Encapsulation of aluminium hydroxide fillers with polymethyl-methacrylate

A process was developed for the microencapsulation of inorganic filler particles with poly-methyl-methacrylate, to increase the interaction between the hydrophilic filler particles and a polymer matrix. The filler utilised was aluminium hydroxide with an average diameter of 1.9 µm and a specific surface area of 5 m2/g. The process comprised a surface modification, in which a monolayer of isopropoxy titanium isostearate was chemically bound to the surface to render it hydrophobic and to ensure a chemical bond between the filler and the organic phase. Then, an encapsulation reaction was carried out by means of an emulsion-like polymerization process at monomer starved conditions. The modified particles were stabilized in water with sodium-dodecyl-sulphate. A redox system consisting of cumene-hydroperoxide in combination with sodium-formaldehyde-sulphoxylate and iron(II) salt was applied for the initiation of the polymerization. Besides surface polymer, free polymer particles were also formed. The parameters which varied were the filler concentration, the concentration of the initiator components and the surfactant concentration. At optimum conditions, ~50% of the added monomer polymerized at the modified filler surface, thus forming encapsulated filler particles. SEM together with TGA analysis indicated that a smooth polymer layer had been formed on the filler surface. At high filler loading, however, coagulation occurred.     

正交试验法优选精乌颗粒的提取工艺

目的:优选精乌颗粒的提取工艺。方法:以二苯乙烯苷(2、3、5、4′-四羟基二苯乙烯-2-Oβ--D-葡萄糖苷)的含量及出膏率为考察指标,采用L9(34)正交设计优选提取工艺条件,确定精乌颗粒的最佳提取工艺。结果:A1B2C2即以8倍量水、煎煮2次、2h/次为最佳工艺。结论:优选出的工艺科学合理,可作为该制剂合理开发的依据。     

Silica nanoparticles induce cytokine responses in lung epithelial cells through activation of a p38/TACE/TGF-α/EGFR-pathway and NF-κΒ signalling

Amorphous silica nanoparticles (SiNPs) have previously been shown to induce marked cytokine (interleukin-6; IL-6 and interleukin-8; CXCL8/IL-8) responses independently of particle uptake in human bronchial epithelial BEAS-2B cells. In this study the involvement of the mitogen-activated protein kinases (MAP-kinases), nuclear factor-kappa Β (NF-κΒ) and in particular tumour necrosis factor-α converting enzyme (TACE) and—epidermal growth factor receptor (EGFR) signalling pathways were examined in triggering of IL-6 and CXCL8 release after exposure to a 50 nm silica nanoparticle (Si50). Exposure to Si50 increased phosphorylation of NF-κΒ p65 and MAP-kinases p38 and JUN-N-terminal protein kinase pathways (JNK), but not extracellular signal regulated kinases (ERK). Inhibition of NF-κΒ and p38 reduced the cytokine responses to Si50, whereas neither JNK- nor ERK-inhibition exerted any significant effect on the responses to Si50. Increases in membrane-bound transforming growth factor-α (TGF-α) release and EGFR phosphorylation were also observed after Si50 exposure, and pre-treatment with inhibitors of these pathways reduced the release of IL-6 and CXCL8, but did not affect the Si50-induced phosphorylation of p38 and p65. In contrast, p38-inhibition partially reduced Si50-induced TGF-α release, while the p65-inhibition was without effect. Overall, our results indicate that Si50-induced IL-6 and CXCL8 responses in BEAS-2B cells were regulated through combined activation of several pathways, including NF-κΒ and p38/TACE/TGF-α/EGFR signalling. The study identifies critical, initial events in the triggering of pro-inflammatory responses by nanoparticles.     

HPLC法测定小儿退热口服液中黄芩苷的含量

目的：建立HPLC法测定小儿退热口服液中的有效成分黄芩苷含量的方法。方法：采用色谱柱为C18柱,流动相为ψ甲醇：水：磷酸)=45：55：0．2,检测波长为315nm。结果：黄芩苷在0.15～1.2μg／mL范围内与峰面积呈线性关系,口服液中黄芩苷的平均回收率为98,07％,RSD=1．05％。结论：方法简便、稳定,能有效地控制该制剂的质量。     

Mathematical modeling of molecular diffusion through mucus

The rate of molecular transport through the mucus gel can be an important determinant of efficacy for therapeutic agents delivered by oral, intranasal, intravaginal/rectal, and intraocular routes. Transport through mucus can be described by mathematical models based on principles of physical chemistry and known characteristics of the mucus gel, its constituents, and of the drug itself. In this paper, we review mathematical models of molecular diffusion in mucus, as well as the techniques commonly used to measure diffusion of solutes in the mucus gel, mucus gel mimics, and mucosal epithelia.     

小儿肺热咳喘口服液防治甲型H1N1流感病毒感染免疫低下小鼠的研究

目的:评价小儿肺热咳喘口服液对免疫低下小鼠感染甲型H1N1流感病毒的防治作用。方法:ICR小鼠sc环磷酰胺造成免疫低下,以甲型H1N1流感病毒滴鼻感染造成肺炎模型,造模同时及造模前ig 20,10,5 mL·kg-1小儿肺热咳喘口服液4 d后观察肺部炎症、计算肺指数,死亡率和生命延长率,Real-time RT-PCR法检测肺组织中病毒载量,酶联免疫法检测血清中免疫因子的含量。结果:小儿肺热咳喘口服液治疗性给药或预防性给药后能明显降低流感病毒FM1株和PR8株感染后免疫低下小鼠的肺指数、降低死亡率、延长平均存活天数、显著降低小鼠肺组织中的病毒载量,明显升高小鼠血清中CD4/CD8的比值。结论:小儿肺热咳喘口服液对甲型H1N1流感病毒感染免疫低下小鼠造成的病毒性肺炎具有明显的防治作用。     

双波长分光光度法测定小儿肺热咳喘口服液中黄芩甙的含量

采用双波长分光光度法测定中药复方制剂小儿肺热咳喘口服液中黄芩的主要成分黄芩甙的含量。样品可不经分离,用双波长法消除共存的干扰,直接进行测定。同时使用UV-3000和751型分光光度计,所得结果基本一致。     

姜胆咳喘片微生物限度检查方法的验证

目的:建立姜胆咳喘片的微生物限度检查方法。方法:参照《中国药典》2005年版,采用5种阳性对照菌回收率试验测定其是否含抑菌成分。结果:该品种对金黄色葡萄球菌和枯草芽孢杆菌有抑菌活性,采用离心沉淀集菌和培养基稀释联用的方法进行细菌数的测定,采用常规法进行霉菌和酵母菌数的测定及控制菌的检查。结论:用该法进行微生物限度检查,可以客观地反映药物中微生物的污染状况,可行性强,能达到检测目的。     

小儿健脾止泻颗粒联合蒙脱石散治疗婴幼儿肺炎继发性腹泻疗效观察

目的：探讨小儿健脾止泻颗粒联合蒙脱石散治疗婴幼儿肺炎继发性腹泻的效果。方法：将156例婴幼儿肺炎继发性腹泻患儿随机分为两组,治疗组给予小儿健脾止泻颗粒和蒙脱石散口服,对照组单用蒙脱石散口服,并进行疗效分析判断。结果：治疗组总有效率为91.25%,对照组总有效率为69.73%,两组差异有显著性（P〈0.005）。结论：小儿健脾止泻颗粒联合蒙脱石散治疗婴幼儿肺炎继发性腹泻疗效满意,是安全有效的治疗方法。     

清洁磨损钛微粒对巨噬细胞释放破骨性细胞因子的影响

目的:探讨人工关节磨损清洁钛微粒的大小及不同微粒-细胞比对巨噬细胞释放破骨性细胞因子:肿瘤坏死因子-α(TNF-α)、白细胞介素-1(IL-1)、白细胞介素-6(IL-6)和前列腺素(PGE2)的影响。方法:清洁钛微粒按直径大小分为(0.35±0.09),(1.5±0.38),(6.25±2.13)μm组,分别以微粒-细胞比1:1,10:1,100:1,500:1,1000:1与巨噬细胞联合培养,用酶联免疫吸附法(ELISA)检测细胞培养上清液TNF-α、IL-1、IL-6、PGE2含量。结果:各组清洁钛微粒在微粒-细胞比10:1时,巨噬细胞释放TNF-α较对照组显著增高(P<0.05),500:1时释放TNF-α达到高峰,1000:1时分泌量下降。(0.35±0.09)μm清洁钛微粒组较(1.5±0.38)μm和(6.25±2.13)μm清洁钛微粒组,(1.50±0.38)μm清洁钛微粒组较(6.25±2.13)μm清洁钛微粒组,分别在微粒-细胞比10:1,100:1,500:1时,巨噬细胞释放更多TNF-α,具有统计学差异(P<0.05)。各组间IL-1、IL-6含量无显著性差异(P>0.05)。微粒-细胞比500:1,1000:1时,PGE2含量显著增高(P<0.01),巨噬细胞存活率显著下降(P<0.01)。结论:清洁磨损钛微粒大小及微粒-细胞比是决定磨损微粒生物细胞学反应的重要参量。磨损微粒越小,微粒-细胞比越高,生物细胞学毒性越大,能刺激巨噬细胞释放更多破骨性细胞因子TNF-α。清洁钛微粒本身并不能刺激巨噬细胞释放IL-1、IL-6、PGE2。