一类多因素HIV模型的研究

研究了一类多因素HIV模型.建立了一个标准型的DI模型,证明了无病平衡点的局部渐近稳定性和全局渐近稳定性.     

一种适合视频瞄准具的电子分划叠加电路系统

对视频电子分划瞄准具进行了设计。根据视频图像电子叠加原理,完成了屏幕存储映射方式的电子分划线及操作提示符场叠加。系统核心是由单片机、视频叠加显示芯片、数字电位器和单稳态延时电路组成,具有叠加图像与场景图像同显、手动二维调节瞄准分划线位置及改变OLED亮度对比度、热图极性转换和手动非均匀校正等功能。     

高效率多程折叠Nd:YVO4激光放大器

采用具有近共焦、非稳腔特点的多程折叠光路结构,使激光光束多次通过增益介质,实现了高提取效率的激光放大器.实验中在注入22W种子激光的条件下,以43.9%的提取效率得到了63 W的激光输出,斜效率超过52%,激光放大器的输出光束质量从种子激光的M2X=2.08,M2Y=1.92变为M2X=2.84,M2Y=1.79.     

基于二维光栅分光的同步移相干涉测量技术

为了干涉测量的抗振目的,提出了一种新的同步移相干涉测量方案并搭建了实验装置。整个测量系统在迈克耳孙偏振移相干涉仪的基础上,利用一个正交的二维光栅产生对称分光,选取对于理想光栅衍射效率一致的(±1,±1)级衍射光作为测量分光路,使之分别通过偏振方向依次相差45°的一个偏振片组,从而分别形成0°、90°、180°和270°相移的四幅移相干涉图,按照传统的四步移相算法,对被测波面进行了复原。分析了光强畸变和移相误差对系统的测量误差的影响。利用该系统测量一球面系统,结果与在ZYGO干涉仪上相比较,球面系统的均方根误差相差0.012λ,峰谷值相差0.051λ。     

双螺旋叠栅条纹检测光束准直性的两种方法

介绍双螺旋叠栅条纹检测光束准直性的基本原理,进一步就双螺旋叠栅条纹的特征参量与被测光束发散角(即光束准直精度)的关系进行分析和推导。在分析双螺旋叠栅条纹进行时,首先采用频域低通滤波提取纯叠栅条纹,然后提取纯叠栅条纹的特征参量。提出两种特征参量的提取方法,一种依次进行傅里叶变换计算相位信息的傅里叶变换方法,另一种是受传统时间相移算法启发而提出的空间相移算法,讨论了在两种方法中极坐标的重采样问题和相应的计算公式,并进行了计算机模拟。结果表明,傅里叶变换方法和空间相移算法实质都是获取叠栅条纹全场趋势的平均值,使最终光束发散角的检测具有很高的精度,对自成像条纹周期的检测误差在±2.8‰以内。     

新型PTP 1B抑制剂喹啉腙及酰腙化合物的合成与活性研究

喹啉腙及喹啉酰腙类化合物具有广泛的生物活性.本文设计合成了29个未见报道的4-(2-芳基)喹啉芳腙和芳酰腙类化合物,采用光吸收检测法测试所合成化合物对蛋白酪氨酸磷酸酶PTP 1B的抑制作用.结果 表明,喹啉腙类化合物对PTP 1B具有显著的酶抑制作用,在20μ g/mL浓度时,有21个化合物对PTP 1B抑制率在80％...     

OMIS图像条带噪音消除方法研究

分析了OMIS高光谱图像条带噪音产生的主要原因及条带噪音的特点.提出了两种改进的空域和小波域OMIS条带噪音消除新方法.比较了实验图像和数据.结果表明,两种新方法均具有良好的消除OMIS条带噪音的能力,并能较好地保持图像的纹理细节信息,效果明显优于原有方法.     

Research on Preparation Methods of Carbon Nanomaterials Based on Self-Assembly of Carbon Quantum Dots

Here, based on self-assembly of carbon quantum dots (CDs), an innovative method to prepare nanomaterials under the action of a metal catalyst was presented. CDs were synthesized by a one-step hydrothermal method with citric acid (CA) as the carbon source, ethylenediamine (EDA) as the passivator and FeSO₄•7H₂O as the pre-catalyst. In the experiment, it was found that the nano-carbon films with a graphene-like structure were formed on the surface of the solution. The structure of the films was studied by high-resolution transmission electron microscopy (HRTEM), Fourier transform infrared (FT-IR), etc. The results demonstrated that the films were formed by the self-assembly of CDs under the action of the gas–liquid interface template and the metal catalyst. Meanwhile, the electrochemical performance of the films was evaluated by linear cyclic voltammetry (CV) and galvanostatic charge discharge (GOD) tests. In addition, the bulk solution could be further reacted and self-assembled by reflux to form a bifunctional magnetic–fluorescent composite material. Characterizations such as X-ray diffractometer (XRD), fluorescence spectra (FL), vibrating sample magnetometer (VSM), etc. revealed that it was a composite of superparamagnetic γ-Fe₂O₃ and CDs. The results showed that self-assembly of CDs is a novel and effective method for preparing new carbon nanomaterials.     

Concurrent suppression of Aβ aggregation and NLRP3 inflammasome activation for treating Alzheimer's disease

Alzheimer''s disease (AD) is a neurodegenerative illness accompanied by severe memory loss, cognitive disorders and impaired behavioral ability. Amyloid β-peptide (Aβ) aggregation and nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome play crucial roles in the pathogenesis of AD. Aβ plaques not only induce oxidative stress and impair neurons, but also activate the NLRP3 inflammasome, which releases inflammatory cytokine IL-1β to trigger neuroinflammation. A bifunctional molecule, 2-[2-(benzo[d]thiazol-2-yl)phenylamino]benzoic acid (BPBA), with both Aβ-targeting and inflammasome-inhibiting capabilities was designed and synthesized. BPBA inhibited self- and Cu²⁺- or Zn²⁺-induced Aβ aggregation, disaggregated the already formed Aβ aggregates, and reduced the neurotoxicity of Aβ aggregates; it also inhibited the activation of the NLRP3 inflammasome and reduced the release of IL-1β in vitro and vivo. Moreover, BPBA decreased the production of reactive oxygen species (ROS) and alleviated Aβ-induced paralysis in transgenic C. elegans with the human Aβ₄₂ gene. BPBA exerts an anti-AD effect mainly through dissolving Aβ aggregates and inhibiting NLRP3 inflammasome activation synergistically.

Bifunctional molecule BPBA inhibits Aβ aggregation and NLRP3 inflammasome activation, thereby decreasing ROS and IL-1β in vitro and vivo; it synergistically prevents Alzheimer''s disease via alleviating Aβ neurotoxicity and reducing neuroinflammation.