正交设计法优选洁肤康洗剂的制备工艺

目的优选洁肤康洗剂的制备工艺。方法以处方中黄芩的主要药效成分黄芩苷含量为考察指标,采用正交设计法,筛选最佳制备工艺条件。结果结合生产实际需要,优化出的条件为加水量12倍,浸泡1.0h,煎煮3次,每次40min。结论采用优化方案能保证产品质量。     

RP-HPLC法测定参龙补肾胶囊中淫羊藿苷的含量

建立参龙补肾胶囊中淫羊藿苷的高效液相测定方法。色谱柱为Hypersil C18ODS,流动相为甲醇-水(54∶46),流速:1.0mL.m in-1,检测波长为270nm。淫羊藿苷线性范围为0.38~3.07μg,r=0.9999,平均回收率为97.8%,RSD=0.7%。方法简便,准确可靠,适用于该制剂的质量控制。     

浅议如何确定药品行政处罚对象的主体资格

我国《行政处罚法》和相关法律，明确规定了行政处罚对象的主体资格，但是尚未对其进行细化，在执法实践中由于对法律法规条文理解不一，在一定程度上造成了难以确定行政处罚对象主体资格的情况。本文结合《行政处罚法》、《药品管理法》等相关法律法规，对如何确定行政处罚对象的主体资格进行探讨。     

干咳清糖浆的质量控制

目的：建立干咳清糖浆的质量控制。方法：采用TLC法对干咳清糖浆中贝母进行定性鉴别；采用HPLC法测定糖浆中的栀子苷含量，色谱柱：Diamonsil C18（250mm×4．6mm，5μm）；流动相：乙腈-水（15：85）；波长：238nm结果：在TLC色谱中检出贝母；栀子苷线性范围为0．50μg-4．02μg，平均回收率为99．3％，RSD为1.2％。结论：方法准确可行，可用于该制剂的质量控制。     

奥硝唑阴道凝胶剂的制备及质量考察

目的:制备奥硝唑阴道凝胶剂并考察其稳定性。方法:以卡波姆为基质制备奥硝唑凝胶剂,采用HPLC法测定含量。结果:奥硝唑含量测定方法稳定,重复性好,奥硝唑凝胶剂对热和光较稳定。结论:奥硝唑凝胶的制备及质量控制方法可行。     

散瘀接骨精在四肢骨关节损伤康复中的应用

为观察散瘀接骨精在四肢骨关节损伤康复中应用的疗效,将208例由于四肢骨关节损伤所致的组织粘连和瘢痕形成引起的陈旧性伤痛患者分两组治疗。对照组99例,在医师指导下行功能训练、物理治疗等常规处理;治疗组109例,加用散瘀接骨精以手法在损伤部位反复按揉20分钟,每天2次,7～10天为1个疗程;分别观察两组病人用药前后疼痛、肿胀、压痛、功能障碍等症状体征。均于治疗2个疗程后第4周观察疗效,结果治疗组显愈率80.7%,总有效率99.1%,对照组显愈率31.3%,总有效率82.8%,两组疗效差异有显著性。表明散瘀接骨精在四肢骨关节损伤康复治疗中效果显著。     

一种抗转移层粘连蛋白核心三糖的合成

本文完成了一种具有潜在转移活性的层粘连蛋白核心三糖β—D—Gal-（1→4）-β—D—GlcpNAc-（1→6）-α-D—Manp—OMe的合成。以2-碘代叠氮乳糖为供体采用“叠氮碘糖基化”反应一步完成了2-脱氧-2-氨基乳糖结构及1，2-反式-氨基乳糖糖苷键的立体选择性构建。这种方法能简易、高效地合成含氨基乳糖的寡糖，较好地避免了直接使用活性较差的2-氨基糖衍生物构建氨基乳糖模块。     

HPLC法测定银马解毒颗粒中绿原酸、甘草酸铵的含量

目的：研究以HPLC法同时测定银马解毒颗粒中绿原酸、甘草酸铵含量的方法。方法：采用高效液相色谱法。色谱柱：AgilentSB-C18柱（250mm×4．6mm，5μm）；流动相：以乙腈-0．4％磷酸梯度洗脱，流速1．0ml·min^-1；检测波长：λ1=327nm，λ2=250nm；柱温：30℃。结果：绿原酸在0．4992～4．9920μg范围内线性关系良好（r=0．9997），平均回收率为99．33％，RSD=0．67％（n=6）；甘草酸铵在0．1515～1．5150μg范围内线性关系良好（r=0．9999），平均回收率为99．30％，RSD=034％（n=6）。结论：该法操作简便，结果准确可靠，可作为银马解毒颗粒的质量控制方法。     

Studies on interaction between Vitamin B12 and human serum albumin

The binding reaction between Vitamin B12 (B12, cyanocobalamin) and human serum albumin (HSA) was investigated by fluorescence quenching, UV–vis absorption and circular dichroism (CD) spectroscopy. Under simulative physiological conditions, fluorescence quenching data revealed that the quenching constants (K_sv) are 3.99 × 10⁴, 4.33 × 10⁴, 4.76 × 10⁴ and 5.16 × 10⁴ M⁻¹ at 292, 298, 304 and 310 K, respectively. The number of binding sites, n is almost constant around 1.0. On the basis of the results of fluorescence quenching the mechanism of the interaction of B12 with HSA has been found to be a dynamic quenching procedure. Thermodynamic parameters ΔH^Θ = −13.38 kJ mol⁻¹, ΔS^Θ = 66.73 J mol⁻¹ K⁻¹ were calculated based on the binding constant. These suggested that the binding reaction was enthalpy and entropy driven, and the electrostatic interaction played major role in stabilizing the reversible complex. The binding distance r = 5.5 nm between HSA and B12 was obtained according to Förster theory of energy transfer. The effect of B12 on the conformation of HSA was analyzed by synchronous fluorescence and CD spectroscopy. Synchronous spectra indicated that the polarity around the tryptophan (Trp214) residues of HSA was decreased and its hydrophobicity was increased; however, the α-helix content of the protein was predominant in the secondary structure but the CD spectra indicated that B12 induced minor conformational changes of HSA.     

L‐type Ca2+ channel opener BayK 8644‐induced Ca2+ influx and Ca2+ release in human oral cancer cells (OC2)

The effect of BayK 8644, a chemical widely used to activate L‐type Ca²⁺ channels, on cytosolic free Ca²⁺ concentrations ([Ca²⁺]_i) in human oral cancer cells (OC2) has not been explored to date. The present study examined whether BayK 8644 altered basal [Ca²⁺]_i levels in suspended OC2 cells by using fura‐2. BayK 8644 (10 pM–10 µM) increased [Ca²⁺]_i in a concentration‐dependent manner. The Ca²⁺ signal was reduced partly by removing extracellular Ca²⁺. BayK 8644‐induced Ca²⁺ influx was blocked by nifedipine, but was not altered by the store‐operated Ca²⁺ entry inhibitors, econazole and SKF96365; protein kinase C modulators phorbol 12‐myristate 13‐acetate (PMA) and GF109203X; the protein kinase A inhibitor H89; and the phospholipase A₂ inhibitor, aristolochic acid. In Ca²⁺‐free medium, after pretreatment with 1 µM BayK 8644, 1 µM thapsigargin (an endoplasmic reticulum Ca²⁺ pump inhibitor)‐induced [Ca²⁺]_i rises were abolished; and conversely, thapsigargin pretreatment abolished BayK 8644‐induced [Ca²⁺]_i rises. Inhibition of phospholipase C with U73122 did not change BayK 8644‐induced [Ca²⁺]_i rises. Collectively, in OC2 cells, BayK 8644 induced [Ca²⁺]_i rises by causing phospholipase C‐independent Ca²⁺ release from the endoplasmic reticulum; and Ca²⁺ influx via L‐type Ca²⁺ channels. Drug Dev Res 69: 2008. © 2008 Wiley‐Liss, Inc.