RNA Sequencing Demonstrates That Circular RNA Regulates Avian Influenza Virus Replication in Human Cells

Circular RNAs (circRNAs) are involved in diverse biological processes. Avian influenza virus (AIV) can cross the species barrier to infect humans. Here, we employed RNA sequencing technology to profile circRNA, microRNA, and mRNA expression in human lung carcinoma cells in response to AIV or human influenza A virus (IAV) infection at viral replication. The analysis revealed that the expression of 475 common circRNAs were significantly regulated. The 381 and 1163 up-regulated circRNAs were induced by AIV at 8 and 16 h, respectively. Subsequently, gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses were also conducted for the AIV-specific up-regulated circRNAs. Moreover, the circRNAs were characterized, of which six were verified by quantitative real-time PCR. We further confirmed that expression of the selected circRNAs only increased following AIV infection. Knocking down the selected circRNAs promoted AIV proliferation, and overexpression of three of the candidate circRNAs restricted AIV replication and proliferation. We further analyzed that AIV-specific up-regulated circRNA mechanisms might function through the ceRNA network to affect the “Endocytosis” pathway and the “Cell cycle process”. These data provide the first expression profile of AIV-specific up-regulated circRNAs and shed new light on the pathogenesis of AIV infection. Our findings also suggest that these circRNAs serve an important role in AIV infection.     

Nanoparticle Emulsions Enhance the Inhibition of NLRP3

Antibacterial delivery emulsions are potential materials for treating bacterial infections. Few studies have focused on the role and mechanism of emulsions in inflammation relief. Therefore, based on our previous analysis, in which the novel and natural Pickering emulsions stabilized by antimicrobial peptide nanoparticles were prepared, the regulation effect of emulsion on inflammasome was explored in silico, in vitro and in vivo. Firstly, the interactions between inflammasome components and parasin I or Pickering emulsion were predicted by molecular docking. Then, the inflammasome stimulation by different doses of the emulsion was tested in RAW 264.7 and THP-1 cells. Finally, in Kunming mice with peritonitis, NLRP3 and IL-1β expression in the peritoneum were evaluated. The results showed that the Pickering emulsion could combine with ALK, casp-1, NEK7, or NLRP3 to affect the assembly of the NLRP3 and further relieve inflammation. LPNE showed a dose–dependent inhibition effect on the release of IL-1β and casp-1. With the concentration of parasin I increased from 1.5 mg/mL to 3 mg/mL, the LDH activity decreased in the chitosan peptide-embedded nanoparticles emulsion (CPENE) and lipid/peptide nanoparticles emulsion (LPNE) groups. However, from 1.5 to 6 mg/mL, LPNE had a dose–dependent effect on the release of casp-1. The CPENE and parasin I-conjugated chitosan nanoparticles emulsion (PCNE) may decrease the release of potassium and chloride ions. Therefore, it can be concluded that the LPNE may inhibit the activation of the inflammasome by decreasing LDH activity, potassium and chloride ions through binding with compositions of NLRP3.     

FgCsn12 Is Involved in the Regulation of Ascosporogenesis in the Wheat Scab Fungus Fusarium graminearum

Fusarium head blight (FHB), caused by the fungal pathogen Fusarium graminearum, is a destructive disease worldwide. Ascospores are the primary inoculum of F. graminearum, and sexual reproduction is a critical step in its infection cycle. In this study, we characterized the functions of FgCsn12. Although the ortholog of FgCsn12 in budding yeast was reported to have a direct interaction with Csn5, which served as the core subunit of the COP9 signalosome, the interaction between FgCsn12 and FgCsn5 was not detected through the yeast two-hybrid assay. The deletion of FgCSN12 resulted in slight defects in the growth rate, conidial morphology, and pathogenicity. Instead of forming four-celled, uninucleate ascospores, the Fgcsn12 deletion mutant produced oval ascospores with only one or two cells and was significantly defective in ascospore discharge. The 3′UTR of FgCsn12 was dispensable for vegetative growth but essential for sexual reproductive functions. Compared with those of the wild type, 1204 genes and 2240 genes were up- and downregulated over twofold, respectively, in the Fgcsn12 mutant. Taken together, FgCsn12 demonstrated an important function in the regulation of ascosporogenesis in F. graminearum.     

Cordycepin Inhibits Growth and Metastasis Formation of MDA-MB-231 Xenografts in Nude Mice by Modulating the Hedgehog Pathway

We previously found that cordycepin inhibits the growth and metastasis formation of MDA-MB-231 cells through the Hedgehog pathway but has not validated this in vivo. In this study, we confirmed cordycepin’s anti-triple-negative breast cancer (TNBC) effect in nude mice and documented its mechanism. We found that cordycepin reduced the volume and weight of MDA-MB-231 xenografts and affected the expression of proliferation-, apoptosis-, epithelial–mesenchymal transition-, and matrix metalloproteinase-related proteins without side effects. RNA sequencing screening, pathway enrichment, and the protein network interaction analysis revealed enriched pathways and targets mainly concentrated on the Hedgehog pathway and its core components of SHH and GLI2. This indicates that the Hedgehog pathway plays a central role in the cordycepin-mediated regulation of growth and metastasis formation in TNBC. The database analysis of the Hedgehog pathway markers (SHH, PTCH1, SMO, GLI1, and GLI2) revealed that the Hedgehog pathway is activated in breast cancer tissues, and its high expression is not conducive to a patient’s survival. Finally, we verified that cordycepin effectively inhibited the Hedgehog pathway in TNBC through Western blotting and immunohistochemistry. This study found that cordycepin could regulate the growth and metastasis formation of TNBC through the Hedgehog pathway in vivo, which provides new insights for targeting and treating breast cancer.     

废弃锂电池电极材料中有价金属的赋存状态

这是一篇冶金工程领域的论文。以废旧磷酸铁锂电池正极粉为对象,开展了以Na₂S₂O₈作为氧化剂,并添加低浓度乙酸作为浸出剂选择性浸锂的研究,考查了Na₂S₂O₈加入量、乙酸浓度、浸出温度、浸出液固比和浸出时间等对锂选择性浸出影响。在乙酸浓度0.3 mol/L、Na₂S₂O₈加入量为理论量的1.1倍,浸出液固比10 mL/g、室温浸出2 h条件下,锂、铁、磷的浸出率分别为98.05%、4.49%和2.46%。     

真空开关电器中接触触点热过程的仿真研究

金属蒸气是真空开关电弧存在的根源, 基于流体动力学理论, 建立真空开关开断初期分离最终电接触触点由固体、金属液桥到金属蒸气相变过程的完整模型。考虑了金属触点的熔化变形边界, 同时关注金属液桥断裂后金属蒸气的扩散过程, 计算结果表明电触点最高温度点出现在接触触点的中心, 也正是金属桥断裂形成的初始位置。金属液桥相变过程中伴随金属蒸气的蒸发, 并在真空环境中迅速扩散, 在阴极斑点形成之前, 金属蒸气密度高达1.092×10²⁵ m^-3, 并沿着扩散半径迅速降低。计算结果表明, 随着电极加载电流的增大, 金属液桥完全断裂时间大大缩短。     

Circadian Rhythm Disorders Aggravate Periodontitis by Modulating BMAL1

Circadian rhythms regulate the body’s homeostasis through the temporal control of tissue-specific circadian rhythm control genes. Circadian rhythm disorders (CRD) affect the expression levels of circadian rhythms-associated genes in brain and muscle aryl hydrocarbon receptor nuclear translocator-like-1(BMAL1), which is thought to contribute to metabolic disorders and an altered immune system. However, the relationship between CRD and the development of periodontitis was poorly reported. Therefore, this study aimed to investigate the role played by BMAL1 in periodontitis. We used a modified multi-platform approach (MMPM) to induce circadian rhythm disturbances in rats to investigate the role of BMAL1 in periodontitis. Our results showed significant downregulation of BMAL1 in the CRD with periodontitis group, significant resorption of alveolar bone, increased osteoclast differentiation, and upregulation of the inflammatory signaling molecule NF-κB. In addition, apoptosis and oxidative stress levels were increased in periodontal tissues. Collectively, our study suggests that BMAL1 is a key regulator in periodontitis exacerbated by CRD and that CRD may lead to the downregulation of BMAL1, thereby exacerbating oxidative stress and apoptosis in periodontal tissues. Our study found that BMAL1 may be associated with the progression of periodontitis and provides a new perspective on the treatment of periodontitis.     

桥梁结构时变可靠度计算的新方法

为提高桥梁结构时变可靠度的计算效率,该文提出了新的计算方法。该方法基于结构时变可靠度分析的基本理论,利用Taylor级数展开,将可靠度计算从传统的积分运算形式转换为代数运算的形式,从而简化计算过程,提高计算效率。为了考虑桥梁初始承载力和衰减过程的不确定性,该文基于全概率方法,给出了计算劣化结构时变可靠度的显式公式。通过将该文方法应用于某钢筋混凝土桥梁进行时变可靠度分析,并与Monte Carlo模拟方法进行对比,表明了该文方法的准确性和高效性。     

太赫兹技术在医学科学中的应用及研究进展

近年来太赫兹光(0.1 THz~10 THz)因其良好的探测能力和非电离特性受到研究者们的关注。根据不同的检测方式和信号处理方法,可分为太赫兹成像技术和太赫兹光谱技术两大类。太赫兹技术在医学科学中发展迅速,其中生物大分子检测和组织成像令人印象深刻。水含量和结构差异是太赫兹成像技术的理论基础,据此可对生物组织进行检测识别。不同的生物组织具有不同的太赫兹特征谱,太赫兹光谱技术通过检测吸收系数、折射系数和反射系数来识别不同的生物分子、细胞或组织。实时、无标记的检测方式有望在临床实践中发挥重要作用,但仍需克服生物安全性不明等困难。综述介绍了太赫兹技术在医学科学中的应用及研究进展,同时探讨了太赫兹技术目前需要克服的难题和潜在的生物安全性问题。

     

适用于离焦状态相机的相位编码标定方法

现阶段通用的相机标定方法需要使用者提供准确的标定板特征点像素坐标。但对某些成像位置特殊的相机而言,一般标定物(如长宽在厘米级别的标定板)的使用范围在其清晰成像范围之外。使用这些相机拍摄一般标定物,只能得到离焦的模糊图像,无法准确提取特征点像素坐标。本文分析了光学系统离焦状态对基于正弦光栅的结构光(简称正弦结构光)相位的影响。利用正弦结构光相位与相机对焦状态无关的性质,提出了一种利用相移法正弦结构光编码的方法,对标定物上特征点进行相位编码,实现了相机在离焦状态下的标定。经过实验验证,标定结果焦距长度与真实值之间最大偏差为0.47%,最大像素重投影误差为0.17 pixels。该方法为具有特殊成像范围的相机的标定提供了一种解决方案。