Pulse-to-pulse periodic signal sorting features and feature extraction in radar emitter pulse sequences

A novel class of periodically changing features hidden in radar pulse sequence environment,named G features,is proposed.Combining fractal theory and Hilbert-Huang transform,the features are extracted using changing characteristics of pulse parameters in radar emitter signals.The features can be applied in modern complex electronic warfare environment to address the issue of signal sorting when radar emitter pulse signal parameters severely or even completely overlap.Experiment results show that the proposed feature class and feature extraction method can discriminate periodically changing pulse sequence signal sorting features from radar pulse signal flow with complex variant features,therefore provide a new methodology for signal sorting.

NOVEL RADAR SIGNAL SORTING METHOD BASED ON GEOMETRIC COVERING

With the increase of complexity of electromagnetic environment and continuous appearance of advanced system radars,signals received by radar reconnaissance receivers become even more intensive and complex.Therefore,traditional radar sorting methods based on neural network algorithms and support vector machine(SVM) cannot process them effectively.Aiming at solving this problem,a novel radar signal sorting method based on the cloud model theory and the geometric covering algorithm is proposed.By applying the geometric covering algorithm to divide input signals into different covering domains based on their distribution characteristics,the method can overcome a typical problem that it is easy for traditional sorting algorithms to fall into the local extrema due to the use of complex nonlinear equation to describe input signals.The method uses the cloud model to describe the membership degree between signals to be sorted and their covering domains,thus it avoids the disadvantage that traditional sorting methods based on hard clustering cannot deinterleave the signal samples with overlapped parameters. Experimental results show that the presented method can effectively sort advanced system radar signals with overlapped parameters in complex electromagnetic environment.

Multi-Parameter Signal Sorting Algorithm Based on Dynamic Distance Clustering

A multi-parameter signal sorting algorithm for interleaved radar pulses in dense emitter environment is presented. The algorithm includes two parts, pulse classification and pulse repetition interval （PRI） analysis. Firstly, we propose the dynamic distance clustering （DDC） for classification. In the clustering algorithm, the multi-dimension features of radar pulse are used for reliable classification. The similarity threshold estimation method in DDC is derived, which contributes to the efficiency of the algorithm. However, DDC has large computation with many signal pulses. Then, in order to sort radar signals in real time, the improved DDC （IDDC） algorithm is proposed. Finally, PRI analysis is adopted to complete the process of sorting. The simulation experiments and hardware implementations show both algorithms are effective.

Network Sorting Algorithm of Multi-Frequency Signal with Adaptive SNR

An signal noise ratio（ SNR） adaptive sorting algorithm using the time-frequency（ TF）sparsity of frequency-hopping（ FH） signal is proposed in this paper. Firstly,the Gabor transformation is used as TF transformation in the system and a sorting model is established under undetermined condition; then the SNR adaptive pivot threshold setting method is used to find the TF single source. The mixed matrix is estimated according to the TF matrix of single source. Lastly,signal sorting is realized through improved subspace projection combined with relative power deviation of source. Theoretical analysis and simulation results showthat this algorithm has good effectiveness and performance.

Exploring the role of N-acetyltransferases in diseases:a focus on N-acetyltransferase 9 in neurodegeneration

Acetyltransferases,required to transfer an acetyl group on protein are highly conserved proteins that play a crucial role in development and disease.Protein acetylation is a common post-translational modification pivotal to basic cellular processes.Close to 80%-90%of proteins are acetylated during translation,which is an irreversible process that affects protein structure,function,life,and localization.In this review,we have discussed the various N-acetyltransferases present in humans,their function,and how they might play a role in diseases.Furthermore,we have focused on N-acetyltransferase 9 and its role in microtubule stability.We have shed light on how N-acetyltransferase 9 and acetylation of proteins can potentially play a role in neurodegenerative diseases.We have specifically discussed the N-acetyltransferase 9-acetylation independent function and regulation of c-Jun N-terminal kinase signaling and microtubule stability during development and neurodegeneration.

Study on the role of JAK/STAT signaling pathway during chicken spermatogonial stem cells generation based on RNA-Seq

Spermatogonia! stem cells（SSCs） form the foundation for spermatogenesis and sustain male fertility.To explore the regulatory mechanisms of chicken SSCs generation,we obtained highly purified chicken embryonic stem cells（ESCs）,primordial germ cells（PGCs） and SSCs by fluorescence-activated cell sorting（FACS）.High-throughput analysis methods（RNA-Seq） were used to sequence the transcriptome level of these cells.Gene ontology and Kyoto encyclopedia of genes and genomes（KEGG） pathway enrichment were used to analyze RNA-Seq results.BMP4 was used to induce chicken ESCs differentiation to SSCs-like cells in vitro.The quantitative real-time（qRT）-PCR was used to detect the expression changes of the key genes.The results showed that 22 relevant critical pathways were found by RNA-Seq,one of them was the Janus kinase/signal transducer and activator of transcription（JAK/STAT） signaling pathway.Total of 103 related genes were detected in this pathway.Protein-protein interactions analysis found that 87 proteins were significantly related to 19 key proteins in this pathway.These 87 proteins were enriched in 21 biological processes and 18 signaling pathways.Moreover,during the differentiation of chicken ESCs to SSCs-like cells induced by BMP4 in vitro,JAK2 and STAT3 were activated.The qRT-PCR results showed that the expression trends of JAK2 and STAT3 were basically the same as in vivo.We concluded that JAK/STAT signaling pathway plays an important role in the process of chicken SSCs generation both in vivo and in vitro;it may achieve its function through multiple biological processes and other related pathways.

SIGNAL MECHANISM OF INHIBITION OF BIFIDOBACTERIA ON GROWTH OF COLON CANCER

Objective: To explore the antitumor mechanisms of bifidobacteria adolescence in vivo. Methods: The content of extracellular signal regulated proteins (ERK)1/2, C-Jun N-terminal kinase (JNK), p38, c-fos and c-jun in nude mouse transplanted large bowel carcinoma was detected by using laser confocal microscopy. The expression of NF-κB was determined by immunohistochemistry. Results: After the nude mouse transplanted tumor was treated with bifidobacteria, the average fluorescent strength of ERK1/2, JNK, c-fos and c-jun was significantly lower than that in tumor control group (P<0.01). The average fluorescent strength of p38 was not obvious difference in the two groups (P>0.05). The positive cell density of NF-κB in large bowel carcinoma transplantation tumors in Bifidobacterium injection group was markedly lower than that in tumor group(P<0.01). Conclusion: bifidobacteria adolescence could markedly decrease the activity of ERK1/2 and JNK, the expression c-fos and c-jun, and the activity of NF-κB.

Smad3 phospho-isoform signaling in hepatitis C virus-related chronic liver diseases

The risk of hepatocellular carcinoma (HCC) development increases as hepatitis virus C (HCV)-related liver diseases progress, especially in patients with active inflammation. Insight into hepatic carcinogenesis have emerged from recent detailed analyses of transforming growth factor-&#x003b2; and c-Jun-N-terminal kinase signaling processes directed by multiple phosphorylated (phospho)-isoforms of a Smad3 mediator. In the course of HCV-related chronic liver diseases, chronic inflammation and host genetic/epigenetic alterations additively shift the hepatocytic Smad3 phospho-isoform signaling from tumor suppression to carcinogenesis, increasing the risk of HCC. Chronic inflammation represents an early carcinogenic step that provides a nonmutagenic tumor-promoting stimulus. After undergoing successful antiviral therapy, patients with chronic hepatitis C could experience a lower risk of HCC as Smad3 phospho-isoform signaling reverses from potential carcinogenesis to tumor suppression. Even after HCV clearance, however, patients with cirrhosis could still develop HCC because of sustained, intense carcinogenic Smad3 phospho-isoform signaling that is possibly caused by genetic or epigenetic alterations. Smad3 phospho-isoforms should assist with evaluating the effectiveness of interventions aimed at reducing human HCC.

Signaling interactions among neurons impact cell fitness and death in Alzheimer's disease

The pathology of Alzheimer’s disease involves a long preclinical period,where the characteristic clinical symptoms of the changes in the brain are undetectable.During the preclinical period,homeostatic mechanisms may help prevent widespread cell death.Evidence has pointed towards selective cell death of diseased neurons playing a potentially protective role.As the disease progresses,dysregulation of signaling pathways that govern cell death contributes to neurodegeneration.Aberrant activation of the c-Jun N-terminal kinase pathway has been established in human and animal models of Alzheimer’s disease caused by amyloid-beta 42-or tau-mediated neurodegeneration.Clonal mosaic studies in Drosophila that examine amyloid-beta 42 in a subset of neurons suggest complex interplay between amyloid-beta 42-expressing and wild-type cells.This review examines the role of c-Jun N-terminal kinase signaling in the context of cell competition and short-range signaling interactions between amyloid-beta 42-expressing and wild-type neurons.Cell competition is a conserved phenomenon regulating tissue integrity by assessing the fitness of cells relative to their neighbors and eliminating suboptimal cells.Somatic clones of amyloid-beta 42 that juxtapose genetically distinct neuronal cell populations show promise for studying neurodegeneration.Generating genetic mosaics with labeled clones of amyloid-beta 42-or tau-expressing and wild-type neurons will allow us to understand how short-range signaling alterations trigger cell death in neurons and thereby contribute to the progression of Alzheimer’s disease.These approaches have the potential to uncover biomarkers for early Alzheimer’s disease detection and new therapeutic targets for intervention.

Arrestin-mediated signaling: Is there a controversy?

The activation of the mitogen-activated protein(MAP) kinases extracellular signal-regulated kinase(ERK)1/2 was traditionally used as a readout of signaling of G protein-coupled receptors(GPCRs) via arrestins, as opposed to conventional GPCR signaling via G proteins. Several recent studies using HEK293 cells where all G proteins were genetically ablated or inactivated, or both non-visual arrestins were knocked out, demonstrated that ERK1/2 phosphorylation requires G protein activity, but does not necessarily require the presence of non-visual arrestins. This appears to contradict the prevailing paradigm. Here we discuss these results along with the recent data on gene edited cells and arrestinmediated signaling. We suggest that there is no real controversy. G proteins might be involved in the activation of the upstream-most MAP3Ks, although in vivo most MAP3K activation is independent of heterotrimeric G proteins, being initiated by receptor tyrosine kinases and/or integrins. As far as MAP kinases are concerned, the best-established role of arrestins is scaffolding of the three-tiered cascades(MAP3K-MAP2 K-MAPK). Thus, it seems likely that arrestins, GPCRbound and free, facilitate the propagation of signals in these cascades, whereas signal initiation via MAP3K activation may be independent of arrestins. Different MAP3Ks are activated by various inputs, some of which are mediated by G proteins, particularly in cell culture, where we artificially prevent signaling by receptor tyrosine kinases and integrins, thereby favoring GPCR-induced signaling. Thus, there is no reason to change the paradigm: Arrestins and G proteins play distinct non-overlapping roles in cell signaling.

Role of JNK signaling pathway in sensitivity to radiotherapy of nasopharyngeal carcinoma

Objective:The aim of the study was to investigate the effect of c-Jun N-terminal protein kinase(JNK) signaling pathway on influencing the sensitivity to radiotherapy of human nasopharyngeal carcinoma CNE cells.Methods:Human nasopharyngeal carcinoma CNE multicellular spheroids(MCS) were constructed with three dimensional cell culture methods.Western blot was employed to analyze the activity of JNK signaling pathway in MCS after X-ray irradiation,and the expression of caspase-3 protein before and after using SP600125(a special inhibitor of JNK).X-ray induced cell apoptosis in MCS before and after treated with SP600125 were detected by TUNEL.Results:The level of JNK phosphorylation in MCS was a dynamic course after radiation,and there was a phosphorylation peaks at 2 h later,the apoptotic rate of MCS(P < 0.05) and the expression of caspase-3 protein(P < 0.05) were significantly increased after treated with SP600125.Conclusion:The transient activation of JNK played a important role in sensitivity to radiotherapy of CNE MCS via mediating survival signals,blocking this pathway accelerate cell apoptosis,which may be related to the increased expression of caspase-3.

基于改进Fuzzy ART的自适应雷达信号分选

侦察接收机对获取的辐射源波形去交织以分离不同信号,称为信号分选,是电磁频谱战系统的核心技术.复杂电磁环境下脉冲流密度大、时域波形及诸域特征严重交叠,导致多数基于无监督模型的信号分选方法难以胜任.提出一种可自适应调整警戒阈值的模糊自适应共振理论(AVT fuzzy ART)聚类算法,基于对属性差异敏感的曼哈顿距离自适应调整警戒阈值,依据在线累积数据得出的辐射源瞬态聚类概率对警戒阈值动态加权.仿真结果表明,该方法能在无历史先验信息的条件下胜任多类别辐射源信号去交错.

偏联系数集对势的雷达信号多站融合分选算法

针对现有分选算法或多或少存在依赖先验信息或者难以适应多功能雷达的情况,提出基于偏联系数集对势的雷达信号多站融合分选算法。从数学领域的集对分析中引入偏联系数参数建立聚类模型,在此基础上通过多站协同方式,利用到达时间差参数对聚类结果进行决策级融合。经过实测数据及仿真验证,在无须任何先验信息的情况下,该算法可适应搜索捕获跟踪等多功能雷达体制,实现雷达脉冲信号的精确聚类与融合,在干扰脉冲比例不高于60%的情况下,分选正确率达97%以上。

基于脉冲间隔分布矩阵的抗抖性改进算法

为解决利用脉冲间隔分布矩阵(PIDM)进行分选无抗抖性的问题,提出了一种改进算法.借鉴改进PRI变换法交叠PRI箱的思想,以PIDM矩阵中PRI箱交叠范围内的幅度之和替代元素幅度,以此进行主周期行、子序列行和门限计算,并对门限的计算方式进行了改进,对过门限的值进行聚类分析,以簇中均值(子序列提取)或最小值(主周期提取)作为真实PRI值.研究结果表明,改进算法在基本保持了原算法分选成功率的基础上,具有一定的抗抖性(5%~10%),并也能适应于多部辐射源的复杂环境.

基于自适应滑动窗均值偏移算法的雷达信号分选

为了应对复杂体制雷达信号分选的要求,提升信号分选的速度和准确性,解决传统信号分选方法的弊端,本文将均值偏移聚类算法引入雷达信号分选,通过改进算法引入滑动窗的自适应更新摆脱了传统分选方法对预设参数的依赖。实验结果表明:自适应滑动窗均值偏移算法在分选准确性和速度上综合表现优于用于对比的传统分选方法,对不同密度的雷达数据集和在脉冲丢失的情况下都可实现较好的分选效果,对捷变频雷达的分选效果良好,并可推知对其他类似体制的雷达均有良好分选效果。本文研究成果可应用于大量数据的多体制雷达的分选优化。

基于扫描波束特征的信号分选算法研究

针对传统分选算法处理维度不足而产生的电磁参数交叠信号分选准确率低的难题,提出一种基于扫描波束特征的信号分选算法。在对天线扫描波束进行理论分析的基础上,利用不同辐射源之间天线扫描波束的差异对目标进行分选。算法首先提取了信号的主瓣包络簇,然后计算了主瓣包络簇的持续时间,最后对主瓣包络簇的持续时间进行聚类,克服了传统分选对电磁参数的依赖。仿真数据验证表明,与传统分选算法相比,本算法可有效提升电磁参数交叠目标的信号分选能力,分选准确率可提升35%以上。

基于重频熵的自适应方位聚类算法研究

针对传统方位聚类算法由于采用固定门限而难以准确对密集方位目标进行准确分选的难题,提出一种基于重频熵的自适应方位聚类算法。算法首先定义了重频熵数学模型,然后采用一系列不同的方位门限对脉冲进行聚类,并依据重频熵对不同方位门限的脉冲聚类结果进行度量,最后选取最优方位门限对脉冲进行聚类处理。仿真和实际数据验证表明,本算法可处理得到准确的聚类结果,与传统聚类算法相比本算法在密集信号环境下的聚类准确率可提升15%以上。

基于天线扫描特征分析的信号分选算法研究

针对传统分选算法难以对电磁参数交叠、方位相近的密集分布目标进行准确分选的难题,提出一种基于天线扫描特征分析的信号分选算法。首先利用辐射源天线扫描周期的差异性,将脉冲序列按照一定的单位进行量化,然后根据天线扫描周期的相关性提取属于同一辐射源的脉冲,最后根据主瓣时间间隔的一致性对目标进行确认,克服了传统分选算法对电磁参数和方位的依赖。仿真与实际数据验证表明,与传统分选算法相比,本算法可有效提升参数交叠、且方位密集分布环境下的信号分选能力,信号分选准确率可提升30%以上。

Attention U-Net在雷达信号图像化分选中的应用研究

针对海战场复杂电磁环境对雷达信号分选的挑战,采用改进的U-Net网络结合注意力机制提出新的分选方法。首先,将脉冲描述字转化为图像序列以适应深度学习处理。通过优化U-Net架构,融入注意力机制,有效提升模型对关键脉冲特征的识别与提取能力,实现像素级分类。通过此方法,系统能够精准搜索并归类所有雷达脉冲。实验证明,在海战场复杂电磁环境中,该方法显著提升了雷达信号分选准确率,提供了一种应对强干扰环境下的高效解决方案。这一研究成果证实了Attention U-Net在雷达信号智能分选中的优越性和实用性。

Mitochondrial targeting sequence of magnetoreceptor MagR:More than just targeting

Iron-sulfur clusters(ISC)are essential cofactors for proteins involved in various biological processes,such as electron transport,biosynthetic reactions,DNA repair,and gene expression regulation.ISC assembly protein IscA1(or MagR)is found within the mitochondria of most eukaryotes.Magnetoreceptor(MagR)is a highly conserved A-type iron and iron-sulfur cluster-binding protein,characterized by two distinct types of iron-sulfur clusters,[2Fe-2S]and[3Fe-4S],each conferring unique magnetic properties.MagR forms a rod-like polymer structure in complex with photoreceptive cryptochrome(Cry)and serves as a putative magnetoreceptor for retrieving geomagnetic information in animal navigation.Although the N-terminal sequences of MagR vary among species,their specific function remains unknown.In the present study,we found that the N-terminal sequences of pigeon MagR,previously thought to serve as a mitochondrial targeting signal(MTS),were not cleaved following mitochondrial entry but instead modulated the efficiency with which iron-sulfur clusters and irons are bound.Moreover,the N-terminal region of MagR was required for the formation of a stable MagR/Cry complex.Thus,the N-terminal sequences in pigeon MagR fulfil more important functional roles than just mitochondrial targeting.These results further extend our understanding of the function of MagR and provide new insights into the origin of magnetoreception from an evolutionary perspective.