紫外分光光度法测定复方苦参素胶囊中绞股蓝总皂苷含量及稳定性研究

目的 对复方苦参素胶囊中绞股蓝总皂苷的含量及稳定性进行研究,从而对本品质量进行控制。方法 采用紫外分光光度法和经典恒温试验法。结果 人参皂苷R_bl在(0.004-0.020mg·ml^-1)间浓度与吸收度成线性关系,回归方程为A=18.5C-0.012,相关系数r=0.9988;加样回收率为100.7%,RSD为2.3%。复方苦参素胶囊中绞股蓝总皂苷的有效期为1.6年。结论 该法简便易行、快速准确,可作为本品的质量控制。加速试验表明该制剂中绞股蓝总皂苷的稳定性较好。     

长梗绞股蓝的化学成分研究

自长梗绞股蓝( Gynostemma longipes C.Y.Wu )的地上部分分得一个新的三萜皂甙,经化学方法和光谱分析确定其化学结构为19-氧化-3β,20(S),21-三羟基达玛烷-24-烯-3-O-｛[α-L-吡喃鼠李糖基(1→2)][β-D-吡喃木糖基(1→3)]｝α-L-阿拉伯糖甙,命名为长梗绞股蓝皂甙I(gylongiposideI)。     

绞股蓝总皂苷对非酒精性脂肪肝大鼠Treg/Th17免疫功能的影响

目的 研究绞股蓝总皂苷对非酒精性脂肪肝（nonalcoholic fatty liver disease,NAFLD）大鼠肝脏保护作用及免疫调节作用机制。方法 48只SD大鼠随机分为正常对照组,模型对照组,多烯磷脂酰胆碱胶囊组（阳性对照组,150 mg·kg^-1）及绞股蓝总皂苷高、中、低（240,120,60 mg·kg^-1）剂量组,除正常对照组外,其余各组连续饲喂高脂饲料10周,制备NAFLD模型;模型成功后,各组连续给药8周。实验期间,分别于给药0,4,8周眼眶取血检测血清AST、ALT;末次给药后,采用流式细胞技术检测外周血Th17和Treg细胞含量;酶联免疫法检测血清IL-17、IL-10及TNF-α含量。HE染色检查肝组织病理变化和免疫组化法检查肝组织IL-17和Foxp3表达。结果 给药4周,绞股蓝总皂苷高剂量显著降低大鼠血清ALT、AST（P<0.01）;给药8周,绞股蓝总皂苷各剂量均能显著降低血清ALT、AST（P<0.05,0.01）。绞股蓝总皂苷高、中剂量能改善肝组织病变,降低TNF-α水平;高剂量显著降低IL-17、升高IL-10水平（P<0.05,0.01）,降低淋巴细胞IL-17含量,升高CD4⁺CD25⁺Treg含量（P<0.05）,明显减少炎症因子IL-17的表达和增加Foxp3表达。结论 绞股蓝总皂苷能改善NAFLD大鼠肝脏病变,其作用机制可能与调节肝脏Treg/Th17细胞平衡,减少促炎症因子和增加抗炎因子产生相关。     

绞股蓝总苷对慢性脑缺血大鼠海马神经元的保护作用及其机制研究

目的 探讨绞股蓝总苷对慢性脑缺血大鼠海马神经元的保护作用及可能机制。方法 选取50只健康SD大鼠,♂,随机分为假手术组、模型组和绞股蓝高、中、低剂量组,每组10只。通过双侧颈总动脉永久性结扎法,建立慢性脑缺血模型,造模手术后24 h,绞股蓝总苷高、中、低剂量组大鼠分别灌胃100,50,25 mg·kg^-1的绞股蓝总皂苷,每日1次,连续8周。Morris水迷宫法检测大鼠空间学习记忆力;TUNEL法检测海马部位神经元的凋亡情况;Western blot法检测脑组织GSK-3β和TNF-α蛋白的表达,并检测凋亡相关通路蛋白p38及caspase-3的表达。结果 与模型组相比,绞股蓝总苷高、中、低剂量组逃避潜伏期显著缩短（P<0.01）,穿台次数明显增多（P<0.05）;海马部位神经元凋亡数量明显减少（P<0.01）;GSK-3β和TNF-α蛋白的表达显著降低（P<0.01）;caspase-3和P38的表达显著降低（P<0.01）。结论 绞股蓝总苷通过抑制凋亡通路P38/caspase-3的激活,减少神经元凋亡,从而对神经元发挥保护作用。     

HPLC测定绞股蓝中七叶胆苷XLVI和人参皂苷Rb3含量

目的 建立HPLC测定绞股蓝中七叶胆苷XLVI和人参皂苷Rb₃含量的方法。方法 采用Ultimate XB-C₁₈色谱柱（250 mm×4.6 mm，5 μm），以乙腈（A）-水（B）线性梯度洗脱，检测波长203 nm，流速1 mL·min^-1，柱温30℃。结果 七叶胆苷XLVI在3.30~39.62 μg·mL^-1范围内线性良好（r²=0.999 7），平均回收率为113%，RSD为1.84%；人参皂苷Rb₃在3.27~39.26 μg·mL^-1范围内线性良好（r²=0.999 7），平均回收率为102%，RSD为2.82%。结论 该方法有较好的分离效果，准确性、精密度和重复性良好，为绞股蓝的研究和质量控制提供了科学依据。     

基于代谢组学技术研究绞股蓝总皂苷抑制tau蛋白过表达诱导的细胞损伤机制

目的 研究绞股蓝总皂苷(GPs)对tau蛋白过表达细胞代谢的影响,探讨GPs治疗阿尔茨海默病(AD)的机制。方法 通过采用CRISPR/Cas9技术构建微管相关蛋白tau (MAPT)过表达N2a细胞系(MAPT细胞);用CCK-8法检测GPs对N2a、MAPT细胞存活率的影响;体外培养N2a (对照组)、MAPT细胞(模型组),向MAPT细胞中加入GPs (50、100 μg·mL^-1)进行干预,共同孵育24 h后收集细胞,采用Western blotting技术检测总tau蛋白量水平;利用代谢组学技术检测GPs对MAPT细胞内源性代谢产物的影响,明确差异代谢产物及通路。结果 50、100、200 μg·mL^-1 GPs对N2a细胞活力无明显影响;5、50、100、200 μg·mL^-1 GPs对MAPT细胞活力无显著性影响;与对照组相比,MAPT细胞内tau蛋白水平明显增加(P<0.001);与模型组比较,50 μg·mL^-1 GPs可明显减少MAPT细胞内总tau蛋白含量(P<0.05);代谢组学结果显示,按照差异代谢产物数量占比从高到底依次为脂质和类脂分子,有机酸及其衍生物,核苷、核苷酸和类似物等。通过京都基因与基因组百科全书(KEGG)通路分析,差异代谢产物主要富集在核苷酸代谢、氨基酸合成、甘油磷脂代谢等通路。与模型组比较,给药后参与甘油磷脂代谢通路的胞磷胆碱和磷脂酰胆碱水平显著增加(P<0.001),甘油磷酰胆碱、甘油-3-磷乙醇胺水平显著降低(P<0.001)。结论 GPs可以减少细胞内tau蛋白的异常过表达,通过增加胞磷胆碱和磷脂酰胆碱水平、减少甘油磷酰胆碱和甘油-3-磷乙醇胺水平调控甘油磷脂代谢通路。     

扁果绞股蓝化学成分的研究

从扁果绞股蓝(Gynostemma compressum X. X. Chen et D. R. Liang)中分离出四个皂甙,经光谱及化学方法鉴定了它们的化学结构,分别命名为扁果绞股蓝皂甙Ⅰ～Ⅳ(gycomoside Ⅰ～Ⅳ),均为新化合物。     

HPLC波长切换法同时测定心神安胶囊中9种成分的含量

目的 建立HPLC波长切换法同时测定心神安胶囊中9种成分的含量。方法 采用Agilent Eclipse XDB-C₁₈色谱柱,流动相乙腈（A）-0.1%甲酸溶液（B）,梯度洗脱;流速0.9 mL·min^-1;检测波长分别为320 nm[检测远志（口山）酮Ⅲ、3,6''-二芥子酰基蔗糖]、203 nm （检测人参皂苷Rb₁、绞股蓝皂苷XLIX、绞股蓝皂苷XVⅡ）和254 nm （检测毛蕊异黄酮葡萄糖苷、芒柄花苷、毛蕊异黄酮、芒柄花素）;柱温25℃。结果 远志（口山）酮Ⅲ、3,6''-二芥子酰基蔗糖、人参皂苷Rb₁、绞股蓝皂苷XLIX、绞股蓝皂苷XVⅡ、毛蕊异黄酮葡萄糖苷、芒柄花苷、毛蕊异黄酮、芒柄花素分别在2.070~41.40 μg·mL^-1（r=0.999 2）、3.860~77.20 μg·mL^-1（r=0.999 6）、11.29~225.8 μg·mL^-1（r=0.999 8）、5.070~101.4 μg·mL^-1（r=0.999 9）、19.86~397.2 μg·mL^-1（r=0.999 5）、1.280~25.60 μg·mL^-1（r=0.999 1）、0.960 0~19.20 μg·mL^-1（r=0.999 3）、0.670 0~13.40 μg·mL^-1（r=0.999 7）、2.580~51.60 μg·mL^-1（r=0.999 1）内线性关系良好,平均回收率分别为98.04%,99.26%,99.05%,97.42%,100.0%,98.27%,97.81%,96.84%和99.86%,RSD分别为1.28%,0.82%,1.43%,1.43%,0.86%,1.26%,1.38%,1.16%和0.69%。结论 本方法操作简便、准确、重复性好,能够对心神安胶囊中9种成分进行同时含量测定,为提高和完善心神安胶囊的质量标准提供了有效方法。     

黄毛忽木皂甙A的分离和结构测定

黄毛木(Aralia decaisneana Hance)为五加科木属植物。从其根的甲醇提取物中分离得到一个皂甙化合物(I),根据光谱(IR,¹HNMR,¹³CNMR,MS,Longrange ¹H-¹HCOSY和¹H-¹³cHETCOR)解析和化学反应(酸水解,乙酰化和碱水解)证明,化合物1的结构确定为3-O-[β-D-吡喃木糖1→3)]-β-D-吡喃葡萄糖(1→2)-β-D-吡喃葡萄糖-28-O-β-D-吡喃葡萄糖(1→6)-β-D-吡喃葡萄糖酯甙。该化合物是一个新的三萜皂甙,命名为黄毛木皂甙A(aradecoside A)。     

喙果绞股蓝中皂甙成分的研究

首次从喙果绞股蓝(Gymostemma yixingense CY Wu et SK Chen)中分得四个皂甙成分(Ⅰ～Ⅳ),经理化常数测定、光谱解析和化学方法确定了它们的结构。其中Ⅰ为新化合物,命名为喙果皂甙A(yixinosideA),Ⅱ,Ⅲ和Ⅳ分别鉴定为绞股蓝皂甙XLIVXLII(gypensideXLIV,XLII)和具明显调脂作用的人参皂甙Rb₁(ginsenosideRb₁)。此外,Ⅰ经酸水解得到一新皂甙元1β-羟基人参二醇(1β-hydroxylpanaxadiol)(Ⅴ)和一新次级甙,命名为喙果皂甙B(yixinosideB,VI)。     

BOVINE PROTHROMBIN FRAGMENT 1, SEGMENT 1–10

The N-terminal decapeptide methyl ester, H-Ala-Asn-Lys-Gly-Phe-Leu-Gla-Gla-Val-Arg-OCH₃ (16) of bovine prothrombin fragment 1 has been prepared by standard solution techniques, via a fragment coupling strategy. Hexapeptide Boc-Ala-Asn-Lys^e(Boc)-Gly-Phe-Leu-OBzl (9) was obtained by coupling Boc-Ala-Asn-Lys^e (Boc)Gly-OH (6) to the trifluoroacetate salt of H-Phe-Leu-OBzl (8). Hydrogenolysis of (9) followed by coupling to HCl-H-Gla^γ (O^tBu)₂-Gla^γ (O^tBu)₂-Val-Arg(HCl)-OCH₃ (14) gave the fully protected decapeptide (15). Treatment of 15 with 90% trifluoroacetic acid followed by ion exchange chromatography yielded the methyl ester (16). The decapeptide 16 labeled with¹²⁵I using the Bolton-Hunter reagent, did not bind to antibodies specific for the calcium ion-induced conformation of bovine fragment 1.     

Protective effects of Scutellaria lindbergii root extract against oxidative-induced cell and DNA damage in mouse fibroblast-like cells

Context: Scutellaria lindbergii Rech. f. (Lamiaceae) is an Iranian species of Scutellaria which has been shown to exert antimicrobial, antioxidant and cytotoxic effects. Objective: The protective properties of total methanol extract (TME) of S. lindbergii and its fractions (defatted and CH₂Cl₂) were investigated against cytotoxic and genotoxic effects of H₂O₂ in NIH 3T3 cell line as non-malignant cells. Materials and methods: The cells were incubated with different concentrations of S. lindbergii root extracts [TME (15–250?μg ml^?1), defatted fraction (15–500?μg ml^?1) and CH₂Cl₂ fraction (5–40?μg ml^?1)] and toxic concentration of H₂O₂ (200?µM) at 37?°C for 2?h concurrently and Cell viability was quantitated by MTT assay. The antigenotoxic effect of extracts was investigated using comet assay. The cells were incubated with extracts [TME (25–250?μg ml^?1), defatted fraction (25–500?μg ml^?1) and CH₂Cl₂ fraction (5–40?μg ml^?1)] and H₂O₂ (25?µM) at 4?°C for 20?min, then the comet assay was performed. DNA damage was expressed as percentage tail DNA. Results: Total methanol extract of S. lindbergii and its fractions had a significant inhibitory effect on DNA damage. The IC₅₀ values of TME, defatted fraction and CH₂Cl₂ fraction against DNA damage were determined as 48, 138 and 8?μg ml^?1, respectively. Conclusion: S. lindbergii extracts can prevent oxidative DNA damage, which is likely due to its flavonoids and phenolic compounds as antioxidant constituents.     

Preparation of 14C2‐cis‐1,2‐dichloroethylene from 14C2‐trichloroethylene using a cobalt porphyrin catalyst

A protocol for producing ¹⁴C₂‐cis‐1,2‐dichloroethylene (¹⁴C₂‐cis‐DCE) from ¹⁴C₂‐trichloroethylene (¹⁴C₂‐TCE) was developed as an economical alternative to commercial, custom synthesis of ¹⁴C₂‐cis‐DCE. The method uses 5,10,15,20‐tetrakis‐(4‐carboxyphenyl) porphyrin cobalt(II) as a catalyst in the presence of titanium(III) citrate to convert ¹⁴C₂‐TCE to ¹⁴C₂‐cis‐DCE as shown in Figure 1. A purge‐and‐trap technique was used to isolate ¹⁴C₂‐cis‐DCE to provide a methanolic stock solution of high purity (97% cis‐DCE). The overall ¹⁴C₂‐cis‐DCE yield of the process was approximately 53%. Copyright © 2005 John Wiley & Sons, Ltd.     

Pharmacokinetics of sulfaethidole in the rat: Nonlinear multicompartment solution

Sulfaethidole distribution and elimination in the rat was studied over a 90-fold dose range. This experimental design produced marked nonlinearity in the binding of Sulfaethidole to proteins in both interstitial fluid and plasma. Using a multicompartmental model consisting of binding of Sulfaethidole to plasma and interstitial fluid proteins, Sulfaethidole distribution in the body could be simulated. Urinary and biliary elimination of Sulfaethidole depended on the unbound drug mass in the plasma and urine flow. The results confirm the central role of the unbound species in the distribution and elimination of drugs with marked binding to plasma proteins.Nomenclature A ₁ amount of drug in plasma (mg) - A ₂ amount of drug in interstitial fluid (mg) - A ₃ amount of drug in poorly perfused tissues (mg) - A ₄ amount of drug in highly perfused tissues (mg) - fu ₁ fraction of total drug in plasma unbound (dimensionless) - fu ₂ fraction of total drug in interstitial fluid unbound (dimensionless) - fb ₁₁ fraction of drug bound to first binding site on plasma protein (dimensionless) - fb ₁₂ fraction of drug bound to second binding site on plasma protein (dimensionless) - fb ₂₁ fraction of drug bound to first binding site on interstitial fluid protein (dimensionless) - fb ₂₂ fraction of drug bound to second binding site on interstitial fluid protein (dimensionless) - K _d,1 apparent dissociation constant of first binding site on protein (dimensionless) - K _d,2 apparent dissociation constant of second binding site on protein (dimensionless) - B _max,11 ^–1 inverse of maximal binding capacity of first binding site on plasma protein (ml/mg) - B _max ^12–1 inverse of maximal binding capacity of second binding site on plasma protein (ml/mg) - B _max,21 ^–1 inverse of maximal binding capacity of first binding site on interstitial fluid protein (ml/mg) - B _max,22 ^–1 inverse of maximal binding capacity of second binding site on interstitial fluid protein (ml/mg) - k ₁₂ fractional transport rate of unbound drug from plasma to interstitial fluid (h^–1) - k ₂₁ fractional transport rate of unbound drug from interstitial fluid to plasma (h^–1) - k ₂₃ fractional transport rate of unbound drug from interstitial fluid to poorly perfused tissues (h^–1) - k ₃₂ fractional transport rate of unbound drug from poorly perfused tissues to interstitial fluid (h^–1) - k ₁₀ fractional rate of elimination of unbound drug from plasma (h^–1) - k ₁₀ ⁰ value during the first 210 min - k ₁₀ ¹ value after 270 min, linearly increased between 210 and 270 min (Eq. 5) - fup _t fraction of instantaneous binding of drug between plasma unbound drug and highly perfused tissue (dimensionless) - V _p plasma volume (ml) - V _is interstitial fluid volume (ml)     

Crystal structure and conformation of two N-tosyl-protected dipeptides containing amino acids with polar side-chains

X-Ray diffraction studies and energy-minimization calculations were carried out on two dipeptides, N-tosyl-l -Ser-Gly-OMe monohydrate (C₁₃H₁₈N₂O₆S·H₂O, compound A) and N-tosyl-l -Thr-Gly-OMe (C₁₄H₂₀N₂O₆, compound B). Compound A crystallized in the monoclinic system, space group P2₁ with unit cell parameters a= 4.915(1), b= 15.625(4), c= 11.003(1) Å, β= 91.28(1)°, V= 844.8 ų. M_r= 348.4, d= 1.37(2) g cm^?3, Z = 2, λ(Cu Kα) = 1.5418 Å, μ= 1.99 mm^?1, T=293 K. R= 0.032 for 1451 unique reflections with I > 2σ(I). Compound B crystallized in the orthorhombic system, space group P2₁2₁2₁, with unit cell parameters a= 5.050(2), b= 16.483(3), c= 20.769(5) Å, V= 1729.3 ų, Z = 4. M_r= 344.4, d= 1.32(2) g cm^?3, μ(Cu Kα)= 1.90 mm^?1. R= 0.040 for 1060 unique reflections with I > 2σ(I). The major difference in the backbone conformation of the two compounds is in their glycine residues, with the glycine residue in compound A adopting an extended conformation with φ= - 132.6(3)° and ψ= 175.3(3)° and that in compound B having a folded conformation with φ=?56.3(6)° and ψ=?42.6(7)°. In compound A the oxygen atom of the Ser side-chain and the carbonyl oxygen atom of glycine are bridged by the water of crystallization through O—H ··· O hydrogen bonds, resulting in the relatively rare trans conformation [χ=? 175.7(2)°] for this side-chain. The Thr side-chain in compound B is in the sterically preferred (tg^?) conformation [χ^1,1=? 179.4(4)° and χ^1,2=?62.3(5)°]. The conformations were found to be in general agreement with those obtained by an energy-minimization procedure. The energy-minimized structure of N-tosyl-l -Ser-Gly-Ome (anhydrous) showed a strong hydrophobic interaction between the methyl substituents of the tosyl group and the methyl ester (C—C = 4.08 Å).     

Synthesis,biological activity and conformational analysis of cyclic GRF analogs

A novel cyclic GRF analog, cyclo(Asp⁸-Lys¹²)-[Asp⁸,Ala¹⁵]-GRF(1-29)-NH₂, i.e. cyclo^8.12[Asp⁸,Ala¹⁵]-GRF(1-29)-NH₂, was synthesized by the solid phase procedure and found to retain significant biological activity. Solid phase cyclization of Asp⁸ to Lys¹² proceeded rapidly (～2h) using the BOP reagent. Substitution of Ala¹² with d -Ala² and/or NH₂-terminal replacement (desNH₂-Tyr¹ or N-MeTyr¹) in the cyclo^8.12[Asp⁸,Ala¹⁵]-GRF(1-29)-NH₂ system resulted in highly potent analogs that were also active in vivo. Conformational analysis (circular dichroism and molecular dynamics calculations based on NOE-derived distance constraints) demonstrated that cyclo^8.12[Asp⁸,Ala¹⁵]-GRF(1-29)-NH₂ contains a long α-helical segment even in aqueous solution. A series of cyclo^8.12 stereoisomers containing d -Asp⁸ and/or d -Lys¹² were prepared and also found to be highly potent and to retain significant α-helical conformation. The high biological activity of cyclo^8.12[N-MeTyr¹,d -Ala²,Asp⁸,Ala¹⁵]-GRF(1-29)-NH₂ may be explained on the basis of retention of a preferred bioactive conformation.     

Cardiovascular effects elicited by milonine, a new 8,14-dihydromorphinandienone alkaloid

Abstract: The mechanisms underlying the cardiovascular responses evoked by milonine (i.v.), an alkaloid, were investigated in rats. In normotensive rats, milonine injections produced hypotension and tachycardia, which were attenuated after N^w‐nitro‐l ‐arginine methyl esther (l ‐NAME; 20 mg/kg, i.v.). In phenylephrine (10 μM), pre‐contracted mesenteric artery rings, milonine (10^?10 M to 3 × 10^?4 M) caused a concentration‐dependent relaxation (EC₅₀ = 1.1 × 10^?6 M, E_max = 100 ± 0.0%) and this effect was rightward shifted after either removal of the vascular endothelium (EC₅₀ = 1.6 × 10^?5, p < 0.001), or after l ‐NAME 100 μM (EC₅₀ = 6.2 × 10^?5, p < 0.001), hydroxocobalamin 30 μM (EC₅₀ = 1.1 × 10^?4, p < 0.001) or ODQ 10 μM (EC₅₀ = 1.9 × 10^?4p < 0.001). In addition, in rabbit aortic endothelial cells, milonine increased NO₃^? levels. The relaxant effect induced by milonine was attenuated in the presence of KCl (20 mM), a modulator efflux K⁺ (EC₅₀ = 1.2 × 10^?5, p < 0.001), or different potassium channel blockers such as glibenclamide (10 μM) (EC₅₀ = 6.3 × 10^?5, p < 0.001), TEA (1 mM) (EC₅₀ = 2.3 × 10^?5 M, n = 6) or Charybdotoxin (0.2 μM) plus apamin (0.2 μM) (EC₅₀ = 3.9 × 10^?4 M, n = 7). In addition, pre‐contraction with high extracellular potassium concentration prevented milonine‐induced vasorelaxation (EC₅₀ = 1.0 × 10^?4, p < 0.001). Milonine also reduced CaCl₂‐induced contraction in Ca²⁺‐free solution containing KCl (60 mM). In conclusion, using combined functional and biochemical approaches, we demonstrated that the hypotensive and vasorelaxant effects produced by milonine are, at least in part, mediated by the endothelium, likely via nitric oxide release, activation of nitric oxide‐cGMP pathway and opening of K⁺ channels.     

N‐heterocyclic carbenes as ligands in palladium‐mediated [11C]radiolabelling of [11C]amides for positron emission tomography

A model palladium‐mediated carbonylation reaction synthesizing N‐benzylbenzamide from iodobenzene and benzylamine was used to investigate the potential of four N‐heterocyclic carbenes (N,N′‐bis(diisopropylphenyl)‐4,5‐dihydroimidazolinium chloride ( I ), N,N′‐bis(1‐mesityl)‐4,5‐dihydroimidazolinium chloride ( II ), N,N′‐bis(1‐mesityl)imidazolium chloride ( III ) and N,N′‐bis(1‐adamantyl)imidazolium chloride ( IV )) to act as supporting ligands in combination with Pd₂(dba)₃. Their activities were compared with other Pd‐diphosphine complexes after reaction times of 10 and 120 min. Pd₂(dba)₃ and III were the best performing after 10 min reaction (20%) and was used to synthesize radiolabelled [¹¹C]N‐benzylbenzamide in good radiochemical yield (55%) and excellent radiochemical purity (99%). A Cu(Tp*) complex was used to trap the typically unreactive and insoluble [¹¹C]CO which was then released and reacted via the Pd‐mediated carbonylation process. Potentially useful side products [¹¹C]N,N′‐dibenzylurea and [¹¹C]benzoic acid were also observed. Increased amounts of [¹¹C]N,N′‐dibenzylurea were yielded when PdCl₂ was the Pd precursor. Reduced yields of [¹¹C]benzoic acid and therefore improved RCP were seen for III /Pd₂(dba)₃ over commonly used dppp/Pd₂(dba)₃ making it more favourable in this case. Copyright © 2010 John Wiley & Sons, Ltd.     

二室模型药物“静注十静滴”的给药方案计算

本文对静脉注射一定剂量,同时以一定速度恒速静脉滴注,提出了一类确定静注剂量和静滴速度的方法。按这类方法确定的给药方案用药时,可确保从用药一开始直至用药结束,血药浓度一直在有效血药浓度范围内变化。