Adenovirus-mediated wild-type P53 Transfer radiosensitizes H1299 cells to subclinical-dose carbon-ion irradiation through the restoration of p53 function

To determine whether adenovirus-mediated wild-type p53 transfer after radiotherapy could radiosensitize non-small-cell lung cancer (NSCLC) cells to subclinical-dose carbon-ion beam (C-beam), H1299 cells were exposed to a C-beam or -ray and then infected with 5 MOI of AdCMV-p53 or GFP (C-beam or -ray with p53 or GFP).Cell cycle was detected by flow cytometric analysis. The apoptosis was examined by a fluorescent microscope with DAPI staining. DNA fragmentation was monitored by the TUNEL assay. P53 mRNA was detected by reverse-transcriptase polymerase chain reaction. The expression of p53, MDM2, and p21 was monitored by Western blot. Survival fractions were determined by colony-forming assay. The percentages of G1-phase cells in C-beam with p53 increased by 8.2%–16.0%, 5.2%–7.0%, and 5.8%–18.9%, respectively, compared with C-beam only, -ray with p53, or p53 only. The accumulation of G2-phase cells in C-beam with p53 increased by 5.7%–8.9% and 8.8%–14.8%, compared with those in -ray with p53 or p53 only, respectively. The percentage of apoptosis for C-beam with p53 increased by 7.4%–19.1%, 5.8%–11.7%, and 5.2%–19.2%, respectively, compared with C-beam only, -ray with p53, or p53 only. The level of p53 mRNA in C-beam with p53 was significantly higher than that in p53 only. The expression level of p53 and p21 in C-beam with p53 was significantly higher than that in both C-beam with GFP and p53 only. The survival fractions for C-beam with p53 were significantly less than those for the other groups (p 0.05). The data suggested that AdCMV-p53 transfer could more efficiently radiosensitize H1299 cells to subclinical-dose C-beam irradiation through the restoration of p53 function.

potential mechanisms involved in resistant phenotype of MCF-7breast carcinoma cells to ionizing radiation induced apoptosis

In the present study, we investigated the mechanisms of apoptosis resistance and the roles of the phosphorylation of BRCA1, p21, the Bax/Bcl-2 protein ratio and cell cycle arrest in IR-induced apoptosis in MCF-7 cells. X-irradiation, in particular at low dose (1 Gy), but not carbon ion irradiation, had a significant antiproliferative effect on the growth of MCF-7 cells. 1 Gy X-irradiation resulted in G1 and G2 phase arrest, but 4 Gy induced a significant G1 block. In contrast, carbon ion irradiation resulted in a significant accumulation in the G2 phase. Concomitant with the phosphorylation of H2AX induced by DNA damage,carbon ion irradiation resulted in an approximately 1.9–2.8-fold increase in the phosphorylation of BRCA1 on serine residue 1524, significantly greater than that detected for X-irradiation. Carbon ion irradiation caused a dramatic increase in p21 expression and drastic decrease in Bax expression compared with X-irradiation. The data implicated that phosphorylation of BRCA1 on serine residue 1524 might,at least partially, induce p21 expression but repress Bax expression. Together, our results suggested that the phosphorylation of BRCA1 at Ser-1524 might contribute to the G2 phase arrest and might be an upstream signal involved in preventing apoptosis signal via upregulation of p21 and downregulation of the Bax/Bcl-2 ratio.

High-efficiency transfer and expression of AdCMV-p53 in human cervix adenocarcinoma cells induced by subclinical-dose carbon beam radiation

Purpose The aim of this study is to evaluate the eVect of carbon-beam irradiation on adenovirus-mediated p53 transfer in human cervix adenocarcinoma.Materials and methods The HeLa cells pre-exposed to carbon-beam or -ray, were infected with replication-deficient adenovirus recombinant vectors, containing human wild-type p53 (AdCMV-p53) and green Xuorescent protein (GFP) (AdCMV–GFP), respectively. The GFP transfer and p53 expression were detected by Xow cytometric analysis.Results The GFP transfer frequency in C-beam with AdCMV-GFP groups was 38–50% more than that inγ-ray with AdCMV–GFP groups. The percentage of p53 positive cells in the C-beam with AdCMV–p53 groups was 34–55.6% more than that in γ-ray with AdCMV-p53 groups (p < 0.05), suggesting that subclinical-dose C-beam irradiation could signiWcantly promote exogenous p53 transfer and p53 expression, and extend the duration of p53 expression in the HeLa cells. The expression of p21 increased with p53 expression in HeLa cells. The survival fractions for the 0.5–1.0 Gy C-beam with AdCMV-p53 groups were 38–43% less than those for the isodose γ-ray with AdCMV-p53 groups, and 31–40% less than those for the C-beam only groups (p <0.05).Conclusions The subclinical-dose C-beam irradiation could signiWcantly promote the transfer and expression of exogenous p53, extend the duration of p53 expression, and enhance the suppression of p53 on cervix adenocarcinoma cells.

P53及其相关蛋白对X射线照射肝癌细胞周期的调节

X射线照射人肝癌细胞HepG2,照射后细胞存活随照射剂量增大明显下降。流式细胞术分析,不同剂量组照射后24h均发生G2期阻滞。照射后不同时间组的细胞周期分布也有不同,照射后12h,有显著的S期延迟。Western Blot显示照射后24hP53,MDM2,P21蛋白表达上升,并有时间效应:P53在照射后24h之内始终维持较高表达,MDM2和P21分别在照射后6和12h的表达最高。X射线照射通过影响P53及其相关蛋白的表达影响细胞周期。

Cell cycle and apoptosis alteration of human hepatocarcinoma cells by subclinical-dose C-12(6+)-beam irradiation

Objective The purpose of this study is to investigate the effect of subdinical-dose C-12(6+)-beam irradiation on cell cycle and cell apoptosis in hepatocarcinoma cells. Materials and methods The HepG(2) cells were exposed to 0-2.0 Gy of either the C-12(6+) beam or a gamma-ray. Cell survival was detected by clonogenic assay. Cell cycle was determined by flow-cytometry analysis. The apoptosis was monitored by fluorescence microscope with DAPI staining. p53 and p21 expression were detected by Western blot. Results The G(0)/G(1) cells in the irradiated groups were significantly more than those in the control (P<0.05). The C-12(6+)-ion irradiation had a greater effect on the cell cycle of HepG(2) cells (including promoting G(1)-phase and G(2)-phase arrest) than gamma-ray irradiation. The apoptotic cells induced by C-12(6+) beam were significantly more numerous than those induced by gamma-ray (P<0.05). The carbon ions had a stronger effect on p53 and p21 expression than the gamma-ray irradiation. The survival fractions for cells irradiated by C-12(6+) beam were significantly smaller than those irradiated by gamma-ray (P<0.05).

BRCA1 and its phosphorylation involved in caffeine-inhibitable event upstream of G2 checkpoint

Caffeine, which specifically inhibits ATM/ATR kinases, efficiently abrogates the ionizing radiation (IR)-induced G2 arrest and increases the sensitivity of various tumor cells to IR. Mechanisms for the effect of caffeine remain to be elucidated. As a target of ATM/ATR kinases, BRCA1 becomes activated and phosphorylated in response to IR. Thus, in this work, we investigated the possible role of BRCA1 in the effect of caffeine on G2 checkpoint and observed how BRCA1 phosphorylation was regulated in this process. For these purposes, the BRCA1 protein level and the phosphorylation states were analyzed by Western blotting by using an antibody against BRCA1 and phospho-specific antibodies against Ser-1423 and Ser-1524 residues in cells exposed to a combination of IR and caffeine. The results showed that caffeine down-regulated IR-induced BRCA1 expression and specifically abolished BRCA1 phosphorylation of Ser-1524, which was followed by an override of G2 arrest by caffeine. In addition, the ability of BRCA1 to transactivate p21 may be required for MCF-7 but not necessary for Hela response to caffeine. These data suggest that BRCA1 may be a potential target of caffeine. BRCA1 and its phosphorylation are most likely to be involved in the caffeine-inhibitable event upstream of G2 arrest.

p53基因转导联合重离子辐射引起小鼠黑色素瘤细胞生长抑制及其机制的探讨

为了将放射治疗与基因治疗有机结合起来以寻求有效治疗恶性黑色素瘤的方法，采用了AdCMV-p53（AdCMV-GFP）转染B16细胞联合重离子（或X－射线）辐照的方法，观察辐射对基因转移效率的影响、外源性P53蛋白对重离子辐照诱导肿瘤细胞生长抑制和辐射增敏作用，以及外源性P53蛋白对重离子辐照诱导肿瘤细胞内蛋白表达的变化，现将本工作结果总结如下： 1.重离子照射可增加腺病毒载体介导p53基因转导效率，而且先转染后辐照法比先辐照后转染法能更显著的地增加基因转导效率。这样在最大限度提高基因转导效率的基础之上，同时又可以减少病毒使用量及辐照剂量。 2.p53基因转导联合重离子辐照能明显抑制细胞生长，诱导细胞凋亡，促进G0/G1期细胞阻滞。说明外源性野生型p53基因导入联合辐照可增加黑色素瘤细胞系B16的辐射敏感性。 3.重离子照射比X-射线照射能更明显增加腺病毒载体介导p53基因转导效率和G0/G1期细胞所占比例，可能是由于两种射线能量沉积的方式不同造成的。 4.重离子辐照联合p53基因转导诱导B16细胞中细胞信号通路发生变化，使得P53和P21表达明显增多，同时MDM2表达随时间而减少。推测导入的p53基因联合重离子辐照改变细胞内信号通路，从而诱导细胞凋亡和细胞周期阻滞

碳离子束联合p53腺病毒重组体转染对肿瘤细胞生物学效应研究

肿瘤是严重威胁人类生命健康的常见病、多发病，不仅病因复杂、发生发展异常迅速，而且到目前为止，发病机理不完全清楚，尚无适应范围广和有特异疗效的治疗方法。因此，肿瘤治疗方法的探索依然是医学、生物学及其相关学科研究的热点。肿瘤的重离子治疗和基因治疗是近年来发展起来的新的肿瘤治疗方法。但它们同样或多或少存在一些不足。在肿瘤治疗方法的探索中，将两种或两种以上理化特性或生物学作用原理不尽相同的现有治疗方法有机结合，充分利用各自优势，取长补短，使治疗效果叠加，对肿瘤发挥协同或相加抑制作用。本研究将重离子辐射与p53腺病毒重组体(AdCMV-p53)转染有机结合，探讨了重离子辐射联合p53基因转导对肿瘤细胞的生物学作用及其可能机理。在低剂量γ辐射联合AdCMV-p53/GFP转染HT-29和PC-3细胞研究基础上，我们用不同剂量的AdCMV-p53/GFP转染经0.5 Gy、1.0 Gy、2.0 Gy 12C6+束/γ射线预辐射处理的人非小细胞肺癌(H1299细胞系，nullp53)，人肝癌细胞(HepG2细胞系，wtp53)和人宫颈癌细胞(Hela细胞系，wtp53，wtp53低水平表达)。用流式细胞分析法检测肿瘤细胞绿色荧光蛋白(GFP)、p53蛋白表达水平和细胞周期。DAPI染色后用荧光显微镜检测细胞凋亡。用RT-PCR检测外源性p53转录。用Western Blot检测外源性p53、MDM2和p21蛋白表达。用克隆形成法测定肿瘤细胞存活。通过与γ辐射联合腺病毒重组体转染组比较，观察了12C6+ 辐射联合腺病毒重组体转染对肿瘤细胞外源性p53蛋白表达、细胞周期阻滞、细胞凋亡和细胞增殖的影响。结果显示，12C6+ 辐射对AdCMV-GFP转染H1299、HepG2和Hela细胞的诱导作用明显强于γ辐射(p<0.05)。与γ辐射诱导AdCMV-GFP转染组相比，0.5 Gy 12C6+束辐射联合20 MOI AdCMV-p53转染组H1299细胞GFP阳性率增加约50% (其GFP阳性率提高到约90%)。0.5 Gy、1.0 Gy 12C6+辐射联合40 MOI AdCMV-p53转染组HepG2细胞GFP阳性率增加约44%(其阳性率分别达56.6%和76.4%)。0.5 Gy、1.0 Gy 12C6+ 束辐射联合40 MOI AdCMV-p53转染组Hela细胞GFP阳性率分别增加37.8%和50%(其阳性率分别达43.4%和59.8%)。12C6+ 辐射对AdCMV-p53转染H1299、HepG2和Hela细胞外源性p53蛋白表达的增强作用明显强于γ辐射(p<0.05)。12C6+ 辐射联合AdCMV-p53转染组各种细胞p53阳性率明显高于其它处理组同种细胞p53阳性率(p<0.05)。转染后第5天，γ辐射联合AdCMV-p53转染组3种细胞p53阳性率均降至对照水平。转染后第13天，12C6+ 辐射联合AdCMV-p53转染组3种细胞p53阳性率仍高达6－44%。12C6+ 辐射联合AdCMV-p53转染H1299细胞G0/G1、G2/M期细胞所占比例明显高于其它处理组G0/G1、G2/M期细胞所占比例(p<0.05)。与γ辐射联合AdCMV-p53转染组相比，12C6+ 辐射联合AdCMV-p53转染组G0/G1期细胞增加6－36%，G2/M期细胞增加了13－86%。12C6+ 辐射联合AdCMV-p53转染HepG2细胞G0/G1期细胞所占比例明显高于其它处理组G0/G1期细胞所占比例(p<0.05)；转染后第5天，1.0、2.0 Gy 12C6+ 辐射联合AdCMV-p53转染组G2/M期细胞所占比例明显高于γ辐射联合AdCMV-p53转染组G2/M期细胞所占比例(p<0.05)。各12C6+束辐射联合AdCMV-p53转染Hela细胞G0/G1和G2/M期细胞所占比例均明显高于单纯12C6+ 辐射组和γ射线辐射联合AdCMV-p53转染组G0/G1和G2/M期细胞所占比例(p<0.05)。各12C6+ 辐射联合AdCMV-p53转染H1299、HepG2和Hela细胞凋亡率明显高于等剂量12C6+ 单纯辐射和等剂量γ辐射联合AdCMV-p53转染组细胞凋亡率(p<0.05)。与等剂量单纯12C6+辐射和等剂量γ辐射联合AdCMV-p53转染组相比，12C6+ 辐射联合AdCMV-p53转染H1299细胞凋亡率分别增加8.0－66.0%和9.3－63.5%；12C6+束辐射联合AdCMV-p53转染HepG2细胞凋亡率分别增加0.8－32.7%和4.5－27.1%； 12C6+束辐射联合AdCMV-p53转染Hela细胞凋亡率分别增加4.8－30.7%和3.1－22.7%。低剂量12C6+ 辐射联合AdCMV-p53转染细胞存活率明显低于其它处理组同种细胞存活率(p<0.05)。结果提示，低剂量碳离子辐射对腺病毒重组体转染肿瘤细胞和靶细胞内外源p53蛋白表达的促进作用明显强于低剂量γ辐射。碳离子辐射联合AdCMV-p53转染通过促进外源性p53转导、靶细胞外源性p53蛋白表达、细胞周期阻滞和细胞凋亡等增强对肿瘤细胞的抑制。碳离子辐射联合AdCMV-p53转染对肿瘤细胞生物学作用与肿瘤细胞内在p53基因状态有关。总之，我们的研究表明，低剂量碳离子辐射联合AdCMV-p53转染，可通过促进腺病毒重组体对肿瘤细胞的转染、增强靶细胞外源性p53蛋白稳定表达及其由此而诱发的细胞周期阻滞与细胞凋亡等有效抑制肿瘤细胞。在临床上，碳离子辐射联合AdCMV-p53转染有望在提高肿瘤治疗效果的基础上，进一步降低碳离子辐射与AdCMV-p53转染的各自临床用量，减少碳离子辐射的毒副作用，降低AdCMV-p53转染的潜在生物危险性

低剂量重离子辐射诱导小鼠的适应性反应和褪黑素的辐射保护作用研究

研究目的： 1.研究碳离子辐射对小鼠不同组织抗氧化酶活性及细胞周期进程的影响。 2.研究低剂量碳离子预辐射对离体培养的黑色素瘤B16细胞及正常小鼠诱导的适应性反应。 3. 研究褪黑素（MLT）对碳离子的辐射损伤防护效应。 4. 研究碳离子层叠法辐照对H22荷瘤小鼠的治疗效果。研究方法： 1.采用不同剂量的碳离子辐照小鼠，用黄嘌呤氧化酶法检测外周血、肝脏及脑组织中抗氧化酶活性变化，流式细胞仪检测细胞周期阻滞情况。 2.采用低剂量碳离子预辐射离体培养的黑色素瘤B16细胞及正常小鼠，间隔4h后再以攻击剂量辐照，常规组织切片染色观察各组织器官病理变化，流式细胞仪检测细胞周期阻滞情况，黄嘌呤氧化酶法检测小鼠胸腺、脾脏及B16细胞中抗氧化酶活性，Western-blot法检测胸腺细胞及B16细胞中P53及P21蛋白表达情况，RT-PCR法检测CHK2及CDC25mRNA的表达水平。 3.在碳离子辐照小鼠1h前腹腔注射褪黑素，单细胞电泳方法检测胸腺、脾脏细胞的DNA损伤情况，微核法表征外周血的染色体损伤，黄嘌呤氧化酶法测定胸腺、脾脏细胞的抗氧化酶活性。 4.以碳离子层叠法辐照H22荷瘤小鼠，统计不同剂量照射后的肿瘤体积变化、肿瘤抑制率、肿瘤生长延迟天数及治愈率。结果： 1、小鼠血清和肝脏组织在辐射剂量较低（≤0.75Gy）时SOD活性高于对照组，随着辐射剂量的增高，SOD活性趋于降低；MDA含量在辐射剂量较低（≤0.3Gy）时低于对照，随着辐射剂量的增高其含量趋于升高；脑组织GSH浓度在照射剂量较低（≤0.5Gy）时大于对照组，随着照射剂量的升高其浓度趋于降低；低剂量辐射小鼠引起胸腺G2期细胞比例增加，脾脏G1期细胞比例增加。 2、小鼠肝脏、脾脏、肺脏及脑组织在攻击剂量辐射后，出现明显的病理变化，低剂量预辐射处理后病理变化减轻；低剂量预辐射增加胸腺G2期细胞及脾脏G1期细胞比例；相对于单纯攻击剂量辐射组，低剂量预辐射组胸腺组织P53及P21蛋白表达升高；CHK2 mRNA水平升高，CDC25 mRNA水平降低；脾脏及胸腺组织中SOD活性降低程度减弱，MDA含量升高趋势减弱。B16细胞经低剂量预辐射处理后上述指标均未发生明显变化。 3、与辐照处理组相比，褪黑素处理后小鼠的脾脏胸腺细胞DNA损伤拖尾率及彗尾长度明显降低；SOD活性升高，MDA含量降低，外周血微核率降低。 4、在不同剂量的碳离子辐照处理后观察的12天内，各组肿瘤生长速度减慢，生长延迟，肿瘤抑制率随时间而增加。15Gy照射组肿瘤生长速度最慢，肿瘤抑制率最大，肿瘤生长延迟最为明显，而且肿瘤治愈率达到30%。结论： 1． 低剂量12C6+离子全身辐照小鼠应激激活机体抗氧化系统，随辐射剂量的增加，机体抗氧化能力明显降低，导致脂质过氧化发生；低剂量的碳离子辐射导致小鼠胸腺细胞G2期阻滞，脾脏细胞发生G1期阻滞。 2． 低剂量12C6+离子预辐射引发小鼠正常机体产生适应性反应，减轻随后的大剂量辐射造成的损伤；低剂量12C6+离子预辐射对小鼠黑色素瘤B16细胞未引发适应性反应。 3． 15mg/kg的MLT可以对小鼠的重离子辐射损伤产生明显的防护效果。 4． 12C6+离子适形治疗小鼠移植性肿瘤H22，荷瘤鼠的存活时间、肿瘤体积变化、肿瘤的控制率、治愈率等结果显示，15Gy为最佳治疗剂量

BRCA1对人乳腺癌细胞辐射敏感性的影响及其作用机制研究

目的：研究肿瘤抑制子BRCA1在人乳腺癌细胞辐射抗性中的作用，并探讨其作用机制。材料和方法：利用实时细胞分析系统检测辐射对细胞存活的影响；流式细胞术检测辐射对细胞周期分布的影响；RT-PCR检测辐射导致的BRCA1、Bax和Bcl-2在 mRNA水平变化；Western blot方法检测辐射诱导的蛋白表达水平的变化； In-cell western定量检测辐射引起的蛋白表达水平的变化； AO/EB染色法检测辐射导致的细胞死亡情况。结果：第一，分别用1Gy和4Gy x射线和碳离子束辐照人乳腺癌细胞MCF-7，研究MCF-7对不同LET射线的辐射敏感性差异。结果显示，x射线组1Gy辐射导致细胞存活显著下降，4Gy辐射对细胞存活影响不明显；而碳离子束辐射对细胞生长无抑制作用。与x射线组比较，碳离子辐射诱导了更低的亚“G1”期细胞百分数和更显著的G2期阻滞现象。同时碳离子束辐射诱导BRCA1磷酸化水平和p21表达上调，Bax表达下调。以上结果表明MCF-7对辐射的耐受性与凋亡功能相关，而BRCA1 Ser-1524磷酸化作用可能参与细胞周期和凋亡的信号调控。第二，研究BRCA1在咖啡因诱导的辐射增敏效应中作用。当2mM咖啡因联合4Gy的x射线或碳离子束辐射处理MCF-7细胞后，观察到细胞存活显著下降，辐射诱导的G2期阻滞被废除，BRCA1和p21蛋白表达被抑制，而p53表达水平无明显变化。结果表明咖啡因诱导的MCF-7细胞的辐射增敏作用可能与G2期阻滞被废除相关，BRCA1可能参与该过程的信号调节。第三， 利用BRCA1功能正常的MCF-7细胞和BRCA1功能缺失的HCC1937细胞进一步研究BRCA1对细胞辐射敏感性的影响。辐射显著抑制了HCC1937细胞存活，但对MCF-7细胞存活无明显影响。与HCC1937细胞相比，辐射诱导MCF-7细胞发生显著的G2期阻滞。辐射诱导HCC1937细胞发生晚期凋亡，而MCF-7细胞则多发生早期凋亡，且MCF-7细胞凋亡数明显少于HCC1937细胞。RT-PCR检测结果显示，辐射增强了MCF-7细胞中BRCA1的mRNA 水平，抑制了Bax的mRNA 水平，对Bcl-2的影响不明显；而HCC1937细胞中Bax的mRNA表达水平则被增强。同时辐射诱导MCF-7细胞中BRCA1和p21蛋白表达增强，Bax表达下降，Bcl-2水平略有增高。而HCC1937细胞Bax表达水平增强，但p21和Bcl-2的表达水平则检测不到。这些结果表明，正常的BRCA1功能对Bcl-2的转录表达是必须的，BRCA1通过上调p21水平，下调Bax/Bcl-2影响细胞的辐射敏感性。结论： BRCA1在人乳腺癌细胞的辐射抗性发生中发挥重要作用，BRCA1通过上调p21水平诱导G2期阻滞，下调Bax/Bcl-2抑制凋亡信号，使得细胞对辐射诱导的凋亡产生抗性，最终导致细胞对辐射产生耐受性

Applications of homemade kit in mutation detection of genes

Several methods of mutation detection, such as single-strand conformation polymorphism (SSCP), tandem SSCP/heteroduplex analysis and SNaPshot analysis were developed using homemade kit on ABI 310 genetic analyzer, and were successfully applied to mutation detection of 31 colorectal tumor samples. The sieving capability of homemade kit and commercial kit were compared, results demonstrate that homemade kit has higher resolution and shorter analysis time. In clinical tumor samples, 26% K-ras (exon 1) and 24% p53 (exons 7-8) were found to have mutations, and all mutations were single point variations. A majority of mutations occurred in one gene, only 1 tumor contained alterations in the two genes, which indicates that development of colorectal cancer lies on alternate pathways, and may correlate with different gene mutations.

Novel Near-Infrared Luminescent Hybrid Materials Covalently Linking with Lanthanide [Nd(III), Er(III), Yb(III), and Sm(III)] Complexes via a Primary beta-Diketone Ligand: Synthesis and Photophysical Studies

A series of novel, colorless, and transparent sot-gel derived hybrid materials Ln-DBM-Si covalently grafted with Ln(DBM-OH)(3)center dot 2H(2)O (where DBM-OH = o-hydroxydibenzoylmethane, Ln = Nd, Er, Yb, and Sin) were prepared through the primary beta-diketone ligand DBM-OH. The structures and optical properties of Ln-DBM-Si were studied in detail. The investigation results revealed that the lanthanide complexes were successfully in situ grafted into the corresponding hybrids Ln-DBM-Si. Upon excitation at the maximum absorption of ligands, the resultant materials displayed excellent near-infrared luminescence.

Synthesis, characterization, and near-infrared luminescent properties of the ternary thulium complex covalently bonded to mesoporous MCM-41

The crystal structure of a ternary Tm(DBM)(3)phen complex (DBM - dibenzoylmethane; phen = 1. 10-phenanthroline) and the synthesis of hybrid mesoporous material in which the complex covalently bonded to mesoporous MCM-41 are reported. Crystal data: Tm(DBM)(3)phen C59H47N2O7Tm, monoclinic P21/c, a = 19.3216(12) A, b = 10.6691(7) A, c = 23.0165(15)A, alpha = 90, beta = 91.6330(10), gamma = 90, V = 4742.8(5) A(3), Z = 4. The properties of the Tm(DBM)(3)phen complex and the corresponding hybrid mesoporous material [Tm(DBM)(3)phen-MCM-41] have been studied. The results reveal that the Tm(DBM)(3)phen complex is successfully covalently bonded to MCM-41.

Surface plasmon resonance and electrochemistry characterization of layer-by-layer self-assembled DNA and Zr4+ thin films, and their interaction with cytochrome c

Through electrostatic layer-by-layer (LbL) assembly, negatively charged calf thymus double stranded DNA (CTds-DNA), and positively charged Zr4+ ions were alternately deposited on gold substrate modified with chemisorbed cysteamine. Thus-prepared three-dimensional DNA networks were characterized by surface plasmon resonance (SPR) spectroscopy, X-ray photoelectron spectroscopy (XPS) and infrared reflection-absorption spectroscopy (IR-RAS). SPR spectroscopy indicates that the effective thickness of DNA monolayer in the (DNA/Zr4+), bilayer was 1.5 +/- 0.1 nm, which corresponds to the surface coverage of 79% of its full packed monolayer. At the same time, a linear increase of film thickness with increasing number of layers was also confirmed by SPR characterizations. The data of XPS and IR-RAS show that Zr4+ ions interact with both the phosphate groups and nitrogenous bases of DNA and load into the framework of DNA. Furthermore, the interactions between this composite film and heme protein cytochrome c (Cyt c) were investigated by SPR spectroscopy and electrochemistry.

Surface plasmon resonance and electrochemistry characterization of layer-by-layer self-assembled DNA and Zr4+ thin films, and their interaction with cytochrome c

Through electrostatic layer-by-layer (LbL) assembly, negatively charged calf thymus double stranded DNA (CTds-DNA), and positively charged Zr4+ ions were alternately deposited on gold substrate modified with chemisorbed cysteamine. Thus-prepared three-dimensional DNA networks were characterized by surface plasmon resonance (SPR) spectroscopy, X-ray photoelectron spectroscopy (XPS) and infrared reflection-absorption spectroscopy (IR-RAS). SPR spectroscopy indicates that the effective thickness of DNA monolayer in the (DNA/Zr4+), bilayer was 1.5 +/- 0.1 nm, which corresponds to the surface coverage of 79% of its full packed monolayer. At the same time, a linear increase of film thickness with increasing number of layers was also confirmed by SPR characterizations. The data of XPS and IR-RAS show that Zr4+ ions interact with both the phosphate groups and nitrogenous bases of DNA and load into the framework of DNA. Furthermore, the interactions between this composite film and heme protein cytochrome c (Cyt c) were investigated by SPR spectroscopy and electrochemistry. Compared with the adsorption of Cyt c on DNA monolayer, this composite multilayer film can obviously enhance the amount of immobilized Cyt c confirmed by SPR reflectivity-incident angle (R-theta) curves.