双波长HPLC法同时测定止痢宁片中穿心莲内酯和脱水穿心莲内酯的含量

目的:建立高效液相色谱法同时测定止痢宁片中穿心莲内酯和脱水穿心莲内酯含量的方法.方法:色谱柱:CAPCELL PAK-C18柱(150 mm×4.6 mm,5 μm);流动相:甲醇-水(48:52);流速为1.0 ml·min-1;柱温:30℃;检测波长:225 nm(穿心莲内酯)、250 nm(脱水穿心莲内酯);进样量:5 μl.结果:穿心莲内酯在4.17～41.68 μg·ml-1 (r=0.999 9)、脱水穿心莲内酯在4.04～40.40 μg·ml-1(r=0.999 9)浓度范围内线性关系良好;穿心莲内酯回收率为99.21%(RSD=1.3%,n=6),脱水穿心莲内酯回收率98.73%(RSD=1.1%,n=6).结论:该方法简单、准确,可作为止痢宁片的质量控制.     

HPLC-ELSD测定穿心莲超分子提取物中三种穿心莲内酯的含量

目的 建立穿心莲超分子提取物中穿心莲内酯、脱水穿心莲内酯和14-去氧穿心莲内酯的含量测定方法.方法 HPLC-ELSD;色谱柱:Agilent ZORBAX Extent-C18 (4.6 mm×250 mm,5 μm);检测器:蒸发光散射检测器(ELSD);流动相:乙腈-水,线性梯度洗脱,流速0.8 mL·min-1,柱温:40 ℃.结果 穿心莲内酯、脱水穿心莲内酯和14-去氧穿心莲内酯线性范围分别为0.920～9.200 μg(r=0.999 6),0.397～3.952 μg(r=0.999 3)和0.395～3.936 μg(r=0.999 3);三者的回收率分别为98.9%、97.8%和98.4%,RSD分别为1.1%、2.2%和2.1%(n＝6).结论 本法简便,快捷,结果真实可靠,可用于穿心莲超分子提取物穿心莲内酯等有效成分的含量测定.     

HPLC法测定莲芝消炎胶囊中穿心莲内酯和脱水穿心莲内酯的含量

目的:建立反相高效液相色谱法测定莲芝消炎胶囊中穿心莲内酯和脱水穿心莲内酯含量的方法。方法:色谱柱为Kromasil-C_(18)柱(250 mm×4.6 mm,5μm),流动相为甲醇-水(55:45),流速1.0ml·min~(-1),检测波长225 nm,柱温40℃。结果:穿心莲内酯在0.23～2.30μg范围内线性良好。r=0.999 8,平均加样回收率为100.40%,RSD 为2.13%;脱水穿心莲内酯在0.25～2.50μg范围内线性良好,r=0.999 8,平均加样回收率为101.8%,RSD 为2.0%。结论:该方法简便、准确、灵敏度高,可有效控制莲芝消炎胶囊的质量。     

千喜片的定性定量方法研究

目的:建立千喜片的定性定量方法,对制剂质量进行有效控制。方法:采用TLC方法,对方中主药穿心莲和千里光分别进行鉴别。采用HPLC法测定穿心莲中穿心莲内酯和脱水穿心莲内酯的含量,色谱柱为Agela C18(5μm,250 mm×4.6 mm)柱,以甲醇(A)-水(B)为流动相,进行梯度洗脱(0～15 min,45%A;15～35 min,45%A→60%A),流速1.0 mL.min-1,检测波长为225 nm(穿心莲内酯)和254 nm(脱水穿心莲内酯)。结果:穿心莲和千里光的TLC鉴别专属性强;穿心莲内酯和脱水穿心莲内酯的线性范围分别为0.0646～0.968μg(r=0.9998)和0.196～2.94μg(r=0.9999),平均回收率(n=6)分别为99.5%(RSD=1.1%)和103.4%(RSD=1.1%)。结论:本方法简便、可靠、准确,可用于千喜片的质量控制。     

HPLC法测定清火栀麦片中穿心莲内酯、脱水穿心莲内酯的含量

目的建立用HPLC法测定清火栀麦片中穿心莲内酯、脱水穿心莲内酯的含量。方法采用C18柱(250mm×4.6mm5μm);以甲醇-水(55:45)为流动相,穿心莲内酯检测波长为230nm;脱水穿心莲内酯检测波长为250nm,流速:1.0mL·min-1。结果穿心莲内酯在4.02-32.16μg呈良好的线性关系(r=0.9999),回收率为98.8%,RSD为0.37%(n=6);脱水穿心莲内酯在4.12-32.96μg范围内呈良好的线性关系(r=0.9999),回收率为98.8%,RSD为0.38%(n=6)。结论本法快速、准确,可同时测定清火栀麦片中穿心莲内酯、脱水穿心莲内酯的含量。     

HPLC法测定穿心莲注射液中脱水穿心莲内酯的含量

目的:建立HPLC法测定穿心莲注射液中脱水穿心莲内酯的含量。方法:色谱柱:Hypersil ODS2 C_(18)柱(250mm×4.6mm,5μm);流动相:甲醇-水(55:45);流速1.0ml·min~(-1),检测波长250nm。结果:脱水穿心莲内酯在0.18～0.90μg的范围内,与峰面积呈良好的线性关系(r=1.000 0)。回收率为99.5%,RSD=2.0%。结论:本法快速、准确、简便。     

高效液相色谱法测定穿黄消炎片中穿心莲内酯和脱水穿心莲内酯的含量

目的建立HPLC测定穿黄消炎片中穿心莲内酯和脱水穿心莲内酯含量的方法。方法色谱柱为Dikma Di-amonsil C18柱(4.0 mm×250 mm,5μm),以甲醇-水(50∶50)为流动相,脱水穿心莲内酯检测波长254 nm、穿心莲内酯检测波长为225 nm;采用外标法定量。结果穿心莲内酯与脱水穿心莲内酯的线性范围内分别为2.928~146.4μg.mL-1和5.98~299μg.mL-1,相关系数r均为0.999 9;回收率分别为101.82%(RSD=2.2%)和97.52%(RSD=2.4%)。结论本方法操作简便、重现性好,适合于本制剂的含量测定。     

HPLC法同时测定清火栀麦片中3种有效成分的含量

目的:建立清火栀麦片中栀子苷和穿心莲内酯、脱水穿心莲内酯的HPLC测定方法。方法:采用CLC-ODS C18(4.6 mm×150 mm,5μm)色谱柱;流动相为甲醇-乙腈-水,梯度洗脱,流速1.0 mL.min-1;检测波长:238 nm(0～10 min,栀子苷),224 nm(10.1～25 min,穿心莲内酯),250 nm(25.1～30 min,脱水穿心莲内酯)。结果:栀子苷、穿心莲内酯、脱水穿心莲内酯进样量分别在0.20～1.22μg、0.06～0.35μg、0.17～1.03μg范围内有良好的线性关系(r=0.9999)。平均回收率(n=6)分别为98.2%,97.8%,97.9%;RSD分别为0.74%,1.1%,1.0%。结论:该方法简便、快捷、准确,可用于该制剂的质量控制。     

RP—HPLC法测定清火栀麦胶囊中穿心莲内酯和脱水穿心莲内酯的含量

目的:建立反相高效液相色谱法测定清火栀麦胶囊中穿心莲内酯和脱水穿心莲内酯含量。方法:采用 Hypersil C_(18)(250mm×4.6 mm,5μm)柱;流动相为0.01 mol·L~(-1)的磷酸二氢钾(磷酸调 pH 3.0)-乙腈梯度洗脱,洗脱程序为0～43 min 乙腈的体积分数由20%线性递增至37%;流速为1.0 mL·min~(-1);柱温为35℃;检测波长为225 nm。结果:穿心莲内酯在0.047～1.19μg的范围内线性关系良好(r=0.9999);脱水穿心莲内酯在0.084～2.09μg范围内线性关系良好(r=0.9999),两个成分平均回收率均在95%～105%之间。结论:该方法快速、简便,分离度好,能同时测定清火栀麦胶囊中穿心莲内酯和脱水穿心莲内酯的含量,可作为清火栀麦胶囊质量控制的方法。     

HPLC法测定清咽胶囊中穿心莲内酯和脱水穿心莲内酯的含量

目的建立清咽胶囊中穿心莲内酯和脱水穿心莲内酯的含量测定方法。方法应用HPLC法,选用R eliesil C18色谱柱(250×4.6mm,5μm),流动相为甲醇-水(65∶35),流速为:1m.lm in-1,检测波长为250nm。结果本品中穿心莲内酯含量测定线性范围为0.084~0.756μg(r=0.9999),平均回收率为97.5%(RSD=2.26%,n=5);脱水穿心莲内酯含量测定线性范围为0.036~0.324μg(r=0.9998),平均回收率为100.1%(RSD=0.86%,n=5)。结论含量测定方法准确可行,重复性好,作为药品标准可有效地控制清咽胶囊的质量。     

Trichloroethylene. I. Carcinogenicity of trichloroethylene.

Trichloroethylene (TCE) as an industrial pollutant may damage human health and can be considered as carcinogen. TCE has been detected in the environment and in various human organs, e.g., liver, kidney and brain etc. There are histological alterations such as depletion of glycogen and hydropic degeneration in the liver, however, other signs of TCE effects can be found in various organs as well. TCE and its metabolites, e.g., trichlorethanol, trichloro-acetic acid and epoxides were recently identified as strong mutagens in Ames mutagenicity test inducing frameshift and base-substitution mutations. TCE induced predominantly hepatocellular carcinoma after long term administration in mice. In these animals, kidneys and liver were supposed to be primary target organs with low epoxy-hydrolase activity. A high level of mitotic gene conversion (or gene rearrangement) was indicated by the metabolism of TCE after repeated administration. Purified TCE by was a weak mutagen in the presence of S9 microsomal fraction of rats and as a consequence, the carcinogenic activity was low in the kidney of rats. However, a dose related increase of Leydig cell tumors was found in male rats.     

Trichloroethylene. II. Mechanism of carcinogenicity of trichloroethylene.

The cancer inducing effect of trichloroethylene (TCE) was studied by various methods. DNA complexing activity and apoptosis inhibition were found to be the key elements of the carcinogenicity of TCE and its metabolites. The ability of TCE to interact with DNA was low, but its incorporation into the RNA and DNA of the brain, testis, pancreas, kidney, liver, lung and spleen, cannot be excluded. Exposure to TCE and its metabolites provides a selective growth advantage to spontaneously occurring mutations in some K- and H-ras oncogenes (as non specific results of secondary DNA or RNA damage). The amount of DNA-TCE adducts was higher in mouse hepatocytes than in rat hepatocytes. These differences may explain the species difference in carcinogenicity of TCE, which was dose dependent (due to metabolism) in mice but independent in rats. The blood level kinetics of TCE confirmed the faster metabolic rate in mice, including peroxisome proliferation and induction in hepatocytes. Dichloroacetic- and trichloroacetic acid were found to be hepatic carcinogens in mice, and the specificity depends on peroxisome proliferation induction. Possibly, TCE and related compounds down regulated apoptosis in mouse liver, and the reduced ability to remove initiated cells by apoptosis could be responsible for liver cancer induction by TCE.     

Studies in antifertility agents. 11. Secosteroids. 5. Synthesis of 9,11-secoestradiol.

9,11-Secoestradiol (9) and 11-hydroxy-9,11-secoestradiol (12) have been synthesized starting from 17-acetoxyestradiol 3-methyl ether (1) and found to possess significant antifertility activity in rats. 3-Methoxy-9,11-seco-9-oxo-17beta-acetoxyestra-1,3,5(10)-trien-11-oic acid (2), prepared by CrO3 oxidation of 1, on hydrogenolysis gave methyl 17beta-hydroxy-3-methoxy-9,11-secoestra-1,3,5(10)-triene-11-carboxylate (3). The 17-O-THP derivative of 3 was treated with LiAlH4 to give 17beta-(O-tetrahydropyranyl)-3-methoxy-11-hydroxy-9,11-secoestra-1,3,5(10)-triene (5). The 11-O-mesylate of 5 on LiAlH4 reduction followed by mild acid treatment and demethylation under alkaline conditions gave 9. LiAlH4 reduction of 3 gave 9,11-seco-11-hydroxyestradiol 3-methyl ether (11) which on demethylation gave 9,11-seco-11-hydroxyestradiol (12).     

Metabolism of benzothiazole. I. Identification of ring-cleavage products.

1. The metabolic fate of benzothiazole in guinea pig has been investigated following i.p. administration at a dose of 30 mg/kg. 2. Five ring-cleavage products were identified in urinary extracts by g.l.c.-mass spectra. By reference to authentic compounds the three major metabolites were shown to be 2-methylmercaptoaniline (I), 2-methylsulphinylaniline (II) and 2-methylsulphonylaniline (III). On the basis of the mass spectrometric evidence the remaining two metabolites were postulated to be 2-methylsulphinylphenylhydroxylamine (IV) and 2-methylsulphonylphenylhydroxylamine (V). 3. I, II and III were present in conjugated and unconjugated forms; IV and V were identified only after hydrolysis with sulphatase.     

Discussion of S.G. Donald et al. and R. Davidson

Summary This paper discusses aspects of the papers by S.G. Donald et al. and R. Davidson, which were presented at The Econometrics Journal sponsored special session on the econometrics of inequality measurement, held at the Royal Economics Society Meeting in Surrey in 2010.