稀土三元配合物的合成、结构表征及荧光性能研究

合成了铈-草酸-丙烯酸三元固体配合物。利用元素分析、红外光谱（FT-IR）、紫外．可见光谱（UV-Vis）、热重分析（TGA）和荧光光谱等手段研究了配合物的结构和性质。结果表明配合物的组成为[Ce（OOC-COO）（CH2=CH-COO）]·3H2O，荧光光谱表明，配合物中的有机配体能够有效地把吸收的能量传递给中心Ce^3＋离子，强烈敏化Ce^3＋发光，且发射谱线很窄，主发射峰为Ce^3＋的5d→^2F7/2跃迁，这对寻找新型稀土配合物发光材料和制备有机电致发光器件具有一定的价值。     

铕掺杂配合物的合成及其荧光性质研究

采用稀土掺杂的方法以Zn2+与Eu3+、配体对氯苯甲酸(CBA)、邻菲罗啉(Phen)合成铕掺杂配合物铕-锌-对氯苯甲酸-邻菲罗啉(Eu-Zn-CBA-Phen).经元素分析,推测其组成为:Eu1-xZnx(CBA)3-xPhen*H2O(x=0～0.8).红外光谱分析证实,铕与配体发生配位,而紫外与荧光光谱分析表明,随着Zn2+取代配合物中部分Eu3+,配合物的荧光强度明显增加,当掺杂Zn2+与Eu3+摩尔分数比为2∶3时,荧光强度达到最大值.同时还系统地考察了非稀土金属离子的加入对配合物荧光性能的影响和荧光增强机理.     

Sm(Ⅲ),Eu(Ⅲ)-丙烯酸-8-羟基喹啉三元配合物的合成及荧光性质研究

用三异丙氧基钐（铕）与８－羟基喹啉、丙烯酸反应合成具有良好荧光性质的稀土三元配合物,通过元素分析、红外光谱、紫外光谱证实其分子结构,并进行荧光光谱、热分析测试,发现配合物具有较好的荧光性质。     

钇配合物-有机硅薄膜的合成及荧光性能

以葡萄糖为有机配体合成了钇配合物,钇配合物与硅溶胶和甲基三乙氧基硅烷在室温条件下经水解缩聚反应形成钇配合物-有机硅杂化溶胶,在基片上涂膜后固化成膜制得钇配合物-有机硅薄膜,对所得薄膜的结构、耐热性、光学性能和荧光性能进行表征。结果表明钇配合物-有机硅薄膜为Si-O-Si键形成的体型结构,晶型为非晶态的SiO2,钇配合物为粒径100 nm～157 nm的球状粒子;钇配合物-有机硅薄膜的耐热性良好,800℃的质量残余率为88%;钇配合物-有机硅薄膜的平均透光率比未添加钇配合物形成的有机硅薄膜的平均透光率高5.4%,钇配合物-有机硅薄膜具有荧光性能。     

烟酸银镧异核配合物的合成,表征及荧光性质研究

本文以烟酸为配体,稍酸银和氯化镧为原料,处理后的无水乙醇为溶剂用溶液中自组装的合成方法制备了LaAgL(L为烟酸)的配合物,用红外光谱对配合物的结构进行了表征.配合物荧光性能测表明配体烟酸的π-π*电子跃迁导致的荧光被淬灭,配合物荧光带状光谱主要为金属离子的MLCT跃迁.配合物的发光强度低于配体,但其荧光发射峰红移到455至477nm,在光物理和光化学领域有一定的潜在应用价值.     

均苯三甲酸邻菲罗啉稀土配合物的合成、表征及荧光性质

分别合成了以均苯三甲酸(H3BTC)和邻菲罗啉(phen)为配体,以Sm、Eu、Tb和Dy为中心的4种稀土三元配合物,通过元素分析及稀土络合滴定确定了配合物的组成为RELL'1.5 ·2H20(L=BTC,L'= phen);配合物的红外光谱、紫外光谱和荧光光谱测定结果表明,配合物中均苯三甲酸根的羧基氧原子和邻菲罗啉的氮原子均与稀土离子配位成键;四种配合物均可发出稀土离子的特征荧光,铕、铽配合物具有良好的荧光性能,钐、镝配合物也发出较强的特征荧光.     

对苯基苯甲酸铕、铽配合物的合成、表征及荧光性能研究

分别合成了以对苯基苯甲酸为配体,铕、铽及掺杂铕、铽为中心的固态配合物。经元素分析、摩尔电导及差热-热重分析,推测其组成分别为:铕配合物:EuL3.3H2O、Eu0.5La0.5L3.3H2O、Eu0.5Y0.5L3.3H2O;铽配合物:TbL3.2H2O、Tb0.5La0.5L3.2H2O、Tb0.5Y0.5L3.3H2O(L=■-■-COO-。红外光谱、紫外光谱及核磁共振氢谱分析表明,对苯基苯甲酸的羧基氧原子与稀土离子配位。配合物的荧光光谱测定表明,铕系列和铽系列配合物都可发出其特征荧光,铕异核稀土配合物的荧光强度与相同配体的铕配合物相比,均有不同程度提高。     

铕、铽-2-噻吩甲酸-1,10-菲咯啉三元配合物的合成及荧光性质的研究

同时合成了高氯酸铕、铽与2-噻吩甲酸、1,10-菲咯啉(phen)的三元配合物和高氯酸铕、铽与2-噻吩甲酸的二元配合物,对配合物进行了元素分析、稀土络合滴定、红外光谱、摩尔电导测定,确定了配合物组成分别为REL3·2H2O及REL3L'·C2H5OH(RE=Eu,Tb;L=2-噻吩甲酸,L'=1,10-菲咯啉).摩尔电导数据表明,此类配合物为非电解质.红外光谱测定表明,配体2-噻吩甲酸羧基氧与稀土离子配位,配体1,10-菲咯啉两个氮原子与稀土离子配位.荧光光谱实验表明,1,10-菲咯啉加入到铕-2-噻吩甲酸二元配合物和铽-2-噻吩甲酸二元配合物中形成三元配合物后它们的荧光明显增强.     

PVAc-Sm(Ⅲ),Nd(Ⅲ) 配合物的合成、表征及荧光性质

以聚醋酸乙烯酯 (PVAc)为配体 ,分别与SmCl3,NdCl3在乙醇中进行反应 ,生成PVAc Sm(Ⅲ ) ,PVAc Nd(Ⅲ )的配合物。用电导率法确定PVAc Sm(Ⅲ ) ,PVAc Nd(Ⅲ )配合物中Sm3 ,Nd3 与PVAc链节单元 [-CH2 -CH (OCOCH3) -]的配比为 1∶6。IR和XPS测试表明 :PVAc的CH3COO中酯基氧共同提供电子与Sm3 ,Nd3 形成配位键 ,溶剂分子C2 H5OH参与配位 ;TG DTA分析表明 :配合物的热分解温度比PVAc的低 ;荧光光谱显示 :PVAc Sm(Ⅲ ) ,PVAc Nd(Ⅲ )配合物具有荧光特性 ,分别在 42 7,418nm产生荧光。     

新型1D+1D钴共晶配合物[Co(bbbi)(4-mbc)2]的合成、晶体结构及性质

利用水热法合成了一种新型的1D+1D钴共晶配合物[Co(bbbi)(4-mbc)2](bbbi=1,1-(1,4-丁基)二-1H-苯并咪唑,4-Hmbc=对甲苯甲酸).通过元素分析、IR、单晶X射线衍射对配合物的结构进行了表征.结果表明:该配合物属于单斜晶系,C2/c空间群;晶胞参数a=2.137 4(5)nm,B=4.589 3(5)nm,c=1.537 0(5)nm,α=90.000(5)°,β=125.467(5)°,γ=90.000(5)°,Z=16,V=12.279(5)mn3,R1=O.057 9,wR2=-O.164 7.标题配合物有较好的热稳定性.在室温下该固态配合物表现出了弱的荧光性质.     

Synthesis of 1-(beta-D-glycopyranosyl)-3-deazapyrimidines from 2-hydroxy and 2-mercaptopyridines

The synthesis of new 4- and 5-substituted-3-cyanopyridine nucleosides has been performed by reacting the silylated pyridines and penta-omicron-acetyl-alpha -D-glycopyranose in dichloroethane in the presence of SnCl4. The free nucleosides were tested for their potential activity against HIV and different types of tumor.     

Electrical and mechanical effects of a novel antihypertensive quinazoline derivative, 3-[[4-(2-methoxyphenyl) piperazin-1-ly]methyl]-5-(methylthio)-2,3-dihydroimidazo [1,2-c]quinazoline, on guinea pig ventricular muscles

We evaluated the effect of sulindac sulfide (SS), which reduces cell number and induces apoptosis in cultured colon cancer cells (CCCs), on expression of the proliferation markers PCNA and Ki-67 in HT-29 and HCT-15 CCCs; only the former express cyclooxygenases. DNA content and PCNA/Ki-67 expression were analyzed by bivariate flow cytometry. SS inhibited cell proliferation, determined by the reduced expression of PCNA and Ki-67, roughly by half at 72 h, and induced apoptosis (accounting for about two-thirds and one-third of the reduction in cell number, respectively). A similar effect of SS occurred in HT-29 and HCT-15 CCCs, and also in non-colonic cells, indicating that this rather general effect of SS on cultured cells is not dependent on inhibition of prostaglandin synthesis.     

Pyridyloxobutyl adduct O6-[4-oxo-4-(3-pyridyl)butyl]guanine is present in 4-(acetoxymethylnitrosamino)-1-(3-pyridyl)-1-butanone-treated DNA and is a substrate for O6-alkylguanine-DNA alkyltransferase

The lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is activated to reactive metabolites that methylate or pyridyloxobutylate DNA. Previous studies demonstrated that pyridyloxobutylated DNA interferes with the repair of O6-methylguanine (O6-mG) by O6-alkylguanine-DNA alkyltransferase (AGT). The AGT reactivity of pyridyloxobutylated DNA was attributed to (pyridyloxobutyl)guanine adducts. One potential AGT substrate adduct, 2'-deoxy-O6-[4-oxo-4-(3-pyridyl)butyl]guanosine (O6-pobdG), was prepared. This adduct was stable at pH 7.0 for greater than 13 days and to neutral thermal hydrolysis conditions (pH 7.0, 100 degrees C, 30 min). Under mild acid hydrolysis conditions (0.1 N HCl, 80 degrees C), O6-pobdG was depurinated to yield O6-[4-oxo-4-(3-pyridyl)butyl]guanine (O6-pobG). O6-pobdG was hydrolyzed to 4-hydroxy-1-(3-pyridyl)-1-butanone and guanine under strong acid hydrolysis conditions (0.8 N HCl, 80 degrees C). O6-pobG was detected in 0.1 N HCl hydrolysates of DNA alkylated with the model pyridyloxobutylating agent 4-(acetoxymethylnitrosamino)-1-(3-[5-3H]pyridyl)-1-butanone ([5-3H]NNKOAc). When [5-3H]NNKOAc-treated DNA was incubated with either rat liver or recombinant human AGT, O6-pobG was removed, presumably a result of transfer of the pyridyloxobutyl group from the O6-position of guanine to AGT's active site.     

Biliary excretion of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in the rat

The tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a potent pancreas carcinogen in rats. The biliary excretion of NNK was therefore studied in anesthetized female Sprague-Dawley rats following i.p. administration of 0.7 mumol/kg [carbonyl-14C]NNK. The concentration of radioactivity peaked within 30 min and decreased thereafter exponentially. Cumulative excretion of radioactivity reached a plateau at 6-9% of the total dose. HPLC analysis revealed the presence of 4-hydroxy-4-(3-pyridyl)butyric acid (hydroxy acid), 4-oxo-4-(3-pyridyl)-butyric acid (keto acid), 4-(methylnitrosamino)-1-(3-pyridyl)-1-butyl beta-D-glucopyranosiduronic acid (NNAL Glu), 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and NNK. NNAL Glu was the major metabolite contributing 34 +/- 4% of total radioactivity in bile at 30 min and 58 +/- 4% at 5 h. The percentage of acidic metabolites remained constant at approximately 20%. In contrast, the percentage of NNK and NNAL decreased within the first 2 h to < 5% and < 10% respectively. The elimination kinetics of NNK and its metabolites fitted into a one-compartment model with a half-life of 37 min for NNK, 52 min for NNAL and 110 min for NNAL Glu and acidic metabolites. In three rats dosed with 240 mumol/kg NNK i.p., the concentration of radioactivity peaked after 1-2 h and decreased very slowly thereafter. After 5-8 h a total of 12-17% of the dose has been excreted in the bile with no indication of a plateau. At all time points NNAL Glu was the major metabolite contributing up to 95% of total radioactivity in bile. The percentage of acidic metabolites was < 5% throughout the experiment. Whereas NNK contributed one-third of the radioactivity at 30 min and decreased rapidly, the percentage of NNAL in bile remained rather constant at approximately 5-10%. In conclusion, the detection of NNK, NNAL and NNAL Glu gives support to the hypothesis that tobacco-specific carcinogens could reach the pancreas retrograde from the bile, especially at high NNK concentrations.     

Metabolism of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in isolated rat lung and liver

PURPOSE: Assessment of sustained voluntary contraction of the external sphincter is helpful in evaluating the patient who has a defecation disorder on presentation. A new index of external sphincter function is described. METHOD: A prospective registry of patients referred for computerized anal manometry using standard protocols was reviewed. Patients were grouped by primary symptoms; those with overlapping complaints were excluded. The rate of fatigue, defined as the change in stationary squeeze over a 40-second period of voluntary contraction, was calculated by linear regression analysis. Fatigue rate index, a calculated measure of time necessary for the external sphincter to become completely fatigued, was determined to permit comparison of external sphincter fatigue in patients with different complaints. RESULTS: Twenty-six healthy volunteers (15 women; mean age, 45 years), 33 patients with a primary complaint of anal seepage (13 women; mean age, 53 years), 75 patients with gross incontinence (61 women; mean age, 53 years), and 49 patients with severe constipation (41 women; mean age, 45 years) were evaluated. Mean resting and squeeze pressures were 55 mmHg and 107 mmHg for volunteers, 37 mmHg and 97 mmHg for patients with seepage, 30 mmHg and 49 mmHg for incontinent patients, and 56 mmHg and 93 mmHg for constipated patients. Pudendal neuropathy, as evidenced by a prolonged pudendal nerve terminal motor latency (> 2.4 ms), was identified in 13 percent of volunteers, 32 percent of patients with seepage, 54 percent of incontinent patients, and 38 percent of constipated patients. Mean fatigue rate index was 3.3 minutes for volunteers, 2.3 minutes for seepage patients, 1.5 minutes for incontinent patients, and 2.8 minutes for constipated patients. Compared with volunteers and patients with seepage, the incontinent patients had a significantly shorter fatigue rate index (P < 0.05; Student's t-test), which was independent of the variations in resting pressure (P < 0.05; two-way analysis of variance). CONCLUSION: The external anal sphincter is normally subject to fatigue. Patients with worsening degrees of incontinence have a predictably lower fatigue rate index. Fatigue rate index is a simple measure of external sphincter integrity, which may be used in assessment of sphincter function and future treatment protocols.     

Promotional effects of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) on N-nitrosobis(2-oxopropyl)amine (BOP)-initiated carcinogenesis in hamsters

The effects of administration of low doses of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), a tobacco-specific nitrosamine, were investigated in hamsters treated with N-nitrosobis(2-oxopropyl)amine (BOP). Female Syrian golden hamsters were given a single sc injection of BOP at a dose of 10 mg/kg and then administered 2 or 5 ppm NNAL in their drinking water for 52 wk. Additional groups of animals received the BOP injection alone, or only the 2 or 5 ppm NNAL treatments as BOP-negative controls. At wk 53 of the experiment, all surviving animals were killed and the development of proliferative lesions was assessed histopathologically. The total incidence of combined carcinomatous and dysplastic lesions of the exocrine pancreas was significantly higher (P < 0.05) in the BOP/NNAL 5 ppm group than in the BOP alone group, although there was no statistically significant influence of NNAL on the development of either pancreatic adenocarcinomas or dysplastic lesions viewed singly. The treatments with NNAL alone did not induce any proliferative lesions of the exocrine pancreas. No significant intergroup differences were found in either incidence or multiplicity of islet cell proliferative lesions. Immunohistochemical examination of islet cell proliferative lesions (hyperplasias and adenomas) found in the BOP-treated animals showed no significant differences in pancreatic hormone production between NNAL-treated and -untreated groups. The NNAL treatment did not exert any influence on lung, liver or kidney tumorigenesis. Thus, the results suggest that NNAL enhances BOP-induced exocrine but not endocrine pancreatic tumorigenesis in hamsters when given in the post-initiation phase.     

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.     

4-(3-吡啶基)-2-巯基咪唑修饰碳糊电极的研制及微量铜的测定

用化合物4-(3-吡啶基)-2-巯基咪唑(PMI)修饰碳粉制备了化学修饰碳糊电极,基于该氮杂环巯基化合物对Cu2+络合的选择性,Cu2+可富集于该电极表面。修饰电极经富集后再于-0.4 V还原20 s,阳极化扫描,在0.1 V左右可以获得灵敏的铜阳极溶出峰。其二次导数峰电流与Cu2+在5.0×10-9~2.0×10-5mol/L浓度范围内呈线性关系,检出限可达2.0×10-9mol/L(S/N=3)。采用本法不经过预分离,对成分复杂的阳极泥和铝合金等样品中的铜可进行直接测定。     

Studies on organosulfur compounds. XV. Substituent effects on 2-(2-pyridyl)-3-substituted-phenyl-4(3H)-quinazolinone cyclization (author''s transl)

The recovery process of HeLa continuous cells after prolonged storage at nitrogen liquid temperature (--196 degrees C) has been analysed. The karyologic analysis evidence indicates a high stock cell karyostability. A study of cell division, generation cycle parameters and DNA synthesis by autoradiography demonstrated cell adaptation to a continuous passage to be due to the increase of proliferative pool and to the intensitification of generation processes in the multiplicated population. Cell structure changes during adaptation were reversible.     

Inhibition of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced lung tumorigenesis by dietary olive oil and squalene

Epidemiological studies have suggested that frequent olive oil consumption may be a protective factor against lung cancer formation. Squalene, a characteristic compound in olive oil, is an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity and has been proposed to inhibit the farnesylation of ras oncoproteins. The present study investigated the effect of dietary olive oil and squalene in a mouse lung tumorigenesis model. Female A/J mice were fed AIN-76A diets containing 5% corn oil (control), 19.6% olive oil, or 2% squalene starting at 3 weeks before a single dose of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) (103 mg/kg, i.p.). Animals were maintained on their respective diets throughout the study. At 16 weeks after NNK administration, 100% of the mice in the control group had lung tumors with a tumor multiplicity of 16 tumors per mouse. The olive oil and squalene diets significantly (P < 0.05) decreased the lung tumor multiplicity by 46 and 58%, respectively. The squalene diet significantly (P < 0.05) decreased lung hyperplasia by 70%. In mice fed a diet containing 2% squalene for 3 weeks, the activation of NNK was increased by 1.4- and 2.0-fold in lung and liver microsomes, respectively, but its relationship to the inhibition of carcinogenesis is not clear. These results demonstrate that dietary olive oil and squalene can effectively inhibit NNK-induced lung tumorigenesis.