双对苯醌的抗氧化活性分析及其固体发酵条件优化

为探索生物活性未知的双对苯醌（2,7-dihydroxy-3,6,9-trimethyl-9H-xanthene-1,4,5,8-tetraone，DTXT）的抗氧化活性，并提高其发酵产量，考察DTXT的还原力以及对超氧阴离子自由基、羟自由基、1,1-二苯基-2-三硝基苯肼（1,1-diphenyl-2-picrylhydrazyl，DPPH）自由基的清除效果，在单因素试验基础上，采用响应面法优化了DTXT产生菌瓶生顶孢霉（Acremonium cavaraeanum）CA022菌株的固体发酵培养基。结果表明：在200 μg/mL质量浓度下，DTXT的还原力与芦丁差异不显著，高于VE和2,6-二叔丁基-4甲基苯酚，对超氧阴离子自由基清除率达到67.00%，对羟自由基清除率达到78.83%，对DPPH自由基清除率达到76.53%。通过响应面试验，得到最佳培养基配方为葡萄糖0.773%、硝酸钠0.185%、H3BO3 0.032%、VB1 100 μg/100 g，在此条件下实际获得的DTXT产量为4 150.8 mg/kg，是优化前产量的（2 864.83 mg/kg）1.45 倍。     

基于完全互补码波形的非零多普勒目标检测

本文将完全互补码(Complete Complementary Code, CCC)应用于多输入多输出(Multiple Input Multiple Output, MIMO)雷达目标探测中，针对具有非零多普勒的多目标检测问题，提出一种基于广义普洛黑-修-莫尔斯(Generalized Prouhet-Thue-Morse, GPTM)序列和二项式系数加权的信号处理方法。该方法分别在发射端和接收端进行处理，在发射端采用GPTM序列设计方法调整脉冲的发射顺序，以降低由多普勒引起的距离旁瓣；在接收端通过二项式设计(Binomial Design, BD)方法为各接收脉冲加上不同权重，扩大目标多普勒附近的清洁区。为综合上述两次处理的优势，将两次处理得到的距离多普勒谱进行逐点最小化处理，得到最终的距离多普勒谱，然后进行有序恒虚警检测。仿真结果表明，本文所提的信号处理方法具有良好的旁瓣抑制效果和多普勒分辨率，能够有效检测出非零多普勒目标。     

温度对变压器绝缘缺陷影响规律的分析及验证

本文中作者研究了温度对油浸式变压器绝缘纸老化水平的影响,开展了频域介电谱测试得出不同的试验温度下绝缘纸的电导率频域谱.推导了温度、电导率和相对介电常数之间的作用情况,并进行实例验证.     

Role of Endocrine-Disrupting Chemicals in the Pathogenesis of Non-Alcoholic Fatty Liver Disease: A Comprehensive Review

Non-alcoholic fatty liver disease (NAFLD) is considered the most common liver disorder, affecting around 25% of the population worldwide. It is a complex disease spectrum, closely linked with other conditions such as obesity, insulin resistance, type 2 diabetes mellitus, and metabolic syndrome, which may increase liver-related mortality. In light of this, numerous efforts have been carried out in recent years in order to clarify its pathogenesis and create new prevention strategies. Currently, the essential role of environmental pollutants in NAFLD development is recognized. Particularly, endocrine-disrupting chemicals (EDCs) have a notable influence. EDCs can be classified as natural (phytoestrogens, genistein, and coumestrol) or synthetic, and the latter ones can be further subdivided into industrial (dioxins, polychlorinated biphenyls, and alkylphenols), agricultural (pesticides, insecticides, herbicides, and fungicides), residential (phthalates, polybrominated biphenyls, and bisphenol A), and pharmaceutical (parabens). Several experimental models have proposed a mechanism involving this group of substances with the disruption of hepatic metabolism, which promotes NAFLD. These include an imbalance between lipid influx/efflux in the liver, mitochondrial dysfunction, liver inflammation, and epigenetic reprogramming. It can be concluded that exposure to EDCs might play a crucial role in NAFLD initiation and evolution. However, further investigations supporting these effects in humans are required.