掺铒nc-Si/SiO_2薄膜中nc-Si和Er~(3+)与非辐射复合缺陷间相互作用对薄膜发光特性的影响

对nc-Si/SiO_2薄膜中纳米硅(nc-Si)、Er~(3+)和非辐射复合缺陷三者间的关系作了研究.在514.5 nm光激发下,nc-Si/SiO_2薄膜在750nm和1.54μm处存在较强的发光,前者与薄膜中的nc-Si有关,后者对应于Er~(3+)从第一激发态4I13/2到基态4I15/2的辐射跃迁.随薄膜中Er3+含量的提高,1.54μm处的发光强度明显增强,750 nm处的发光强度却降低.H处理可以明显增强薄膜的发光强度,但是对不同退火温度样品,处理效果却有所不同.根据以上实验结果,可得如下结论:在nc-Si颗粒附近的Er~(3+)和其他的缺陷组成了nc-Si颗粒内产生的束缚激子的非辐射复合中心,束缚激子通过Er~(3+)的非辐射复合,激发Er~(3+)产生1.54μm处的发光,同时降低了750nm处的发光强度.nc-Si颗粒附近其他非辐射复合中心的存在会降低Er~(3+)被激发的概率,引起1.54μm处的发光强度降低.

注铒a-SiO_x:H中Er~(3+)发光与薄膜微观结构的关系

采用光致发光（PL）谱和傅里叶变换红外（FTIR）谱研究了掺铒a-SiO_x:H(a-SiO_x:H)薄膜在不同退火温度下光学性质和微观结构的变化。PL谱的测量结果表明：薄膜在1.54μm的Er~(3+)发光和750nm处的可风发光随退火温度有相同的变化趋势，这种变化和薄膜在退火过程中微观结构的变化有着密切关系。FTIR谱的分析表明：a-SiO_x:H薄膜是一种两相结构，富硅相镶嵌在富氧相中。两者的成分可近似用a-SiO_(x≈0.3):H和a-SiO_(x≈1.5):H表示，前者性质接近于氢化非晶硅（a-Si:H），后者性质接近于a-SiO_2。富硅相在退火中的变化对Er~(3+)的发光强度有重要影响。

单晶硅中铒点缺陷及Er-O复合缺陷电子结构的EHMO计算

本文采用集团模型和推广的Hucket分子轨道理论(EHMO)计算c-Si中Er点缺陷及Er-O复合缺陷的原子构型及电子结构。计算结果符合实验及一些文献的第一性原理计算结果,解释了Er有c-Si中的发光特性。

a-SiCx∶H和β-SiC中Er缺陷结构及其1.54μm发光探索

材料科学开放实验室基金,光学信息技术科学教育部开放实验室基金

掺Er凝胶玻璃中Er离子发光性质的研究

用溶胶－凝胶方法合成了掺铒（掺杂浓度10~20/cm~3）的二氧化硅玻璃。在室温下可产生1.45μm波长的红外荧光。实验结果表明

稀土（Er）和氧（O）双掺杂GaAs和Si的高效发光的研究

用光致发光谱(PL)、傅里叶变换红外吸收谱(FTIR)和X射线衍射谱(XRD)等研究了稀土(Er)和氧(O)双离子注入GaAs和Si的发光特性和高效发光机理。测量并分析了该材料的FTIR和XRD谱;对该材料的高效发光机制作了较深入地探讨和澄清。

Crystal-Field Symmetry of Luminescence Center in Er-Implanted Silicon

于2010-11-23批量导入

Er离子在Inp、GaAs和Si中的1.54μm特征发光峰

分别在InP、GaAs和Si中以7×10＜′14＞和1×10＜′15＞cm＜′－2＞的剂量进行Er离子注入, 并采用闭管、快速和炉退火等热处理。低温光致发光（PL）、反射式高等电子衍射和卢瑟福背散射实验研究表明, 上述样品中Er＜′3＋＞离子特征发光的中心波长均出现在1．5μm处, 其中InP的发光峰最强, 而注入损伤的恢复是影响Er＜′3＋＞发光的重要因素之一。卢瑟福背散射分析进一步证实退火后Er原子在Si中向表面迁移, 而在InP中的外扩散较小, 并比较了Er在InP和Si晶格中的占位情况。图7参12

Er~+注入单晶硅中非晶层晶化过程的TEM研究

于2010-11-23批量导入

The influence of oxygen content on photoluminescence from Er-doped SiOx

SiOx films with oxygen concentrations ranging 13-46 at.% were deposited by plasma enhanced chemical vapor deposition (PECVD) technique using: pure SiH4 and N2O mixture. Erbium was then implanted at an energy of 500 KeV with dose of 2x10(15) ions/cm(2). The samples were subsequently annealed in N-2 for 20 sec at temperatures of (300-950 degrees C). Room temperature (RT) photo-luminescence (PL) data were collected by Fourier Transform Infrared Spectroscopy (FTIS) with an argon laser at a wavelength of 514.5 nm and an output power from 5 to 2500 mw. The intense room-temperature luminescence was observed around 1.54 mu m. The luminescence intensity increases by 2 orders of magnitude as compared with that of Er-doped Czochralski (CZ) Si. We found that the Er3+ luminescence depends strongly on the SiOx microstructure. Our experiment also showed that the silicon grain radius decreased with increasing oxygen content and finally formed micro-crystalline silicon or nano-crystalline silicon. As a result, these silicon small particles could facilitate the energy transfer to Er3+ and thus enhanced the photoluminescence intensity.

Yellow luminescence mechanism and persistent photoconductivity in n-GaN single crystal films grown on alpha-Al2O3(0001) substrates by LP-MOCVD

Unintentionally doped and Si-doped single crystal n-GaN films have been grown on alpha-Al2O3 (0001) substrates by LP-MOCVD. Room temperature photoluminescence measurement showed that besides the bandedges, the spectrum of an undoped sample was a broad deep-level emission band peaking from 2.19 to 2.30eV, whereas the spectrum for a Si-doped sample was composed of a dominant peak of 2.19eV and a shoulder of 2.32eV. At different temperatures, photoconductance buildup and its decay were also observed for both samples.. The likely origins of persistent photoconductivity and yellow luminescence, which might be associated with deep defects inclusive of either Ga vacancy(V-Ga)/Ga vacancy complex induced by impurities or N antisite (N-Ga), will be proposed.

Study of infrared luminescence from Er-implanted GaN films

In this study, we report the dependences of infrared luminescence properties of Er-implanted GaN thin films (GaN:Er) on the kinds of substrates used to grow GaN, the growth techniques of GaN, the implantation parameters and annealing procedures. The experimental results showed that the photoluminescence (PL) intensity at 1.54 mum was severely influenced by different kinds of substrates. The integrated PL peak intensity from GaN:Er /Al2O3 (00001) was three and five times stronger than that from GaN:Er /Si (111) grown by molecular beam epitaxy (MBE) and by metalorganic chemical vapor deposition (MOCVD), respectively. The PL spectra observed from GaN:Er/Al2O3 (0001) grown by MOCVD and by MBE displayed a similar feature, but those samples grown by MOCVD exhibited a stronger 1.54 mum PL. It was also found that there was a strong correlation between the PL intensity with ion implantation parameters and annealing procedures. Ion implantation induced damage in host material could be only partly recovered by an appropriate annealing temperature procedure. The thermal quenching of PL from 15 to 300 K was also estimated. In comparison with the integrated PL intensity at 15 K, it is reduced by only about 30 % when going up to 300 K for GaN:Er/Al2O3 sample grown by MOCVD. Our results also show that the strongest PL intensity comes from GaN:Er grown on Al2O3 substrate by MOCVD. (C) 2004 Elsevier B.V. All rights reserved.

Correlation between Er3+ emission and the microstructure of a-SiOx : H < Er > films

Photoluminescence (PL) from Er-implanted hydrogenated amorphous silicon suboxide (a-SiOX:H(x<2.0)) films was measured. Two luminescence bands with maxima at lambda congruent to 750 nm and lambda congruent to 1.54mum, ascribed to the a-SiOX:H intrinsic emission and Er3+ emission, were observed. Peak intensities of the two bands follow the same trend as a function of annealing temperature from 300 to 1000degreesC. Micro-Raman results indicate that the a-SiOX:H films are a mixture of two phases, an amorphous SiOX matrix and amorphous silicon (a-Si) domains embedded there in. FTIR spectra confirm that hydrogen effusion from a-SiOX:H films occurs during annealing. Hydrogen effusion leads to a reconstruction of the microstructure of a-Si domains, thus having a strong influence on Er3+ emission. Our study emphasizes the role of a-Si domains on Er3+ emission in a-SiOX:H films.

瓦山安息香中苯并呋喃促雌激素合成的机理研究

雌激素是人体内重要的激素之一，具有广泛的生理功能。雌激素缺乏与许多疾病相关，如卵巢功能低下，更年期综合征以及骨质疏松等；雌激素过剩也将导致某些疾病，如乳腺癌、卵巢癌、子宫内膜癌等。目前，如何降低肿瘤组织中的雌激素水平而达到治疗肿瘤的目的，已经得到广泛的研究，但促雌激素生成或调节卵巢功能药物或其相关研究则很少。 本实验室前期的研究发现，瓦山安息香属植物果实中的乙醇提取物具有促雌激素生成作用，通过活性追踪和结构鉴定，确认促E2 生成的主要成分为苯并呋喃类化合物。苯并呋喃类化合物的作用与芳香酶有关，但其确切的作用机理有待证实和深入研究。 为了探讨安息香苯并呋喃类化合物的促雌激素合成的作用机理，拟采用如下的实验方案： 1、细胞学方面，对小鼠3T3-L1 前脂肪细胞、人乳腺癌细胞MCF-7、MDA-MB-231 以及人卵巢癌细胞OVCAR-3、OVCAR-4、OVCAR-5、OVCAR-8、IGROV1 等细胞株，采用RT-PCR 和ELISA 方法研究芳香酶Aro基因的表达和雌二醇E2 的生成，芳香酶抑制剂Formestane 作为阳性对照，研究时效曲线和量效曲线，确定安息香苯并呋喃类化合物SP25 的有效浓度和作用时间。 2、RNAi 方面，设计合成了针对人芳香酶Aro基因的3 对RNAi 序列，转染入细胞，芳香酶促进剂Forskolin 和地塞米松、芳香酶抑制剂Formestane 作为阳性对照，采用实时定量PCR 技术，研究RNA 干扰后，安息香苯并呋喃类化合物SP25 对人芳香酶Aro基因表达水平瓦山安息香苯并呋喃促雌激素合成的机理研究的影响。 3、雌激素受体方面，设计一段ERE 的雌激素调控元件，构建重组荧光素酶报告基因载体，瞬时转染人乳腺癌细胞株MDA-MB-231，建立针对雌激素受体的报告基因筛选模型，观察安息香苯并呋喃类化合物SP25 对雌激素受体的选择性和亲和力，从受体水平考察安息香苯并呋喃类化合物SP25 促进雌激素生成的药理学机理。 实验结果显示： 1、分化后的小鼠3T3-L1 前脂肪细胞、人乳腺癌细胞MCF-7 、MDA-MB-231 以及人卵巢癌细胞OVCAR-3、OVCAR-4、OVCAR-8 等细胞株具有芳香酶基因的表达。睾酮向雌二醇的转化能够被芳香酶抑制剂Formestane 所阻断，其中OVCAR-3 最适合进行下一步的RNAi研究。 2、RNAi 实验结果显示，设计的3 对RNAi 序列中R2 的干扰效果最强，相应的阴性对照C2 与R2 的表达量相差118 倍（24 小时）和19 倍（48 小时），显示R2/C2 这组序列可用于进一步的RNAi 试验。以R2 干扰OVCAR-3 细胞株，药物作用24、48 小时后，芳香酶抑制剂Formestane 与R2 相对表达量相比分别为0.83 倍和0.04 倍；芳香酶促进剂Forskolin 与R2 相对表达量相比分别为3.61 和1.84 倍；芳香酶促进剂地塞米松与R2 相对表达量相比分别为5.76 倍和3.49倍；苯并呋喃类化合物SP25 与R2 相对表达量相比分别为8.13 倍和4.59 倍。实验证实安息香苯并呋喃类化合物SP25 能够促进因RNAi 而发生基因沉默的人芳香酶Aro表达水平的上调。 3、雌激素受体实验结果显示，构建成功重组pERE-pGL3-promoter 荧光素酶报告基因载体和基于报告基因系统的雌激素受体激动剂或拮抗剂的细胞筛选模型。实验结果表明安息香苯并呋喃类化合物SP25 与雌激素受体ERα和ERβ亲和力选择性之比约为3：1 ，SP25通过与雌激素受体ERα结合作用其受体，刺激芳香酶的表达。 本课题通过RNA 干扰、ELISA、荧光实时定量PCR、报告基因筛选模型等技术手段，从细胞水平、蛋白酶水平和基因表达水平、雌激素受体水平等方面系统地研究了从瓦山安息香属植物果实中提取的苯并呋喃SP25 促进促雌激素生成的机理研究。试验结果显示苯并呋喃类化合物SP25 促雌激素生成的主要作用机制是直接促进芳香酶基因表达水平，以及与雌激素受体a 结合，刺激芳香酶活性。 Estrogen is an important hormone that has versatile physiologicalfunctions. Lack of estrogen will lead to many diseases such as lower ovarianfunction, climacteric syndrome and osteoporosis. Excessive estrogen alsoinduces breast carcinoma, oophoroma and endometrial carcinoma and otherdiseases. To depress the estrogen level in tumor tissue to cure carcinomawas widely studied, but there is only few studies reported on the induction ofestrogen and on the regulation of ovary function. We found that the extracts from seeds of Styrax perkinsiae couldpromote the synthesis of estrogen. The active compounds benzofurans wereidentified. Effect of benzofurans may be related to aromatase, but the mechanism was not clear. To reveal the mechanism of these benzofurans to promote estrogensynthesis, the following protocols were adopted: 1 Cytology: 3T3-L1 preadipocytes,human ovary carcinoma celllines OVCAR-3,OVCAR-4,OVCAR-5,OVCAR-8,IGROV1 andbreast carcinoma cell lines MCF-7 and MDA-MB-231 were usedto determine Aro gene expression and estrogen production withRT-PCR AND ELISA methods. Formestane, an aromataseinhibitor, was used as positive control. And dose-curve,time-curve and the effective concentration of SP25 were also studied. 2 Designed 3 pairs of RNAi for human aromatase gene, andtransfected into cell. Aromatase inducer Forskolin andDexamethasone, and aromatase inhibitor Formestane were usedas positive controls. We studied the change of Aro expressionlevel with SP25 by using real-time PCR after RNA interfering. 3 Estrogen Receptor: We constructed the recombined Luciferasereport vector and establish a screening system for estrogenagonist and antagon. With this system, we studied the affinity ofSP25 and estrogen receptor. Results: 1 Differentiated 3T3-L1 preadipocytes¡¢human ovary carcinomacell lines:OVCAR-3, OVCAR-4, OVCAR-8 and breast carcinomacell lines MCF-7, MDA-MB-231 had detected aromatase geneexpression.And OVCAR-3 is more suitable for further aromatasegene function research. 2 In RNAi assay, R2 has a strong interfering effcet in OVCAR-3 cellline, and ratio of C2 (the negative control) to R2 were 118 times(24 hours) and 19 times (48 hours). This means sucessful inRNA interfering. After R2 acted on OVCAR-3 cell line, the ratiosof formestane to R2 were 0.83 and 0.04 times, 5.76 and 3.49times (Dex), 3.61 and 1.84 times (forskolin) and 8.13 and 4.59times (sp25) after drug treated 24 or 48 hours respectively.These results indicated that SP25 can directly induce aromatasegene up-regulation. 3 We had constructed pERE-pGL3-promoter recombined vectorand the Luciferase report gene screening system. Luciferasereport gene assay showed that sp25 had a higher affinity with strogen receptor alpha than estrogen receptor beta, this indicated that SP25 can act on estrogen receptor and induce aromatase. Our results revealed that the mechanisms of benzofuran to promoteestrogen were the upregulation aromatase gene expression and promotion ofaromatase activity and have partially elective affinity with estrogen receptoralpha.