高效液相色谱法同时测定黄芪赤风胶囊中芍药苷、升麻素苷等9种成分的含量

 目的 建立HPLC同时测定黄芪赤风胶囊中9种成分的含量。方法 采用Waters Symmetry Shield RP₁₈（4.6 mm×150 mm,5 μm）色谱柱;以甲醇（A）-水溶液（B）为流动相进行梯度洗脱（0～15 min,5%A→20%A;15～55 min,20%A→35%A;55～100 min,35%A→85%A）,流速1.0 mL·min^-1;检测波长：230 nm（0～25 min,芍药苷）,254 nm（25～100 min,毛蕊异黄酮苷等）;柱温35 ℃。结果 芍药苷、升麻素苷、毛蕊异黄酮苷、升麻素、5-O-甲基维斯阿米醇苷、芒柄花苷、亥茅酚苷、毛蕊异黄酮、芒柄花素的线性范围分别为1.51～15.10,0.047～0.94,2.192～10.960,0.052 2～1.044,0.041 4～0.828,1.56～7.80,0.042 2～0.844,0.149～0.744和0.110～0.552 μg（r≥0.999 0）;平均回收率（n=6）分别为99.48%（RSD=2.59%）,103.15%（RSD=1.69%）,102.77%（RSD=1.56%）,99.27%（RSD=2.72%）,101.99%（RSD=2.36%）,102.25%（RSD=2.10%）,101.49%（RSD=3.00%）,100.45%（RSD=1.76%）和97.49%（RSD=2.03%）。结论 所建立的方法快速、准确、专属性强、精密度好,可用于黄芪赤风胶囊的质量控制。     

总序葱臭木茎干的化学成分研究

从总序葱臭木Dysoxylum laxiracemosum茎干分离得到12个化合物,通过波谱分析,化合物结构分别鉴定为sho-reic acid(1),cabraleahydroxylactone(2),cabralealactone(3),cinchonain(4),aurantiamide acetate(5),儿茶素(6),莨菪亭(7),香草酸(8),对羟基苯甲酸(9),1-二十二醇(10),β-谷甾醇(11),胡萝卜苷(12)。其中,化合物1～6,8～12首次从总序葱臭木中分离得到,化合物4～6首次从该属中分离得到。     

达英-35和雌孕激素联合应用治疗青春期功血60例的临床分析

目的：对比达英-35和雌孕激素联合应用治疗青春期功血的临床疗效及再次出血、不良反应情况。方法：对青春期功血患者60例,分两组分别用达英-35和雌孕激素联合应用止血,对比两组止血效果及再次出血、不良反应情况。结果：两组患者治疗效果,完全控制出血的时间差别无统计学意义。止血后两组再次发生出血的情况,达英-35组无此现象,雌孕激素联合应用组6例,经t检验,P〈0.05,差别有统计学意义,不良反应及第一次停药后阴道流血情况达英-35组亦明显少于雌孕激素联合应用治疗组。结论：达英-35治疗青春期功血优于传统的雌孕激素联合应用,此外达英-35服用简单,依从性好,值得临床推广应用。     

反相高效液相梯度洗脱法测定地松磺胺麻黄碱滴鼻液中有效成分含量

 目的 建立同时测定地松磺胺麻黄碱滴鼻液中有效成分含量的反相高效液相梯度洗脱法（reverse-phase high performance liquid chromatography,RP-HPLC）。方法 采用Agilent Eclipse XDB-C18（250 mm×4.6 mm,5 μm）色谱柱,以甲醇（A）-0.1%磷酸水溶液（B）为流动相进行梯度洗脱,梯度洗脱程序为：进样0~10 min,调节流动相A∶B（30∶70,V/V）;10~18 min,流动相A∶B（70∶30,V/V）;18~20 min,流动相A∶B（30∶70,V/V）;流速：1.0 mL/min,检测波长为梯度波长：0~5 min,220 nm;5~8 min,310 nm;8~20 min,240 nm;柱温：30℃,进样量：10 μL。结果 盐酸麻黄碱、磺胺甲噁唑和醋酸地塞米松分别在0.083~0.667 g /L、0.417~3.333 g/L和0.003~0.027 g/ L范围内与峰面积呈良好的线性关系;相关系数分别为：0.999 7、0.999 8和0.999 5;平均回收率分别为：（100.2±1.6）%时RSD为1.61%,（100.4±1.3）%时RSD为1.29%,（99.8±1.4）%时RSD为1.74%。样品中3者平均含量分别为（97.2±3.1）%时RSD为3.06%,（98.6±1.1）%时RSD为1.13%,以及（97.8±1.2）%时RSD为1.23%。结论 该方法简便、快速、专属性强,可用于地松磺胺麻黄碱滴鼻液的质量控制。     

Therapy of multiple sclerosis in children and adolescents

Background

Paediatric multiple sclerosis accounts for up to 10% of all MS cases. The initial course of the disease is relapsing-remitting in most children, with a relapse rate generally higher than that observed in adult patients. There is published experience on the use of first-line disease modifying therapies in children with MS. However, about 1/3 of paediatric MS cases do not respond to IFN-β or glatiramer acetate and continue to develop relapses and disease progression. These patients could be proposed to a second-line treatment.

Methods

A comprehensive review of the published literature related to pharmacologic treatment of MS in adults and paediatric patients was performed. The recent literature has been extracted for new evidence from controlled trials in adult patients, and open treatment studies and reported expert opinion in paediatric patients.

Results

No disease modifying drug has been approved for the treatment of children and adolescents with MS, although the currently available first-line therapies for adults seem to be safe and well tolerated in this population. Further studies are required to assess the safety and efficacy of second-line treatments in children with MS.

Conclusion

The present article constitutes an update of the existing publications regarding treatment of acute events of CNS demyelination in children and adolescents as well as considerations for the use of immunomodulatory therapies.     

Overlapping and distinct mechanisms of action of multiple sclerosis therapies

In the last two decades MS has changed from an idiopathic condition with only symptomatic treatments to a disease with better characterized pathophysiologic underpinnings and several treatments that modify its long-term course based on specific mechanisms of action. There are now several FDA approved options for therapy at the onset of disease, and discussions have begun on choosing the best treatment in individual patients and what option to choose next in patients who are failing their current treatment. Numerous studies have begun to highlight that the underlying pathology of CNS damage may be different in subsets of patients, raising the possibility that some may respond to a treatment with a mechanism of action that is targeted to ‘their’ MS. Trials are ongoing of numerous new agents with different mechanisms of action and some combination therapies. A better understanding of how each therapy works may guide decisions on initiating, combining or changing therapy in a more rational way to improve patient outcomes. Further knowledge of underlying mechanisms of disease in different patients with ‘the same’ disease may lead to more targeted therapies, as will biomarkers that predict clinical response to therapy. Studies of the effects of various agents used in MS reveal both overlapping and distinct mechanisms of actions that may be relevant to their efficacy and side effects in individual patients. However, it is important to remember that most agents are approved based on their reduction of MRI lesions and relapse rates over a short time frame. These measures only partially correlate with long-term disability, which may be the most relevant clinical outcome for people with MS. Fixed disability requires years to become apparent, and there is a lack of large studies of biomarkers for chronic outcomes. In addition, few large studies correlate response to therapy with cognitive outcomes, which are a major cause of chronic disability.     

Reducing agents induce thrombomodulin shedding in human endothelial cells

The level of thrombomodulin (TM) on cell surfaces reflects its biosynthesis, intracellular turnover, proteolytic cleavage, and release in soluble form (sTM). In the present study we examined the mechanisms mediating and regulating sTM release. Inducers of endothelial protein C receptor (EPCR) shedding, such as proinflammatory cytokines, phorbol ester, and ionomycin did not affect sTM release from human umbilical endothelial cells (HUVECs). In contrast, several natural and synthetic reducing compounds (i.e., glutathione, dihydrolipoic acid, homocysteine, N-acetyl-L-cysteine, dithiothreitol, and non-thiol cell-impermeable reductant, tris-(2-carboxyethyl)phosphine), but not oxidized glutathione or α-lipoic acid effectively up-regulated the release of sTM in endothelial cells. In addition, the direct activator of metalloproteases, 4-aminophenylmercuric acetate (APMA), was an effective inducer of TM shedding. Considerable inhibition of protein C activation was found with APMA, which is consistent with the effects of this agent on TM shedding. In addition to metalloproteases, serine proteases were shown by pharmacological inhibition studies to be involved in a similar degree in basal sTM release; however, serine proteases seem preferentially to be involved in thiol-induced TM proteolytic processing. From comparisons of non-thiol containing synthetic substrate with human recombinant TM it was demonstrated that disulfide bonds within TM are most likely modified by thiols making TM more susceptible to serine protease-mediated cleavage. In summary, the study shows that the extracellular redox state plays a crucial role in the regulation of TM shedding in HUVECs thereby offering new strategies to interfere with diminished activation of protein C during inflammatory diseases.     

复方氯已定甲硝唑栓治疗肛窦炎的临床观察

为观察复方氯已定甲硝唑栓治疗肛窦炎的疗效,我们将120例肛窦炎患者随机分为治疗组和对照组,各60例。治疗组应用复方氯已定甲硝唑栓,对照组应用肤痔清软膏。结果显示,治疗组总有效率为95．0％,明显优于对照组78．3％（P〈0．01）。结果表明,复方氯已定甲硝唑栓治疗肛窦炎疗效好,起效快。