多巴胺在硫醇修饰电极上的电化学研究

用十二烷基硫醇在金电极表面形成自组装单分子层,采用循环伏安方法及扫描电化学显微镜对多巴胺在金电极和硫醇修饰电极上的电化学行为进行了研究,并考察了溶液pH及循环伏安扫描速度对多巴胺氧化还原过程的影响。结果表明,多巴胺能够渗透通过硫醇单分子层在电极表面发生氧化还原反应,修饰表面的存在对其氧化过程影响较明显。     

基于电沉积多孔碳修饰电极测定6-苄氨基嘌呤的研究

利用恒电位法沉积多孔碳固定于玻碳电极表面,构建多孔碳修饰电极,利用线性扫描伏安法和差分脉冲伏安法研究了标题化合物在多孔碳修饰电极上的电化学行为,建立了一种测定标题化合物的电化学分析方法。结果表明,与玻碳电极相比,多孔碳修饰电极能显著提高标题化合物的氧化峰电流。在优化的实验条件下,标题化合物的氧化峰电流与浓度在1. 0×10-7~4. 0×10-5mol/L范围内呈较好的线性关系,最低检出限为7. 6×10-8mol/L。本法用于黄豆芽中标题化合物的测定,效果良好。     

光学活性的2-苄基-3-羟基丙酸合成

以丙二酸二乙酯为起始原料,经过苄基化、还原、乙酰化保护、氧化、水解等5个步骤,合成了标题化合物.以水为溶剂,对标题化合物与手性1-苯乙胺形成的非对映异构体盐进行手性拆分,得到了(R)-2-苄基-3-羟基丙酸和(S)-2-苄基-3-羟基丙酸.     

N-对苯甲酸基-1,8-萘酰亚胺的合成及金属离子识别作用研究

以对硝基甲苯为起始原料,通过重铬酸钠氧化再将硝基还原得到对氨基苯甲酸,然后与1,8-萘酐缩合得到标题化合物,并以荧光光谱法研究了标题化合物对Cd2+、Co2+、Cu2+等7种金属离子的识别作用.结果表明,随着各种金属离子的加入,标题化合物的荧光光谱均发生了猝灭现象;标题化合物对Fe3+的识别作用最优,络合常数为1.69...     

L-半胱氨酸在金电极上的自组装及其电化学性能研究

将L-半胱氨酸(L-Cys)自组装到金电极表面制成L-Cys/Au修饰电极,并用电化学方法研究了它的电化学性质。研究了葡萄糖在自组装膜修饰电极上的电化学氧化行为,实验表明,该膜对葡萄糖的氧化有催化作用。     

氧化石墨烯还原过程中产生的缺陷表征北大核心

采用Hummer法对鳞片石墨进行氧化得到氧化石墨,之后经过超声剥离制备氧化石墨烯,最后在水合肼的作用下还原制备石墨烯。采用红外光谱、紫外-可见光光谱、拉曼光谱和原子力显微镜对还原前后的氧化石墨烯进行表征。发现化学还原可以除去氧化石墨烯表面一部分含氧官能团,但同时也引入一些缺陷,还原之后石墨烯的sp^2域的平均尺寸减小。AFM照片分析发现含氧官能团去除之后会在原来的位置产生空洞,从而导致石墨烯缺陷增加。     

氧化石墨烯还原过程中产生的缺陷表征

采用Hummer法对鳞片石墨进行氧化得到氧化石墨,之后经过超声剥离制备氧化石墨烯,最后在水合肼的作用下还原制备石墨烯。采用红外光谱、紫外-可见光光谱、拉曼光谱和原子力显微镜对还原前后的氧化石墨烯进行表征。发现化学还原可以除去氧化石墨烯表面一部分含氧官能团,但同时也引入一些缺陷,还原之后石墨烯的sp~2域的平均尺寸减小。AFM照片分析发现含氧官能团去除之后会在原来的位置产生空洞,从而导致石墨烯缺陷增加。     

铁电极表面2,2’-联吡啶-5,5’-二羧酸盐自组装膜缓蚀性能研究

缓蚀剂分子在金属表面自组装成膜是金属防腐的一种重要方法。选用2,2’-联吡啶-5,5’-二羧酸盐(bpydc)作为缓蚀剂,通过自组装法在铁电极表面形成保护膜。利用电化学法和理论计算相结合,从宏观和微观两个层面研究bpydc在铁电极表面的缓蚀效能以及作用机理。结果表明,bpydc对铁的缓蚀效率达到90.93%,属于阳极型缓蚀剂。理论计算证明bpydc符合优异缓蚀剂的标准,分子中羧基氧原子具有较负的电荷更易吸附在铁电极表面,与全反射红外光谱测试结果一致。     

4-（（4’-N，N-二苯基）苯基）-2，2’-联吡啶的合成与表征

以2,2'-联吡啶和N,N-二苯基-4-溴苯胺为原料,通过氧化、硝化、溴化、脱氧、Suzuki偶联等一系列反应,合成了标题化合物.通过元素分析、核磁共振氢谱对所得化合物的结构进行了表征,并测得它在无水乙醇溶液中的紫外吸收光谱和荧光光谱.     

硅溶胶/热空气复合活化对钒电池电极材料性能的影响

利用硅溶胶/热空气复合活化法改性石墨毡,并对其表面形貌、微观结构以及电化学性能进行了分析研究。结果表明:硅溶胶/热空气复合活化使石墨毡电极的亲液性增强、比表面积增大、氧官能团数量提升,由此组装的钒电池电化学性能显著提高;活化后石墨毡表面的C—O氧官能团是钒电池氧化还原反应的有效活性位点,当硅溶胶添加量为50%(质量分数)时,石墨毡表面的C—O氧官能团数量达到4.18%;当电流密度为40 m A/cm²时,以硅溶胶添加量50%的石墨毡为电极组装钒电池,其库仑效率达到95.58%,能量效率达到86.07%,电压效率达到92.35%,比未活化石墨毡为电极组装的钒电池分别高出10.93%、9.16%、3.22%。     

Photooxidation of Benzo[ de ]naphtho[2,1,8,7- stuv ]anthra[2,1,9,8- hijkl ]pentacene

This article describes the photooxidation of benzo[ de ]naphtho-[2,1,8,7- stuv ]anthra[2,1,9,8- hijkl ]pentacene (BNAP) synthesized by the condensation of naphthanthrone with zinc dust. When an o -dichlorobenzene solution of BNAP was irradiated with light of its maximum absorption wavelength (535 nm), the original absorption band was reduced and a new band appeared at longer wavelengths showing a peak at 606 nm. Excitation of the photobleached sample with 600 nm gave rise to fluorescence on the red side of that of BNAP by about 90 nm. The new fluorescence spectrum showed a vibrational progression of about 1,600 cm m 1 , which corresponds to the stretching of a carbonyl group. No spectral changes occurred in degassed solution. These findings suggest that BNAP reacts with singlet oxygen to form a ketone. Molecular orbital calculations revealed that the carbonyl group of the product is located at the C-18 position and that a hydroxy group is also present at the C-2 position; therefore the product is predicted as 2,18-dihydrobenzo[ de ]-naphtho[2,1,8,7- stuv ]anthra[2,1,9,8- hijkl ]pentacen-18-one.     

3-[3-(1-哌啶甲基)苯氧基]丙胺的合成工艺改进

以间羟基苯甲醛为起始原料，经由氧烷基化、缩合、水解得3-[3-(1-哌啶甲基)苯氧基]丙胺，收率49．1％，结构经NMR确证。     

5-(4-羟基苄叉)-噻唑烷-2,4-二酮的合成

5-(4-羟基苄叉)—噻唑烷-2,4-二酮是抗糖尿病药的关键中间体,本文以硫脲为原料,经闭环、中和、水解、缩合4步反应合成得到目标物,总收率40%。     

3-[4-(甲基磺酰基)-2-氯苯甲酰基]双环[3.2.1]辛烷-2,4-二酮的合成研究

标题化合物是合成稻田除草剂的中间体,以降冰片烯为原料,经二氯卡宾的加成、扩环反应和水解反应生成3-氯双环[3.2.1]-3-辛烯-2-醇;随后烯丙醇氧化制得α,β-不饱和酮;接着在氰化钾催化剂的作用下和氢氧化钠反应,得到双环[3.2.1]辛烷-2,4-二酮;最后再发生酰基化反应得到标题化合物。化合物结构用1HNMR、13CNMR表征,纯度用HPLC确定。     

5-[2-(乙硫基)丙基]-1,3-环己二酮的合成工艺研究

研究优化了合成烯草酮、烯禾定以及cloproxydim等环己烯酮类除草剂的重要中间体5-[2-(乙硫基)丙基]-1,3-环己二酮的合成方法.首先,巴豆醛与乙硫醇在三乙胺中高收率制得3-乙硫基丁醛,然后以乙酰乙酸甲酯为原料,通过碱水解、与3-乙硫基丁醛缩和、脱水三步反应合成6-乙硫基庚烷-3-烯-2-酮,接着6-乙硫基庚烷-3-烯-2-酮与丙二酸二甲酯经Michael加成和Claisen缩合,再通过皂化和脱羧反应生成目标化合物5-[2-(乙硫基)丙基]-1,3-环己二酮,主要中间产物以及目标产品均与标准品对照,经液质联用确认.     

GPR40激动剂的合成

以3-甲硫基丙醇(2)与对甲基苯磺酰氯(3)发生取代反应、氧化反应得3-(甲基磺酰基)丙基-4-甲基苯磺酸(5),再以间苯二酚(6)与4-氯乙酰乙酸乙酯(7)缩合成环、水解、成酯、氢化还原得6-羟基-苯并呋喃-3-乙酸甲酯(11),以4-溴-3,5-二甲基苯酚(12)与3-甲酰基苯硼酸(13)发生suzuki偶联得4'-羟基-2',6'-二甲基-[1,1'-联苯]-3-甲醛(14),再与(4)亲核取代、还原得3-(甲基磺酰基)丙基-4-甲基苯磺酸(16),(16)与(11)缩合,最终水解得到6-({2',6'-二甲基-4'-[3-(甲磺酰基)丙酰基]-联苯}甲氧基)-2,3-二氢苯并呋喃-3-乙酸(18)。     

Labeled oxidation products from [1-14C], [U-14C] and [16-14C]-palmitate in hepatocytes and mitochondria

When [1-¹⁴C], [U-¹⁴C], and [16-¹⁴C]palmitate were oxidized by isolated rat hepatocytes, there was a differential distribution of label as a percent of total oxidized products, such that¹⁴CO₂ from [1-¹⁴C]>[U-¹⁴C]>[16-¹⁴C]-palmitate and acid-soluble radioactivity from [16-¹⁴C]>[U-¹⁴C]>[1-¹⁴C]palmitate. The oxidation of [2,3-¹⁴C]succinate to¹⁴CO₂ by isolated hepatocytes was only 9.1% of that from [1,4-¹⁴C]succinate, demonstrating that the differences in distribution of labeled products are in part due to less¹⁴CO₂ production from label in the even carbon positions entering the citric acid cycle. Apparent total ketone body production from [16-¹⁴C]palmitate was markedly higher than [1-¹⁴C], and [U-¹⁴C]palmitate. In addition, the¹⁴C-acetone:¹⁴CO₂ ratio derived from decarboxylation of labeled acetoacetate from [1-¹⁴C]palmitate was less than 1 and positively correlated to the rate of fatty acid oxidation in hepatocytes. These findings indicate that the known preferential incorporation of the omega-C₂ unit of fatty acids into¹⁴C-ketone bodies also contributed to the differential distribution of labeled products and that this contribution was greatest at the lower rates of fatty acid oxidation. In isolated mitochondria, the distribution of label to¹⁴CO₂ and acid-soluble radioactivity from [1-¹⁴C], [U-¹⁴C] and [16-¹⁴C]palmitate was qualitatively similar to that seen with hepatocytes. The distribution of label from [1-¹⁴C]acetylcarnitine to¹⁴CO₂ and¹⁴C-ketone bodies by mitochondria was identical to that observed from [1-¹⁴C]palmitate, indicating that the higher rates of¹⁴CO₂ production from [1-¹⁴C]palmitate cannot be explained by a preferential oxidation in the citric acid cycle of either extramitochondrial acetyl-CoA (generated in peroxisomes) or the carboxyl terminal of the fatty acid. As shown by others in cell-free systems, we observed that the total oxidation of [16-¹⁴C]palmitate by hepatocytes and mitochondria was significantly less than [1-¹⁴C] and [U-¹⁴C]palmitate, suggesting either incomplete mitochondrial β-oxidation or incomplete degradation of peroxisomal oxidation products. The data indicate that this incomplete oxidation does not, however, contribute to the differential distribution of label to oxidized products.