合格率高低与贮存期有关,建议将呋喃硫胺注射液的贮存期定为2年。     

安定注射液稳定性的动力学研究

本文采用初均速法和紫外分光光度法,对安定注射液的稳定性进行了考察。将实验数据运用Arrhenius指数规律外推室温贮存期。实验结果表明,安定注射液的热解反应的活化能(E)为20。389Kcal/mol;推算室温(25℃)贮存期为5年。     

盐酸半胱氨酸对10％维生素C注射液的稳定作用

据文献报道[药学学报1980,15:234],盐酸半胱氨酸用于25％维生素C注射液作稳定剂,稳定性良好,室温贮存期2.5年。本文将盐酸半胱氨酸用于10％维生素C注射液,样品经热加速试验及室温贮存定期质量考察,证明稳定性较佳,贮存期可长至5年。     

盐酸普鲁卡因注射液的稳定性考察

目的:研究盐酸普鲁卡因注射液的稳定性及贮存期。方法:用双波长法测定盐酸普鲁卡因的含量,将产品用经典恒温法,初均速法和室温留样观察法进行实验。结果:盐酸普鲁卡因的含量随温度升高和时间延长逐渐下降,产品经典恒温法测得25℃的贮存期为17个月。初均速法测得25℃的贮存期为18个月。室温留样观察实验证实:盐酸普鲁卡因注射液放置1年含量为97.46%,放置2年为91.63%。结论:3种实验方法测得的数据基本一致,盐酸普鲁卡因注射液的有效期可暂定为1年。     

脉络宁注射液稳定性的动力学研究

采用初均速法^[1]和紫外分光光度法,对脉络宁注射液的稳定性进行了考察。将实验数据运用Arrhenius指数规律外推室温贮存期。结果表明,脉络宁注射液的热解反应活化能(E)为15．069kCal／mol,推算室温(25℃)贮存期约为5年。     

单点测定法预测25％抗坏血酸注射液的贮存期

对现有25％抗坏血酸注射液处方及工艺曾作了改进,使成本降低,贮存期延长。本文采用单点测定法研究其颜色变化并预测得贮存期约为五年(用经典恒温法作对照,     

甲硝唑注射液稳定性的动力学研究

本文采用化学动力学(经典恒温法)和紫外分光光度法,对甲硝唑注射液的稳定性进行了考察,并预测其室温条件下的贮存期。将实验数据运用零级动力学和一级动力学进行处理。结果表明,甲硝唑注射液的降解反应为一级动力学过程,其热解反应的活化能(E)为19.549Kcal/mol,贮存期(t_0.9)为15年。     

抗坏血酸注射液稳定性的研究——Ⅲ.25%抗坏血酸注射液浓度变化规律的探讨

探讨了25%抗坏血酸注射液在98°、90°、80℃绝氧降解的浓度变化规律,其绝氧降解都是假零级反应,降解速度常数在注射液浓度约为初浓度的85%之上与下,略有差异。以5%的注射液在98℃和12.5%的注射液在90℃的绝氧降解作对照,二者都是假一级反应,其速度常数在注射液浓度约为初浓度的75%之上与下,也略有差异。不含抗氧剂的25%抗坏血酸溶液在98℃的绝氧降解也是假零级反应。     

Effects of the garlic compounds diallyl sulphide and diallyl disulphide on arylamine N-acetyltransferase activity in Klebsiella pneumoniae

Arylamine N-acetyltransferase (NAT) activities with 2-aminofluorene (2-AF) were determined in the bacterium Klebsiella pneumoniae. Cytosols or suspensions of K. pneumoniae with or without specific concentrations of diallyl sulphide (DAS) or diallyl disulphide (DADS) as co-treatment showed different percentages of 2-AF acetylation. The data indicated that there was decreased NAT activity associated with increased levels of DAS or DADS in K. pneumoniae. In growth studies on K. pneumoniae it was demonstrated that DAS or DADS elicited a dose-dependent bacteriocide effect on K. pneumoniae. For the cytosol examinations, the apparent values of Km and Vmax were 0.96+/-0.09 mM and 7.87+/-0.79 nmol min(-1) mg(-1) protein, respectively, for 2-AF. However, when DAS or DADS was added to the reaction mixtures, the apparent values of Km and Vmax were 0.16+/-0.04 mM and 0.99+/-0.16 nmol min(-1) mg(-1) protein with DAS, respectively, and 0.14+/-0.18 mM and 0.85+/-0.10 nmol min(-1) mg(-1) protein with DADS, respectively, for 2-AF. For the intact bacteria examination, the apparent values of Km and Vmax were 0.57+/-0.06 mM and 2.00+/-0.14 nmol min(-1) per 10x10(10) CFU, respectively, for 2-AF. However, when DAS or DADS was added to the reaction mixtures, the apparent of values of Km and Vmax were 0.41+/-0.04 mM and 1.30+/-0.10 nmol min(-1) per 10x10(10) CFU with DAS, respectively, and 0.34+/-0.04 mM and 1.08+/-0.08 nmol min(-1) per 10x10(10) CFU with DADS, respectively, for 2-AF. This report is the first demonstration to show that the garlic components DAS and DADS would affect K. pneumoniae growth and NAT activity.     

呋噻米注射液在自然光及灯光照射下的稳定性研究

目的:探讨呋噻米注射液在自然光和不同灯光照射下的稳定性,以找出不同光源对该药物稳定性的等效关系。方法:采用在室温下进行光照加速试验的方法。结果:该药物在光照试验中颜色变化遵从零级动力学规律:A=A0 kEt。结论:根据光对呋噻米注射液稳定性的影响规律,预测了该药物在室内自然光照射下的贮存期约为41天。     

抗坏血酸在注射液中的降解途径

研究了中性抗坏血酸注射液在无氧条件下的降解产物和降解反应。检测出的降解产物有;2-酮-L-古洛糖酸、二氧化碳和木糖,分离、鉴定了新的降解产物——丙酮醛,并研究了抗坏血酸的水解与2-酮-L-古洛糖酸脱羧的反应动力学,提出了中性抗坏血酸注射液在无氧条件下可能的降解途径。     

抗坏血酸在注射液中的降解途径

研究了中性抗坏血酸注射液在无氧条件下的降解产物和降解反应。检测出的降解产物有;2-酮-L-古洛糖酸、二氧化碳和木糖,分离、鉴定了新的降解产物——丙酮醛,并研究了抗坏血酸的水解与2-酮-L-古洛糖酸脱羧的反应动力学,提出了中性抗坏血酸注射液在无氧条件下可能的降解途径。     

利用Excel规划求解法计算药物静脉注射药动学方程参数最优解

目的:利用Excel规划求解功能建立一种简便的计算药物静脉注射药动学方程参数最优解的方法。方法:采用Excel规划求解功能获得药物静脉注射后一、二室模型药动学参数和隔室模型参数,并与DAS和残数法得到的结果进行比较。结果:Excel规划求解可在一定约束条件下获得一、二室模型参数的最优解,与DAS运行结果完全一致。结论:Excel规划求解法可用于临床药物静脉注射后一、二室模型参数的计算。     

Post-initiation modulating effects of allyl sulfides in rat hepatocarcinogenesis.

Effects of administration of diallyl sulfide (DAS) and diallyl disulfide (DADS) on the promotion stage of hepatocarcinogenesis were investigated in rats using the Ito model. They were compared with those of phenobarbital (PB), a well-known liver promoter in rats. Initiation was induced by a single dose of N-nitrosodiethylamine (NDEA) and 3 weeks later, a partial hepatectomy was conducted. Two weeks after the NDEA injection, rats received either 0.05% allyl sulfides, PB or both in their diet for 8 weeks. Feeding with DAS increased the number of liver preneoplastic foci by 63% with respect to the untreated group. However, rats fed DAS showed a lower foci development than rats fed PB. The DADS group did not differ from control group for any of the measured morphometric parameters. Simultaneous administration of DADS with PB partially reduced the promotional activity of PB whereas DAS co-treatment did not modify PB properties. These findings confirm that DAS can act as a promoter in rat liver but exerts no co-promoting effect. Conversely, DADS was found to have promotion-inhibiting ability, suggesting that DADS has greater value than DAS as a chemopreventive agent.     

Differential induction of apoptosis by type A and B trichothecenes in Jurkat T-lymphocytes.

Several studies have shown that the mycotoxins T-2 toxin, diacetoxyscirpenol (DAS), deoxynivalenol (DON) and nivalenol (NIV) affect lymphocyte functioning. However, the molecular mechanisms underlying the immunomodulatory effects of these trichothecenes are not defined yet. In this study, the potency of the type A trichothecenes T-2 toxin and DAS, and the type B trichothecenes DON (and its metabolite de-epoxy-deoxynivalenol; DOM-1) and NIV to reduce mitochondrial activity and to induce apoptosis of Jurkat T cells (human T lymphocytes) were examined. T-2 toxin and DAS are much more cytotoxic at low concentrations than DON and NIV as shown by the AlamarBlue cytotoxicity assay. In addition, the mechanism whereby DON and NIV induced cytotoxicity is mainly via apoptosis as we observed phosphatidylserine externalization, mitochondrial release of cytochrome c, procaspase-3 degradation and Bcl-2 degradation. In contrast, type A trichothecenes reduce the mitochondrial activity at approximately 1000-fold lower concentrations than the type B trichothecenes, resulting in necrosis. These data suggest that the mechanisms resulting in cytotoxic effects are different for type A and type B trichothecenes.     

富马酸氯马斯汀注射液在健康人体内药物动力学研究

目的：研究富马酸氯马斯汀注射液在健康人体内单次和多次给药后药物动力学特征。方法：12名健康受试者单次肌内注射富马酸氯马斯汀注射液2mg;间隔10d后,连续3d肌注富马酸氯马斯汀注射液2mg,bid。给药后LC—MS／MS测定富马酸氯马斯汀血药浓度,DAS2．0药动学软件计算药动学参数。结果：单次和多次给药后主要药动学参数：Cmax分别为（2．43±1．45）、（5．50±0．74）ng·ml^-1;tmax分别为（0．40±0．24）、（0．43±0．26）h;AUC0-12分别为（13．70±6．70）、（49．80±720）ng·h·ml^-1;AUC0-96分别为（65．10±15．70）、（256．90±33．00）ng·h·ml^-1;AUC0-∞分别为（82．50±18．00）、（355．10±116．00）ng·h·ml^-1;t1／2分别为（39．90±7．30）、（46．60±19．10）h。结论：连续3d肌注富马酸氯马斯汀注射液,药物在体内存在蓄积。     

Cytotoxicity of diacetoxyscirpenol is associated with apoptosis by activation of caspase-8 and interruption of cell cycle progression by down-regulation of cdk4 and cyclin B1 in human Jurkat T cells

To understand the mechanism underlying T-cell toxicity of diacetoxyscirpenol (DAS) from Fusarium sambucinum, its apoptogenic as well as growth retardation activity was investigated in human Jurkat T cells. Exposure to DAS (0.01-0.15 microM) caused apoptotic DNA fragmentation along with caspase-8 activation, Bid cleavage, mitochondrial cytochrome c release, activation of caspase-9 and caspase-3, and PARP degradation, without any alteration in the levels of Fas or FasL. Under these conditions, necrosis was not accompanied. The cytotoxicity of DAS was not blocked by the anti-Fas neutralizing antibody ZB-4. Although the DAS-induced apoptotic events were completely prevented by overexpression of Bcl-xL, the cells overexpressing Bcl-xL were unable to divide in the presence of DAS, resulting from the failure of cell cycle progression possibly due to down-regulation in the protein levels of cdk4 and cyclin B1. The DAS-mediated apoptosis and activation of caspase-8, -9, and -3 were abrogated by either pan-caspase inhibitor (z-VAD-fmk) or caspase-8 inhibitor (z-IETD-fmk). While the DAS-mediated apoptosis and activation of caspase-9 and caspase-3 were slightly suppressed by the mitochondrial permeability transition pore inhibitor (CsA), both caspase-8 activation and Bid cleavage were not affected by CsA. The activated normal peripheral T cells possessed a similar susceptibility to the cytotoxicity of DAS. These results demonstrate that the T-cell toxicity of DAS is attributable to not only apoptosis initiated by caspase-8 activation and subsequent mitochondrion-dependent or -independent activation of caspase cascades, which can be regulated by Bcl-xL, but also interruption of cell cycle progression caused by down-regulation of cdk4 and cyclin B1 proteins.