1-(4-硝基苯基)-3-(3,5-二溴吡啶)三氮烯的合成及其与铜的显色反应

合成了显色剂1-(4-硝基苯基)-3-(3,5-二溴吡啶)三氮烯(NPDBPDT),并研究了其与铜的显色反应。在pH11.0的Na2B4O7-NaOH缓冲溶液介质中,表面活性剂OP存在下,铜与NPDBPDT生成组成比为1∶4的络合物。该络合物在460nm处有最大正吸收峰,540nm处有最大负吸收峰,以540nm为参比波长,460nm为测量波长进行双波长测定络合物的吸光度。体系表观摩尔吸光系数为2.02×105L.mol-1.cm-1,铜量在8～480μg/L范围内符合比尔定律,方法检出限为7.43×10-9g/mL。所拟方法用于铜矿和铝合金样品中铜的测定,结果与原子吸收光谱法相吻合,相对标准偏差分别为1.63%和1·56%。     

4-(3,5-二溴-2-吡啶重氮氨基)-4'-硝基偶氮苯的合成及其与镉(Ⅱ)显色反应的研究

合成了新显色剂4-(3,5-二溴-2-吡啶重氮氨基)-4'-硝基偶氮苯(简称DBPNAB),研究了在非离子表面活性剂Triton X-100存在下其与Cd(Ⅱ)的显色反应.结果表明,在pH 10.2的Na2B4O7-NaOH缓冲介质中,该试剂与Cd(Ⅱ)形成摩尔比为2:1的红色络合物,最大吸收波长位于581 nm,表观摩尔吸光系数为1.61×105L·mol-1·cm-1,镉的质量浓度在0～0.7μg/mL范围内遵守比尔定律.所拟方法用于废水中微量镉(Ⅱ)的直接测定,相对标准偏差为2.0%～3.3%,回收率为97.4%～103.6%.     

4-(2-噻唑偶氮)连苯三酚分光光度法测定钢中微量钨

在稀硫酸介质及溴化十六烷基吡啶(CPB)存在下,试剂4-(2-噻唑偶氯)连苯三酚(TATB)与钨(Ⅵ)发生显色反应,据此建立了分光光度法测定钢样中微量钨的方法.研究发现:TATB与钨(Ⅵ)形成2:1的红色络合物,该络合物的最大吸收波长在530 nm处.25 mL溶液中,钨质量在0～40μg范围内服从比尔定律,测得表观摩尔吸光系数为6.16×104L·mol-1·cm-1.方法用于钢样中微量钨的测定,结果同硫氰酸盐光度法所得结果相吻合.     

4-(3,5-二溴-2-吡啶重氮氨基)-4′-硝基偶氮苯的合成及其与镉(Ⅱ)显色反应的研究

合成了新显色剂4-(3,5-二溴-2-吡啶重氮氨基)-4′-硝基偶氮苯(简称DBPNAB),研究了在非离子表面活性剂Triton X-100存在下其与Cd(Ⅱ)的显色反应。结果表明,在pH10.2的Na2B4O7-NaOH缓冲介质中,该试剂与Cd(Ⅱ)形成摩尔比为2∶1的红色络合物,最大吸收波长位于581 nm,表观摩尔吸光系数为1.61×105L.mol-1.cm-1,镉的质量浓度在0～0.7μg/mL范围内遵守比尔定律。所拟方法用于废水中微量镉(Ⅱ)的直接测定,相对标准偏差为2.0%～3.3%,回收率为97.4%～103.6%。     

4-硝基-4′-氟苯基重氮氨基偶氮苯双波长分光光度法测定镍

报道了新含氟显色剂4-硝基-4′-氟苯基重氮氨基偶氮苯与镍(Ⅱ)的显色反应。试验表明,在pH 8.6 Na2B4O7-HCl缓冲溶液、Tween-85存在下,试剂与镍(Ⅱ)形成4∶1的稳定紫红色络合物。最大吸收正峰为504 nm,负峰为424 nm;且在25 mL显色液中镍(Ⅱ)的量在0~4μg范围内符合比尔定律。在两最大正负吸收波长处分别进行单波长分光光度法测定,表观摩尔吸光系数分别为1.13×105,1.06×105L.mol-1.cm-1。再以424 nm为参比波长、504 nm为测量波长进行吸光度叠加的双波长光度法测定,表观摩尔吸光系数为2.17×105L.mol-1.cm-1。加入混合掩蔽剂NaF-硫脲,可消除常见共存离子的干扰。本法可用于测定多元素混合标准溶液和不锈钢中的镍(Ⅱ),回收率为96%~98%,混合标准溶液的测定值与认定值相一致。     

Ce（Ⅳ）-（DBC-偶氮胂）-OP乳化剂体系分光光度法测定铈

研究了Ce(IV)-(DBC-偶氮胂)-乳化剂OP体系分光光度法测定铈的最佳条件及分光光度性质,考察了某些表面活性剂对体系性质的影响.在0.72 mol/L硫酸介质中,体系最大吸收波长为530 nm,表观摩尔吸光系数为ε530nm =1.05×104 L· mol-1·cm-1, Ce(Ⅳ)质量浓度在30～300 μg/25 mL范围内遵守比耳定律.本法用于测定钢样中微量铈,结果令人满意.     

1-(2-苯并噻唑偶氮)-2-羟基-3-萘甲酸与镍(Ⅱ)的显色反应研究及应用

用分光光度法研究了新试剂1-(2-苯并噻唑偶氮)-2-羟基-3-萘甲酸(BTAHN)与镍Ⅱ的显色反应性能。在pH4·6~10·4范围内,BTAHN与镍Ⅱ形成2∶1的蓝色络合物,该络合物的最大吸收波长λmax在612nm处,25mL溶液中镍的质量在0~34μg范围内服从比尔定律,测定的表观摩尔吸光系数ε612为3·52×104,所拟方法用于合金钢样品中微量镍的测定,结果满意。     

Ce(IV)-(DBC-偶氮胂)-OP乳化剂体系分光光度法测定铈

研究了Ce(IV)-(DBC-偶氮胂)-乳化剂OP体系分光光度法测定铈的最佳条件及分光光度性质,考察了某些表面活性剂对体系性质的影响.在0.72 mol/L硫酸介质中,体系最大吸收波长为530 nm,表观摩尔吸光系数为ε530nm =1.05×104 L· mol-1·cm-1, Ce(Ⅳ)质量浓度在30～300 μg/25 mL范围内遵守比耳定律.本法用于测定钢样中微量铈,结果令人满意.     

4-(4-氯苯重氮氨基)-4'-硝基偶氮苯的合成及其与镉(Ⅱ)的显色反应

合成了一种新显色剂4-(4-氯苯重氮氨基)-4'-硝基偶氮苯(简称CDANA),并研究了该试剂与Cd(Ⅱ)的高灵敏显色反应。在60~65℃温度下,亚硫酸氢钠与甲醛反应半小时之后滴入苯胺生成苯胺基甲基磺酸钠,另将硝基苯胺重氮化得到重氮盐溶液滴入苯胺基甲基磺酸钠中得到4'-硝基-4-氨基偶氮苯,然后将其滴入氯苯胺重氮化后的重氮盐溶液中,得经红外光谱检验和元素分析证实的目标产物。分光光度的研究结果表明,在Triton X-100存在下,于pH 10.5的Na2B4O7-NaOH缓冲介质中,镉(Ⅱ)与试剂形成1∶2的橙红色络合物,其最大吸收波长位于558 nm处,表观摩尔吸光系数为1.42×105L.mol-1.cm-1,镉(Ⅱ)的质量浓度在0~0.75μg/mL范围内服从比尔定律。所拟方法用于废水中微量镉的直接测定,结果与原子吸收光谱法一致。     

1—（6—硝基—2—苯并噻唑）—3—（4—硝基苯）—三氮烯与镉的显色反应研究

研究表明,新显色剂1-(6-硝基-2-苯并噻唑)-3-(4-硝基苯)-三氮烯与镉反应,可生成稳定的橙黄色络合物,分别在444nm和530nm波长处有一正一负两个吸收峰,建立以530nm为参比波长,444nm为测定波长的双峰双波长测定法,表观摩尔吸光系数达2.82×105,镉含量在0～280μg/L符合比尔定律,测定了实验室废水和人发中的镉含量,结果满意.     

(3R,4S)-3-[4-(4-fluorophenyl)-4-hydroxypiperidin-1-yl]chroman-4,7-diol: a conformationally restricted analogue of the NR2B subtype-selective NMDA antagonist (1S,2S)-1-(4-hydroxyphenyl)-2-(4-hydroxy-4-phenylpiperidino)- 1-propanol

(1S,2S)-1-(4-Hydroxyphenyl)-2-(4-hydroxy-4-phenylpiperidino)-1-propanol (CP-101,606, 1) is a recently described antagonist of N-methyl-D-aspartate (NMDA) receptors containing the NR2B subunit. In the present study, the optimal orientation of compounds of this structural type for their receptor was explored. Tethering of the pendent methyl group of 1 to the phenolic aromatic ring via an oxygen atom prevents rotation about the central portion of the molecule. Several of the new chromanol compounds have high affinity for the racemic [3H]CP-101,606 binding site on the NMDA receptor and protect against glutamate toxicity in cultured hippocampal neurons. The new ring caused a change in the stereochemical preference of the receptor-cis (erythro) compounds had better affinity for the receptor than the trans isomers. Computational studies suggest that steric interactions between the pendent methyl group and the phenol ring in the acyclic series determine which structures can best fit the receptor. The chromanol analogue, (3R,4S)-3-[4-(4-fluorophenyl)-4-hydroxypiperidin-1- yl]chroman-4,7-diol (12a, CP-283,097), was found to possess potency and selectivity comparable to CP-101,606. Thus 12a is a new tool to explore the function of the NR2B-containing NMDA receptors.     

1-(2,6-二氯-4-硝基苯)-3-(4-硝基苯)-三氮烯分光光度法测定钴

研究了新试剂1-(2,6-二氯-4-硝基苯)-3-(-4-硝基苯)-三氮烯(DCNPNPT)与钴(Ⅱ)显色反应的适宜条件.在表面活性剂Triton X-100存在下,Na2B4O7-NaOH缓冲液(pH.9.3)介质中,钴(Ⅱ)与DCNPNPT形成黄色络合物(12),其最大吸收波长为545nm,用双峰双波长法测定络合物的表观摩尔吸光系数ε=1.08×105,钴在0～240μg/L范围内符合比尔定律.此法已用于VB12针剂和矿样中微量钴(Ⅱ)的测定,结果满意.     

N-[4-(1,1''-biphenyl)methyl]-4-(4-thiomorpholinylmethyl) benzenamines as non-oxazolidinone analogues of antimycobacterial U-100480

Twenty-three patients underwent conventional arteriography and 3D contrast enhanced magnetic resonance angiography explorations. The study was limited to the iliofemoral arteries (13 segments for each patient). Each segment was classified as having 0-49%, 50-99% or 100% stenosis. Overall results were excellent with K = 0.822, sensitivity 92% and specificity 93%. Segment by segment analysis corroborated the overall results except for the internal iliac arteries and the deep femoral arteries, demonstrating the limitations of this technique in this series.     

2-氨基-4-(4-甲氧基苯基)-6-(哌啶-1-基)-3,5-二腈基吡啶的三组分合成与表征

在甲醇溶剂中,以丙二腈、4-甲氧基苯甲醛、哌啶为原料,常温下经三组分一锅法合成得到了未见文献报道的新化合物2-氨基-4-(4-甲氧苯基)-6-(哌啶-1-基)-3,5-二腈基吡啶,收率40%.其化学结构经过1H NMR、MS及单晶衍射进行表征.     

Preparation and antirheumatic activity of optically active 2-acetylthiomethyl-4-(4-methylphenyl)-4-oxobutanoic acid (KE-298)

2-Acetylthiomethyl-4-(4-methylphenyl)-4-oxobutanonic acid (KE-298) is an antirheumatic agent. To elucidate the effects of optically active KE-298, we resolved the racemic acid and obtained the two optical isomers. (+)-KE-298 was converted to the 4-bromobenzyl ester derivative and the absolute structure was confirmed as (S) by X-ray crystallographic analysis. The pharmacological activities of the optical isomers and racemic KE-298 were compared by using the characteristic tests for KE-298. Though (+)-KE-298 showed a stronger suppressive effect on rat adjuvant arthritis than (-)-KE-298, no difference between the two isomers was detected in in vitro tests (enhancing effect on lymphocyte transformation, IL-1 antagonistic effect).     

Absence of metabolism of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) by flavin-containing monooxygenase (FMO)

The N-nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a potent lung carcinogen present in tobacco and tobacco smoke. Carbonyl reduction, alpha-carbon hydroxylation (activation) and N-oxidation of the pyridyl ring (detoxification) are the three main pathways of metabolism of NNK. In this study, metabolism of NNK was studied with lung and liver microsomes from F344 rats, Syrian golden hamsters and pigs and cloned flavin-containing monooxygenases (FMOs) from human and rabbit liver. Thermal inactivation at 45 degrees C for 2 min reduced FMO S-oxygenating activity but did not affect N-oxidation of NNK, leading to the conclusion that FMOs are not implicated in the detoxification of NNK. Detoxification of NNK was not increased by n-octylamine or by incubation at pH 8.4, supporting the conclusion that FMOs are not involved in the metabolism of NNK. SKF-525A (1 mM) significantly reduced N-oxidation and alpha-carbon hydroxylation, suggesting that these two pathways were catalyzed by cytochromes P450. Metabolism of NNK was lower with lung microsomes than with liver microsomes. Inhibition of metabolism of NNK by SKF-525A was also observed with rat lung microsomes, leading to the conclusion that cytochromes P450 are involved in pulmonary metabolism of NNK. Cloned FMOs did not metabolize NNK. In conclusion, cytochromes P450 rather than FMOs are involved in N-oxidation of NNK. The high capacity of hamster liver microsomes to activate NNK does not correlate with the resistance of this tissue to NNK-induced hepatocarcinogenesis.     

Dual inhibition of human type 4 phosphodiesterase isostates by (R, R)-(+/-)-methyl 3-acetyl-4-[3-(cyclopentyloxy)-4-methoxyphenyl]-3- methyl-1-pyrrolidinecarboxylate

Purified recombinant human type 4 phosphodiesterase B2B (HSPDE4B2B) exists in both a low- and a high-affinity state that bind (R)-rolipram with Kd's of ca. 500 and 1 nM, respectively [Rocque, W. J., Tian, G., Wiseman, J. S., Holmes, W. D., Thompson, I. Z., Willard, D. H., Patel, I. R., Wisely, G. B., Clay, W. C., Kadwell, S. H., Hoffman, C. R., and Luther, M. A. (1997) Biochemistry 36, 14250-14261]. Since the tissue distribution of the two isostates may be significantly different, development of inhibitors that effectively inhibit both forms may be advantageous pharmacologically. In this study, enzyme inhibition and binding of HSPDE4B2B by (R, R)-(+/-)-methyl 3-acetyl-4-[3-(cyclopentyloxy)-4-methoxyphenyl]-3-methyl-1-pyrrolidin ecarboxylate (1), a novel inhibitor of phosphodiesterase 4 (PDE 4), were investigated. Binding experiments demonstrated high-affinity binding of 1 to HSPDE4B2B with a stoichiometry of 1:1. Inhibition of PDE activity showed only a single transition with an observed Ki similar to the apparent Kd determined by the binding experiments. Deletional mutants of HSPDE4B2B, which have been shown to bind (R)-rolipram with low affinity, were shown to interact with 1 with high affinity, indistinguishable from the results obtained with the full-length enzyme. Bound 1 was completely displaced by (R)-rolipram, and the displacement showed a biphasic transition that resembles the biphasic inhibition of HSPDE4B2B by (R)-rolipram. Theoretical analysis of the two transitions exemplified in the interaction of (R)-rolipram with HSPDE4B2B indicated that the two isostates were nonexchangeable. Phosphorylation at serines 487 and 489 on HSPDE4B2B had no effect on the stoichiometry of binding, the affinity for binding, or the inhibition of the enzyme by 1. These data further illustrate the presence of two isostates in PDE 4 as shown previously for (R)-rolipram binding and inhibition. In contrast to (R)-rolipram, where only one of the two isostates of PDE 4 binds with high affinity, 1 is a potent, dual inhibitor of both of the isostates of PDE 4. Kinetic and thermodynamic models describing the interactions between the nonexchangeable isostates of PDE 4 and its ligands are discussed.