高功率微波辐照对雄性大鼠生殖细胞的影响

 采用激光扫描共聚焦显微镜观察受不同参数高功率微波辐照后的大鼠精子细胞内Ca²⁺的变化，同时观察了辐照后大鼠的生殖细胞微核率、畸形率、精子数量、存活率和顶体酶反应的变化。实验表明：此条件下的高功率微波辐照对雄性大鼠的生殖细胞微核率和畸形率没有明显的损伤效应，但4×10⁵次脉冲的高功率微波辐照对大鼠的顶体酶反应有较明显的抑制作用，可能通过改变细胞内第二信使的Ca²⁺浓度来影响其生殖细胞功能。     

L波段微波脉冲对微型计算机的辐照效应实验

 在L波段使用1.3 GHz载波频率的微波脉冲辐照微型计算机主板，通过改变脉冲宽度、重复频率和脉冲串长度等参数，实验研究了微波脉冲辐照导致微型计算机失去响应的功率阈值的变化规律，讨论了L波段微波脉冲辐射的积累效应。实验结果表明：当微波脉冲宽度增加时，微波功率阈值下降；当微波脉冲重复频率升高时，微波功率阈值呈下降趋势；在固定重复频率的条件下，微波脉冲数目的增加也会导致微波功率阈值的下降；微波脉冲功率阈值始终小于连续波微波的功率阈值。当微波脉冲间隔时间较长或者脉冲宽度较宽时，微波功率阈值由单个微波脉冲的参数确定，与脉冲重复频率没有明显关系。利用假设的微波脉冲辐射积累效应，可以定性解释和分析微波脉冲辐照微型计算机实验中功率阈值变化的趋势。     

等离子体鞘套低频通信电磁波透射率与辐照微波场强关系仿真研究

高超声速飞行器飞行期间,由于表面激波的影响,飞行器表面会生成等离子体鞘套。等离子体鞘套会吸收、反射和散射电磁波,导致通信信号发生衰减甚至中断,从而形成“黑障”问题。理论上来说,等离子体鞘套与微波的相互作用随微波电场幅值的变化呈现非线性,所以可能存在一个合适的电场幅值和辐照时间区间,使等离子体鞘套的电磁波透射率上升。针对这种可能性,采用有限元分析方法,对飞行器表面等离子体鞘套流场与电磁场进行二维耦合仿真,得到微波照射后等离子体鞘套透射率的改变情况。分别使用电场幅值为5×10^(4)、1×10^(5)、2.5×10^(5)、5×10^(5) V·m^(−1)的微波对等离子体鞘套进行30 ns的辐照,在辐照后等离子体鞘套对1.2 GHz和1.6 GHz的电磁波的最大透射率提升,为解决“黑障”问题提供了新的可能。     

脉冲电磁场对大鼠血清荧光光谱影响的研究

采用荧光光谱结合组织病理学方法,研究脉冲电磁场辐照后大鼠脑组织结构的变化情况,探讨血清荧光光谱变化与脑损伤的关系。将雄性SD大鼠随机分为假辐照组和辐照组,辐照组暴露于宽频脉冲电磁场,在辐照后5个不同时间点采集血样,分析血清荧光光谱和S100B蛋白表达情况,并观察脑组织病理切片。结果发现,脑损伤程度和辐射剂量有一定的关系,辐射剂量越大,损伤越严重,其变化趋势和S100B蛋白表达、脑组织病理观察结果一致。说明血清荧光光谱法可能适用于对电磁脉冲作用后生物体和脑损伤效应的分析。     

超声作用可以提高公猪的生殖能力与质量

本实验研究了0.88和2.64 MHz高频超声对公猪精液质量的影响。采用的超声声强为0.05W/cm~2,辐照时间15、30s和1、2 min。超声波形分连续波和宽度为2、4、10ms的脉冲波。经超声处理过精子的活动性和绝对存活率分别增加到23％。最佳辐照时间30s而脉冲波宽度2ms。实验揭示了超声对猪的生理、生化特性和产仔的短期与长期影响。采用0.88MHz的超声辐照猪的生物活性点(BAP)和睾丸,精     

微型计算机微波辐照效应的实验研究

 微波辐照频率为1.2~2.0 GHz时，利用宽带天线对微型计算机主板进行微波辐照，考察了微波辐照载波频率、调制方式和调制深度对微波辐照效应的影响，得到了计算机分别处于满负荷工作、内存读写操作、磁盘读写操作和系统空闲4种工作状态下的微波辐照干扰功率阈值。实验结果表明：微波辐照的载波频率为1.47 GHz时，辐照干扰功率阈值最低,为32.7 dBm，计算机最易被干扰；瞬时功率是干扰微型计算机的关键参数，调制方式、调制频率和深度对微波辐照干扰功率阈值影响不大；处于高负荷工作状态的微型计算机更易于被微波辐射干扰；计算机启动的干扰功率阈值为32.0 dBm，小于正常工作状态时的阈值。     

Ⅰ层厚度对限幅器热损伤效应的影响

基于器件物理模拟分析法研究PIN限幅器二极管的微波脉冲热效应,利用Sentaurus-TCAD仿真器建立了PIN二极管二维多物理场仿真模型,研究了在5.3,7.5,9.4 GHz的微波脉冲作用下,不同Ⅰ层厚度的二极管模型的峰值温度变化。仿真结果表明:Ⅰ层厚度对PIN二极管微波脉冲热效应的影响分两个阶段,拐点前厚度增加,峰值温度提高,拐点后厚度增加峰值温度降低;一定范围内微波脉冲频率的变化对拐点影响不明显。     

重复频率可调谐的超低抖动光窄脉冲源的研究

提出了一种新型的基于光电振荡器的重复频率可调谐的超低抖动光窄脉冲源. 光电振荡器系统可以产生超低相位噪声的微波信号; 被该信号调制的直调光经过两次相位调制之后, 使光脉冲的啁啾增强; 再通过一段色散补偿光纤, 光脉冲被进一步压窄. 实验中使用YIG可调滤波器, 可以得到8–12 GHz内步进为200 MHz的可调谐微波信号, 因此光脉冲的重复频率具有可调谐性. 当微波信号即脉冲重复频率为9.6 GHz时, 测得脉冲宽度为3.7 ps, 相位噪声为-130.1 dBc/Hz@10 kHz. 由此得出光脉冲的瞬时抖动为60.1 fs (100 Hz–1 MHz), 因此该方案产生的光窄脉冲源具有超低的抖动.     

建筑物对微波脉冲响应仿真与实验

 建立了微波脉冲在建筑物内传播、反射及透射过程的3维仿真模型,提取了空间电场时域最大值进行统计分析。分析表明：不同入射角窄带调制方波脉冲激励下,场增强区域大小与微波通过窗户和门能直接照射到的区域大小呈正比,窗户的大小对建筑物内空间场强增强区域的大小有显著影响;同时在微波脉冲的传播方向上,窗沿后的区域场强幅值明显减小;脉冲宽度对建筑物内空间场强增强区域的大小及空间场强最大值影响很小;无上升下降沿的窄带调制方波脉冲激励下,空间电场叠加增强效应更强。测量了微波脉冲辐照下,建筑物内空间功率密度分布,验证了仿真结果。     

9.33 GHz高功率脉冲微波对IAR20鼠肝细胞和L-02人肝细胞增殖的影响

研究了9.33 GHz高功率脉冲微波对IAR20鼠肝细胞和L-02人肝细胞增殖的影响,利用噻唑蓝比色法测量细胞增殖并对实验数据进行拟合,得到脉冲个数、场强和脉宽与细胞增殖之间的关系。当脉冲微波场强与脉宽保持不变,脉冲微波细胞效应随脉冲个数呈现非线性的指数递增规律。当脉冲微波的脉冲个数、脉宽一定时,场强越大,细胞增殖被抑制的程度越大;当脉冲个数、场强不变,脉宽越大,细胞增殖受到抑制的作用越明显,即脉冲微波细胞效应与场强和脉宽成正比。相同脉冲微波参量对不同种类细胞增殖的影响是不同的,对IAR20鼠肝细胞的影响比对L-02人肝细胞的影响略大。     

二（2-苯并咪唑亚甲基）胺合镝的合成及其与DNA作用的光谱研究

首次微波合成二（2-苯并咪唑亚甲基）胺（L）及其稀土金属镝的配合物[DyL2（NO3）2]NO3,用红外、元素分析、核磁共振、摩尔电导对其进行表征。用紫外可见光谱、荧光光谱、粘度研究了该配合物与鲑鱼精脱氧核糖核酸（DNA）的作用规律,结果表明：配合物以部分插入和静电作用模式与DNA键合。     

脉冲微波辐照影响心肌细胞膜蛋白构象及其机制的研究

应用显微傅里叶变换红外光谱技术研究了脉冲微波辐照对心肌细胞膜蛋白质构象、功能的影响和相关分子机制。结果表明,辐照可对心肌细胞的细胞膜蛋白质结构产生明显影响。细胞膜脂质中—CH₂—、磷脂结构中CO、蛋白质酰胺Ⅰ,Ⅱ带的伸缩振动峰消失或位移。辐照后心肌细胞膜蛋白质二级结构也出现明显变化,α-螺旋和β-折叠结构减少,二级结构无序化程度增加。上述变化均与辐照剂量呈正相关。结果提示受脉冲微波辐照后,心肌细胞膜蛋白构象的完整性受损,膜稳定性及流动性下降,膜上多种生物活性结构被破坏,上述变化构成了细胞膜功能丧失、细胞形态和结构损伤、细胞凋亡等病理学效应的生物化学基础。文章首次从蛋白质构象角度阐述了微波辐照对心肌细胞膜损伤的分子病理机制。     

PIN限幅器的高功率微波单脉冲效应研究

基于PIN限幅器的等效电路模型,构建了PIN限幅器HPM效应ADS等效电路仿真模型,利用HPM注入实验和等效电路仿真相结合的方法,研究了单个微波脉冲作用下PIN限幅器的响应规律,获取了HPM作用结束后限幅器限幅持续时间与注入脉冲功率、脉宽的对应关系,并对限幅器的限幅持续过程进行了分析。仿真与实验结果表明:PIN限幅器限幅持续时间随着微波脉冲功率和脉宽的增大而变大,实验和仿真结果趋势一致,该研究使用的ADS等效电路模型可以应用于PIN限幅器的高功率微波瞬态响应特性分析研究。     

引信高功率微波电磁辐射效应数据的FCM分析

高功率微波(HPM)电磁脉冲对引信辐照实验的数据分析是研究其电磁效应中的一个重要问题,数据分析的主要困难在于HPM电磁效应数据的高维复杂性。通过聚类算法设计,采用模糊C均值聚类(FCM)算法对某无线电引信的高功率微波电磁效应数据进行分析处理,利用其类内相似和类间相异的原则,经迭代运算,实现HPM对无线电引信效应数据的脉宽、峰值功率、功率密度等参数间的识别和分类。结果表明:采用FCM算法能够得到HPM对某引信的最佳聚类中心,即致使引信失效的最佳干扰阈值,证明了算法的有效性。     

Ignition of thin liquid hydrocarbon films via surface microwave discharge generated in a paired-pulse mode

The process of ignition and combustion of liquid hydrocarbon films under the conditions of a self-maintained surface microwave discharge in still air that is generated on a dielectric antenna in the paired pulse mode is investigated. The effect of the medium pre-excitation, which occurs during the first pulse on the period of induction and intensity of hydrocarbon combustion during the second microwave pulse, is demonstrated.     

和厚朴酚对非小细胞肺癌细胞的辐射增敏效应

研究了和厚朴酚（HNK）对非小细胞肺癌（NSCLC）细胞系A549和H1299对低线性能量转移（LET） X射线和高LET碳离子的辐射增敏效应。首先用CCK-8检测了HNK对A549和H1299细胞的生长抑制情况,发现20 μmol/L的HNK处理对细胞的生长抑制作用较弱。用该浓度HNK预处理细胞2 h后给予不同剂量X射线或碳离子的照射,克隆存活法检测细胞的辐射敏感性,Annexin-PI双染法检测细胞凋亡,γH2AX焦点法检测DNA的双链断裂（DSB）损伤。实验结果显示:与X射线相比,NSCLC细胞对碳离子更敏感,HNK预处理仅对碳离子照射有辐射增敏作用;与碳离子单独照射相比,HNK预处理联合碳离子照射诱导了更明显的细胞凋亡;在照射后24 h,HNK预处理联合碳离子照射引起的细胞γH2AX焦点阳性率维持在较高水平,而X射线照射没有这些效应。实验结果表明,HNK预处理抑制了NSCLC细胞DNA的DSB修复,诱导了细胞凋亡的发生,从而提高了细胞对碳离子的辐射敏感性。The radiosensitizing effect of Honokiol (HNK) on non-small cell lung carcinoma (NSCLC) cell lines A549 and H1299 to low-linear energy transfer (LET) X-rays and high-LET carbon ions was investigated in this study. First, the inhibitory effects of HNK on the growth of A549 and H1299 cells were detected by CCK-8 assay, and 20 μmol/L HNK treatment was found to induce a growth inhibitory effect slightly in these two cell lines. Cells were pre-treated with HNK and then irradiated with X-rays and carbon ions of different doses. Cellular radiosensitivity, apoptosis and DNA damage were analyzed by clonogenic survival, Annexin-PI staining and γH2AX foci, respectively. The results showed the cells were more sensitive to carbon ion irradiation compared to X-rays and the radiosensitization of HNK was only observed after carbon ion irradiation. Furthermore, the co-treatment led to higher apoptosis rate 48 h after irradiation and increased the positive rate of γH2AX foci 24 h after irradiation in A549 and H1299 cells compared with those in the groups treated with carbon ion irradiation alone. These phenomena were not observed after X-ray irradiation. Our data suggest that the pre-treatment with HNK inhibited DNA DSB repair, induced apoptosis and then enhanced the cellular radiosensitivity to carbon ions in NSCLC cells.     

Theoretical treatment of pulsed Overhauser dynamic nuclear polarization: Consideration of a general periodic pulse sequence

A general theoretical approach to pulsed Overhauser-type dynamic nuclear polarization (DNP) is presented. Dynamic nuclear polarization is a powerful method to create non-thermal polarization of nuclear spins, thereby enhancing their nuclear magnetic resonance signals. The theory presented can treat pulsed microwave irradiation of electron paramagnetic resonance transitions for periodic pulse sequences of general composition. Dynamic nuclear polarization enhancement is analyzed in detail as a function of the microwave pulse length for rectangular pulses and pulses with finite rise time. Characteristic oscillations of the DNP enhancement are found when the pulse-length is stepwise increased, originating from coherent motion of the electron spins driven by the pulses. Experimental low-field DNP data are in very good agreement with this theoretical approach.     

Initiation of self-propagating high-temperature synthesis by a pulsed microwave discharge

It is shown that a metal plasma with a temperature of 10 kK arises on the surface of a metal-insulator powder subjected to a 0.3-to 1.0-ms-long microwave pulse. The pulse triggers an exothermal chemical reaction in the Ti-B or Al-Fe₂O₃ powder mixture, the delay between the end of the pulse and inflammation of the mixture reaching 10–20 ms. The microwave irradiation results in a high local energy deposition causing evaporation and rapid mixing of the reactants. This distinguishes the early stage of the reaction triggered by microwave radiation from the reaction in the case of conventional thermal initiation.     

开放空间重复频率微波脉冲击穿概率理论与实验研究

综合考虑有效初始电子产生理论、雪崩电子击穿理论等过程中的击穿延迟时间,探讨了开放空间微波脉冲的击穿延时概率分布,提出了重复频率微波脉冲击穿概率模型,定义了基于概率模型的微波脉冲击穿阈值。利用S波段微波准光学反射聚焦系统对一定气压大气击穿过程进行了模拟,监测击穿放电发光时刻作为击穿时间,分别在铯137放射源存在与否情况下开展了系列实验。研究结果表明,提高种子电子产生率相较于提高电离率是增大脉冲击穿概率更有效的方法;重复频率过程中,若存在累积效应,击穿延时概率分布曲线将左移并趋于稳定,击穿后的气体在短时间内容易再次击穿。     

Radiation-induced kidney injury: a role for chronic oxidative stress?

Kidney irradiation clearly leads to a progressive reduction in function associated with concomitant glomerulosclerosis and/or tubulointerstitial fibrosis. However, the particular cell types, mediators and/or mechanisms involved in the development and progression of radiation nephropathy remain ill defined. Angiotensin II (Ang II) plays a major pathogenic role; administration of Ang II blockers markedly abrogates the severity of radiation nephropathy in experimental models. Both ionizing radiation and Ang II signal via generation of reactive oxygen species (ROS). Thus, we hypothesized that localized kidney irradiation might lead to a chronic oxidative stress. In view of the difficulty in measuring ROS in vivo we adopted an indirect immunohistochemical approach in which we used a monoclonal antibody specific for 8-hydroxy-2'-deoxyguanosine (8-OHdG), one of the most commonly used markers of DNA oxidation.The right kidney of 7-8 week-old male Sprague-Dawley rats was removed. Five to 6 weeks later the remaining hypertrophied kidney was irradiated with single doses of 0-20.0 Gy X-rays. Groups of rats, three per dose, were killed at 4, 8, 16 and 24 weeks post-irradiation, their kidneys fixed, and sections stained with the 8-OHdG-specific antibody N45.1.For quantitation of glomerular DNA oxidation with the N45.1 antibody stained sections, 50 glomeruli/animal were counted. The presence of any intensely stained nuclei within the glomerular tuft was scored as positive. Quantitation of tubular DNA oxidation employed a 10 x 10 point ocular grid. Sections were examined at 400 magnification; 250 tubular profiles were counted. All tubules with any nuclear staining were scored as positive.Sham-irradiated kidneys showed little evidence of DNA oxidation over the experimental period. In contrast, localized kidney irradiation led to a marked, dose-independent increase in glomerular and tubular cell nuclear DNA oxidation. This increase was evident at the first time point studied, i.e. 4 weeks after irradiation, and persisted for up to 24 weeks postirradiation. DNA oxidation in the irradiated kidney was only seen in apparently viable glomerular and tubular cells. Thus, while from 16 to 24 weeks post-irradiation structural alterations had progressed to glomerular sclerosis and tubular atrophy, positive staining for 8-OHdG was not observed in severely atrophic tubules. Similarly, fewer positive staining cells were noted in glomeruli undergoing sclerosis, while none were seen in totally sclerotic glomeruli. These data support the hypothesis that renal irradiation is associated with a chronic and persistent oxidative stress.