Multi-Omics Revealed Molecular Mechanisms Underlying Guard Cell Systemic Acquired Resistance

Systemic Acquired Resistance (SAR) improves immunity of plant systemic tissue after local exposure to a pathogen. Guard cells that form stomatal pores on leaf surfaces recognize bacterial pathogens via pattern recognition receptors, such as Flagellin Sensitive 2 (FLS2). However, how SAR affects stomatal immunity is not known. In this study, we aim to reveal molecular mechanisms underlying the guard cell response to SAR using multi-omics of proteins, metabolites and lipids. Arabidopsis plants previously exposed to pathogenic bacteria Pseudomonas syringae pv. tomato DC3000 (Pst) exhibit an altered stomatal response compared to control plants when they are later exposed to the bacteria. Reduced stomatal apertures of SAR primed plants lead to decreased number of bacteria in leaves. Multi-omics has revealed molecular components of SAR response specific to guard cells functions, including potential roles of reactive oxygen species (ROS) and fatty acid signaling. Our results show an increase in palmitic acid and its derivative in the primed guard cells. Palmitic acid may play a role as an activator of FLS2, which initiates stomatal immune response. Improved understanding of how SAR signals affect stomatal immunity can aid biotechnology and marker-based breeding of crops for enhanced disease resistance.     

Human Milk Antibodies against S1 and S2 Subunits from SARS-CoV-2, HCoV-OC43, and HCoV-229E in Mothers with a Confirmed COVID-19 PCR,Viral SYMPTOMS,and Unexposed Mothers

Background: Preexisting immunity to SARS-CoV-2 could be related to cross-reactive antibodies to common human-coronaviruses (HCoVs). This study aimed to evaluate whether human milk antibodies against to S1 and S2 subunits SARS-CoV-2 are cross-reactive to S1 and S2 subunits HCoV-OC43 and HCoV-229E in mothers with a confirmed COVID-19 PCR test, in mothers with previous viral symptoms during COVID-19 pandemic, and in unexposed mothers; Methods: The levels of secretory IgA (SIgA)/IgA, secretory IgM (SIgM)/IgM, and IgG specific to S1 and S2 SARS-CoV-2, and reactive to S1 + S2 HCoV-OC43, and HCoV-229E were measured in milk from 7 mothers with a confirmed COVID-19 PCR test, 20 mothers with viral symptoms, and unexposed mothers (6 Ctl1-2018 and 16 Ctl2-2018) using ELISA; Results: The S2 SARS-CoV-2 IgG levels were higher in the COVID-19 PCR (p = 0.014) and viral symptom (p = 0.040) groups than in the Ctl1-2018 group. We detected a higher number of positive correlations between the antigens and secretory antibodies in the COVID-19 PCR group than in the viral symptom and Ctl-2018 groups. S1 + S2 HCoV-OC43-reactive IgG was higher in the COVID-19 group than in the control group (p = 0.002) but did not differ for the other antibodies; Conclusions: Mothers with a confirmed COVID-19 PCR and mothers with previous viral symptoms had preexisting human milk antibodies against S2 subunit SARS-CoV-2. Human milk IgG were more specific to S2 subunit SARS-CoV-2 than other antibodies, whereas SIgA and SIgM were polyreactive and cross-reactive to S1 or S2 subunit SARS-CoV-2.     

Coagulation Signaling through PAR1 as a Therapeutic Target in Pancreatic Ductal Adenocarcinoma

Pancreatic ductal adenocarcinoma (PDAC) is a highly fatal disease with a 5-year survival rate of less than 10% following diagnosis. The aggressive and invasive properties of pancreatic cancer tumors coupled with poor diagnostic options contribute to the high mortality rate since most patients present with late-stage disease. Accordingly, PDAC is linked to the highest rate of cancer-associated venous thromboembolic disease of all solid tumor malignancies. However, in addition to promoting clot formation, recent studies suggest that the coagulation system in PDAC mediates a reciprocal relationship, whereby coagulation proteases and receptors promote PDAC tumor progression and dissemination. Here, upregulation of tissue factor (TF) by tumor cells can drive local generation of the central coagulation protease thrombin that promotes cell signaling activity through protease-activated receptors (PARs) expressed by both tumor cells and multiple stromal cell subsets. Moreover, the TF-thrombin-PAR1 signaling axis appears to be a major mechanism of cancer progression in general and PDAC in particular. Here, we summarize the current literature regarding the role of PAR1 in PDAC and review possibilities for pharmacologically targeting PAR1 as a PDAC therapeutic approach.     

跳频通信系统的建模与仿真

在Matlab/Simulink仿真的平台上,利用跳频通信基本原理,在给定仿真条件下,建立了跳频通信系统模型,对系统进行了仿真,得到了宽带噪声干扰下的误码率信噪比曲线。通过跳频仿真图形前后对比,得出跳频通信系统的抗干扰能力优于传统的定频通信,在现代通信中有更高可靠性的结论。     

模块化免疫神经网络平衡态检测模型*

基于神经网络原理、免疫系统和遗传算法的相关机理,构造了一个网络安全平衡器。该平衡器建立了抗原与抗体平衡态检测的数学模型、抗原与抗体的促进和抑制函数,提出了安全平衡态的概念,给出了抗原与抗体浓度的计算公式和模块化多层分类处理模型,利用促进、抑制函数和遗传算法适应度函数使已受攻击的网络再次达到一种新的安全平衡状态,这为网络安全提供了一个新的途径。理论证明网络安全方案是有效的。     

一种改进的PID参数整定的研究及仿真

传统PID控制由于依赖于对象的数学模型和控制参数难以精确整定,使其很难适应具有非线性系统的控制。针对非线性系统,本文提出了一种结合免疫的思想改进PSO的PID的控制算法,从而解决PID控制的鲁棒性差及受模型限制的问题,并结合了Matlab强大的矩阵计算和系统仿真功能,对文中实例的PID参数进行了优化整定。仿真结果表明,该控制算法有较强的抗干扰和适应参数变化及鲁棒性和自适应性。     

异常入侵检测系统虚警率问题研究

入侵检测系统的虚警率影响检测结果的可信性.通过分析入侵检测系统的可信问题及异常入侵检测系统的虚警率问题,提出了降低虚警率的方法:基于进程检测行为的入侵检测方法、多检测系统协作工作模式.重点描述了基于人工免疫思想,动态构建正常系统轮廓,抑制虚警率的方法,并对其进行了仿真实验.实验表明,本方法可以提高检测效率,有效降低系统虚警率.     

具有最大代数免疫度的奇数元布尔函数的构造

构造一个具有最大代数免疫度的奇数元布尔函数等价于在某一已知矩阵中寻找一个可逆子矩阵。如何在这一矩阵中有效地寻找可逆子矩阵仍然是一个难题。针对上述问题研究矩阵的性质,简化矩阵的刻画方式,给出构造最大代数免疫度的奇数元布尔函数的构造方法。构造时只需对低维数的向量进行操作,避免了子矩阵可逆性的判断,能够有效地构造具有最大代数免疫度的奇数元布尔函数。     

“免疫软件人”概念及其协商控制模型

在研究生物免疫机理和软件人(SM)技术的基础上,将生物免疫特性融入SM技术中,提出了免疫软件人(ISM)的概念,设计了一种能够对动态网络环境进行实时监控和故障预警的多免疫软件人(MISM)联盟的协商控制模型;在对模型进行形式化描述的基础上,构造出一种新颖的ISM协商控制算法.以此构建的MISM联盟系统具有更强的灵活性、鲁棒性和局部更新能力,是一个适用于动态网络环境的自组织系统.     

带多比特记忆组合生成器的密码分析

带记忆的组合生成器可以提高生成器的代数次数和相关免疫阶数,是一种重要的密钥流生成器。为此,研究带多比特记忆的组合生成器的概率模型,分析带多比特记忆的组合生成器的k阶相关免疫的充分必要条件,计算其输出序列与输入序列相关系数的平方和,并给出平方和的一般计算公式。分析结果表明,满足一定条件的带多比特记忆的组合生成器可以较好地抵抗相关攻击。