BPM方法在SOI结构中的应用

采用交错隐式算子分裂（ADI）算法，设计、实现了一种高速、高精度的波束传播方法（BPM）来模拟SOI波导中不同偏振态的光传输，研究了PML边界层的选取对虚传播计算基模和基模传播常数的影响，给出了大光腔SOI波导结构不同偏振的基模传播常数。

铟镓氮薄膜的光电特性

用金属有机物气相外延设备，在氮化镓/蓝宝石复合衬底上快速外延生长铟镓氮薄膜，并对其进行了X射线三晶衍射、光致发光、反射光谱及霍尔测量等实验测试。确定该薄膜为单晶，其中In组分可以从0增加到0.26；在光致激发下发光光谱为单峰，且峰值波长在360～555nm范围内可调；其发光机理被证实为膜内载流子经带隙跃迁而直接复合；并具有很高的电子浓度。但InGaN薄膜的结晶质量却随着In含量的增加而变差。

4 * 4区域调制多模干涉耦合器SOI光波导开关的设计

根据区域调制多模干涉耦合器光开关的工作原理，以2 * 2区域调制多模干涉光开关为基础，采用级联的方式设计了4 * 4区域调制多模干涉SOI光波导开关。用有限差分二维BPM方法模拟了器件在不同工作状态下的光场传输情况。器件工作波长为1.55 μm，在不计耦合损耗时器件的平均插入损耗小于2.0 dB/cm。

(Ga, Mn, As)/GaAs的发光谱

利用低能双离子束外延技术，在400 ℃条件下生长样品（Ga, Mn, As）/GaAs。样品光致发光谱出现三个峰，即1.5042eV处的GaAs激子峰、1.4875eV处的弱碳峰和低能侧的一宽发光带。宽发光带的中心位置在1.35eV附近，半宽约0.1eV在840 ℃条件下对样品进行退火处理，退火后的谱结构类似退火前，但激子峰和碳杂质峰的峰位分别移至1.5066eV和1.4894eV，同时低能侧的宽发光带的强度大大增加。这一宽发射的来源还不清楚，原因可能是体内杂质和缺陷形成杂质带，生成Mn_2As新相，Mn占Ga位或形成GaMnAs合金。

窄条宽MOCVD选区生长InP系材料的速率增强因子

报道了窄条宽选区生长有机金属化学气相沉积（NSAG－MOCVD）成功生长的InP系材料，并提出在NSAG－MOCVD生长研究中，引入填充因子的必要性，给出速率增强因子随填充因子变化的经验公式，计算得出速率增强因子随填充因子的变化关系。与实验结果作了比较，发现InP的速率增强因子主要取决于掩膜宽度，InGaAsP的速率增强因子不仅与掩膜宽度有关，同时也依赖于生长厚度，且这种依赖性随掩膜宽度的增加而增加。

平顶陡边响应的谐振腔增强型（RCE）光电探测器的分析

报道了一种具有平顶陡边响应的谐振腔增强型（RCE）光电探测器。使用数值模拟的方法对这种新型谐振腔增强型（RCE）光电探测器与传统的RCE光电探测器的响应曲线和串扰特性进行了分析和对比，分析了在半导体材料生长时厚度偏差对平顶陡边响应的RCE光电探测器响应曲线的影响，还分析了入射光的入射角和偏振态对平顶陡边响应的RCE光电探测器响应曲线的影响。

室温铁磁性半导体Mn_xGa_(1-x)Sb

采用离子注入、离子沉积及后期退火方法制备了稀磁半导体单晶Mn_xGa_(1-x)Sb，在室温下（300 K）获得了单晶的磁滞回线。用X射线衍射方法分析了铁磁性半导体单晶Mn_xGa_(1-x)Sb的结构，用电化学C-V法分析了单晶的载流子浓度分布。由X射线衍射得知，Mn_xGa_(1-x)Sb中Mn含量逐渐由近表面处的x = 0.09下降到晶片内部的x = 0。电化学C-V测得单晶的空穴浓度高达1 * 10~(21)cm~(-3)，表明Mn_xGa_(1-x)Sb单晶中大部分Mn原子占据Ga位，起受主作用。

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.

低剂量碳离子束辐射增强AdCMV-p53转染对非小细胞肺癌细胞的治疗效果

探讨低剂量碳离子束预辐照对AdCMV-p53转染非小细胞肺癌细胞的影响, 观察了20和40 MOI AdCMV-p53转染经12C6+ 束流或γ 射线预辐照的H1299细胞后, 外源性p53的表达、细胞周期、细胞凋亡和细胞存活等. 结果显示, 经碳离子束预辐照后 AdCMV-p53转染细胞p53阳性细胞所占比例高达90%多, 明显高于γ 射线预辐射后AdCMV-p53 转染细胞p53阳性率. 低剂量碳离子预辐照明显阻止AdCMV-p53转染细胞G0/G1阻滞的发生,促进 G2/M 阻滞和细胞凋亡的发生. 碳离子束辐射诱导 AdCMV-p53 转染组相对生物学效应(RBE)比单纯碳离子束辐照组增加 30%~60%, 比单纯 AdCMV-p53 转染组增加20%~130%, 比单纯γ 辐射诱导 AdCMV-p53 转染组增加 30%~70%. 结论: 低剂量碳离子束预照射明显增强外源性 p53 的表达和AdCMV-p53 转染对非小细胞肺癌细胞的抑制.

重离子诱导人舌鳞癌细胞凋亡和Bax/Bcl-2蛋白表达的变化

In order to investigate the effect of carbon ion irradiation on apoptosis and Bax/Bcl-2 expression inhuman tongue carcinoma cells, exponentially growing human tongue carcinoma cells (Tb) cultured in vitro were irradiated with 0, 0.5, 1.0, 2.0 or 4.0 Gy of 12C6+ ions respectively. Survival rate of irradiated cells at various doses were measured by MTT assay. The nucleus changes of apoptosis and necrosis of cells stained by Hochest/PI were observed through fluorescence microscope. The cell cycle changes were detected by flow cytometry (FCM). The expressions of Bax and Bcl-2 were detected by Western blot analysis. The results show that the viability of Tb cells decreases gradually with increment of irradiation doses of carbon ions. The proportions of apoptosis cells in the irradiated groups are significantly higher than those in the control group. There is a positive correlation between irradiation doses and retardation strength in G2 /M phase at 24 h after irradiation (P<0.05). And the expressions of Bax and bcl-2 are significantly up-regulated and down-regulated respectively by 12C6+ ion irradiation. It can be concluded from above that cell apoptosis induced by heavy ion with high-LET may be mediated through the Bax/Bcl-2 expression pathway. 探讨重离子辐照对人舌鳞癌Tb细胞的凋亡及Bax/Bcl-2蛋白表达的影响。采用0、0.5、1.0、2.0、4.0 Gy重离子束辐照人舌鳞癌 Tb 细胞，应用 MTT 法检测细胞存活，流式细胞技术检测细胞周期变化，Hoechst33258/PI 复染法观察 Tb 细胞凋亡形态，并采用 Western-blot 法检测 Bax/Bcl-2 蛋白表达情况。结果发现，Tb细胞经12C6+离子束辐照后存活率显著下降，呈剂量依赖性的生长抑制；Tb细胞呈现蓝色荧光浓集成团的凋亡形态，且凋亡比例随辐照剂量增加；G2/M 期细胞百分数随照射剂量增加而增加（P＜0.05） 。Western-blot结果显示 Bax 蛋白表达水平随辐照剂量逐渐上升，但在 4 Gy 组其表达不再增高，Bcl-2 蛋白在 1.0、2.0、4.0 Gy组随剂量增大呈下降趋势。以上结果提示重离子束辐照对 Tb 细胞有抑制作用，Bax/Bcl-2 蛋白表达是重离子治癌的机制之一。

低剂量连续辐射引起的小鼠免疫系统的变化

为了评估低剂量X射线连续辐射对BALB/c小鼠健康机体免疫系统的影响,实验采用X射线全身连续照射BALB/c小鼠,照射第一天剂量为0.07Gy,剂量率0.2Gy/min,之后每天照射0.08Gy,共照射12d,累积剂量1.03Gy,照射后24和48h取血、胸腺和脾脏。流式细胞仪检测免疫细胞周期和凋亡的变化,胸腺和脾脏指数用重量法获取。实验结果表明,小鼠胸腺细胞的周期在照射后24h被阻滞在G2/M期;外周血淋巴和胸腺细胞周期48h被阻滞在G0/G1期,细胞凋亡比例在照射后两个时间点都显著增加;脾脏淋巴细胞周期24h被阻滞在G0/G1期,48h被阻滞在S期,细胞凋亡比例在24和48h显著减少;脾脏指数在照射后48h显著减少。故低剂量X射线连续全身照射BALB/c小鼠可激活免疫细胞不同的周期监测点,引起免疫细胞凋亡比例发生变化,造成一定的辐射损伤,且这种影响随着免疫器官的不同而不同。

低剂量~(12)C~(6+)离子束预辐照对小鼠肝脏细胞DNA损伤和周期进程的影响

研究低剂量重离子束预辐照对小鼠肝脏辐射损伤程度的影响。分别用低剂量12C6+离子束全身均匀预辐照处理小鼠,剂量分别为0、0.05、0.1、0.25、0.5Gy,剂量率为1Gy/min,4h后用4Gy的12C6+离子束全身均匀辐照,照射8h后用流式细胞仪检测辐照小鼠肝脏细胞在各细胞周期时相的百分率,并用单细胞电泳技术检测辐照损伤小鼠肝脏细胞的DNA损伤程度。结果显示,和对照组相比,低剂量预辐射处理可以减轻辐照损伤小鼠肝脏细胞G0/G1期和G2/M的阻滞,促进肝脏细胞在S期的积累。此外,辐照小鼠肝脏细胞的拖尾率及拖尾长度也显著减少,其中以0.1Gy处理组效果最为显著(P<0.01)。提示:低剂量重离子预辐照能使细胞产生适应性反应,有效减轻辐照小鼠肝脏细胞G0/G1期和G2/M的阻滞,并显著减轻肝脏细胞DNA的辐射损伤程度。

低剂量碳离子束辐射增强AdCMV-p53转染对人非小细胞肺癌细胞的治疗效果

探讨低剂量碳离子束预辐照对AdCMV-p53转染非小细胞肺癌细胞的影响,观察了20和40MOIAdCMV-p53转染经12C6+束流或γ射线预辐照的H1299细胞后,外源性p53的表达、细胞周期、细胞凋亡和细胞存活等.结果显示,经碳离子束预辐照后AdCMV-p53转染细胞p53阳性细胞所占比例高达90%多,明显高于γ射线预辐射后AdCMV-p53转染细胞p53阳性率.低剂量碳离子预辐照明显阻止AdCMV-p53转染细胞G0/G1阻滞的发生,促进G2/M阻滞和细胞凋亡的发生.碳离子束辐射诱导AdCMV-p53转染组相对生物学效应(RBE)比单纯碳离子束辐照组增加30%~60%,比单纯AdCMV-p53转染组增加20%~130%,比单纯γ辐射诱导AdCMV-p53转染组增加30%~70%.结论:低剂量碳离子束预照射明显增强外源性p53的表达和AdCMV-p53转染对非小细胞肺癌细胞的抑制.

重离子诱导人舌鳞癌细胞凋亡和Bax/Bcl-2蛋白表达的变化

探讨重离子辐照对人舌鳞癌Tb细胞的凋亡及Bax/Bcl-2蛋白表达的影响。采用0、0.5、1.0、2.0、4.0Gy重离子束辐照人舌鳞癌Tb细胞,应用MTT法检测细胞存活,流式细胞技术检测细胞周期变化,Hoechst 33258/PI复染法观察Tb细胞凋亡形态,并采用Western-blot法检测Bax/Bcl-2蛋白表达情况。结果发现,Tb细胞经12C6+离子束辐照后存活率显著下降,呈剂量依赖性的生长抑制;Tb细胞呈现蓝色荧光浓集成团的凋亡形态,且凋亡比例随辐照剂量增加;G2/M期细胞百分数随照射剂量增加而增加(P<0.05)。Western-blot结果显示Bax蛋白表达水平随辐照剂量逐渐上升,但在4Gy组其表达不再增高,Bcl-2蛋白在1.0、2.0、4.0Gy组随剂量增大呈下降趋势。以上结果提示重离子束辐照对Tb细胞有抑制作用,Bax/Bcl-2蛋白表达是重离子治癌的机制之一。