陀螺仪装配工艺设计

介绍大批量生产的某型陀螺仪装配工艺设计的过程.经过生产实践证明,提高了工作效率,保证了产品质量,取得了良好的效益.     

对邮件过滤技术发展现状的比较与分析

对自学习的过滤技术进行比较和分析,包括已经商品化的方法和目前还处于理论研究阶段的方法,尤其介绍基于机器学习的过滤技术的发展现状,重点研究该领域内的一些新兴过滤技术.在综合比较了一系列的过滤技术的优缺点之后,分析结果表明基于规则的方法和贝叶斯方法是最有潜力的过滤技术.     

异形结构施工总承包项目中智慧建造技术的综合应用—景德镇御窑博物馆项目

智慧建造的特点就在于依靠IT技术、云技术、新型建造设备等传统建造不具备的资源,达到减少重复性人力劳动的目的,使建造过程处于智能技术的精准控制下,解决了人力难以甚至无法达到的高效建造模式。在位于江西省景德镇市的景德镇御窑博物馆项目中,中建一局团队利用了无人机、Hololens全息眼镜、智能放样机器人以及三维激光扫描仪等智能建造设备,整合出了一套质量控制全过程全过程质量控制的解决方案。     

Caudatin attenuates inflammatory reaction by suppressing JNK/AP-1/NF-κB/caspase-1 pathways in activated HMC-1 cells

One of the interfering factors in Coronavirus disease 2019 (COVID-19) is the cytokine storm, which contributes to hyperinflammation. Mast cells cause COVID-19 hyperinflammation by increasing inflammatory cytokine levels. We investigated whether caudatin, an active compound of Cynanchum auriculatum, could suppress inflammatory response signaling in human mast cell line, HMC-1 cells. Caudatin suppressed activation of c-Jun N-terminal kinase (JNK) and activator protein-1 (AP-1) in HMC-1 cells. Caudatin suppressed nuclear translocation of catalytic subunit (p65) of nuclear factor (NF)-κB by blocking IκBα phosphorylation and degradation. Caudatin also reduced levels of activated-caspase-1 protein and activation of caspase-1. Non-toxic caudatin doses inhibited the mRNA expression and protein synthesis of pro-inflammatory cytokines. A significant finding was that caudatin inhibited JNK/AP-1/NF-κB/caspase-1 signaling molecules, reducing the secretion of inflammatory cytokines. Consequently, we propose that caudatin might be used as a material in health functional foods to alleviate mast cell-mediated inflammatory conditions like COVID-19.     

高Nb X80管线钢焊接热影响区显微组织与韧性

为研究Nb含量对焊接热影响区微观组织和性能的影响,采用熔化极气体保护焊(gas metal arc welding,GMAW)和手工焊条电弧焊(shielded metal arc welding,SMAW)对0.055%Nb和0.075%Nb含量的X80钢管进行环焊. 采用夏比冲击试验和金相分析方法,研究热影响区的微观组织差异和夏比冲击韧性. 并借助扫描电镜和超高温激光共聚焦显微镜分析不同Nb含量X80管体的微观组织对热影响区性能的影响. 结果表明,在0 ℃和−20 ℃时,0.075%Nb和0.055%Nb的X80钢管GMAW环焊接头热影响区均具有较高的冲击韧性,其平均冲击吸收能量均高于150 J. 其中0.055%Nb略高于0.075%Nb的GMAW环焊接头热影响区夏比冲击吸收能量;焊接热输入较低时,0.055%Nb低于0.075%Nb的X80环焊接头粗晶区的韧脆转变温度,具有更好的低温韧性. 焊接热输入较高时,0.075%Nb的X80环焊接头粗晶区具有更高的上平台冲击吸收能量,且上平台温度和韧脆转变温度也更低,其低温韧性也更优异;还发现了X80环焊接头热影响区的冲击韧性不仅与热输入量和热影响区马氏体−奥氏体组织(M-A)的形状、大小、分布有关,而且还受管体中Nb含量、原始的强度与韧性、微观组织状态的遗传影响.

     

Nicotinamide Mononucleotide Protects against Retinal Dysfunction in a Murine Model of Carotid Artery Occlusion

Cardiovascular abnormality-mediated retinal ischemia causes severe visual impairment. Retinal ischemia is involved in enormous pathological processes including oxidative stress, reactive gliosis, and retinal functional deficits. Thus, maintaining retinal function by modulating those pathological processes may prevent or protect against vision loss. Over the decades, nicotinamide mononucleotide (NMN), a crucial nicotinamide adenine dinucleotide (NAD⁺) intermediate, has been nominated as a promising therapeutic target in retinal diseases. Nonetheless, a protective effect of NMN has not been examined in cardiovascular diseases-induced retinal ischemia. In our study, we aimed to investigate its promising effect of NMN in the ischemic retina of a murine model of carotid artery occlusion. After surgical unilateral common carotid artery occlusion (UCCAO) in adult male C57BL/6 mice, NMN (500 mg/kg/day) was intraperitoneally injected to mice every day until the end of experiments. Electroretinography and biomolecular assays were utilized to measure ocular functional and further molecular alterations in the retina. We found that UCCAO-induced retinal dysfunction was suppressed, pathological gliosis was reduced, retinal NAD⁺ levels were preserved, and the expression of an antioxidant molecule (nuclear factor erythroid-2-related factor 2; Nrf2) was upregulated by consecutive administration of NMN. Our present outcomes first suggest a promising NMN therapy for the suppression of cardiovascular diseases-mediated retinal ischemic dysfunction.     

The Integration of Genome-Wide Association Study and Homology Analysis to Explore the Genomic Regions and Candidate Genes for Panicle-Related Traits in Foxtail Millet

Panicle traits are important factors affecting yield, and their improvement has long been a critical goal in foxtail millet breeding. In order to understand the genetic basis of panicle formation, a large-scale genome-wide association study (GWAS) was performed in this study for six panicle-related traits based on 706,646 high-polymorphism SNP loci in 407 accessions. As a result, 87 quantitative trait loci (QTL) regions with a physical distance of less than 100 kb were detected to be associated with these traits in three environments. Among them, 27 core regions were stably detected in at least two environments. Based on rice–foxtail millet homologous comparison, expression, and haplotype analysis, 27 high-confidence candidate genes in the QTL regions, such as Si3g11200 (OsDER1), Si1g27910 (OsMADS6), Si7g27560 (GS5), etc., affected panicle-related traits by involving multiple plant growth regulator pathways, a photoperiod response, as well as panicle and grain development. Most of these genes showed multiple effects on different panicle-related traits, such as Si3g11200 affecting all six traits. In summary, this study clarified a strategy based on the integration of GWAS, a homologous comparison, and haplotype analysis to discover the genomic regions and candidate genes for important traits in foxtail millet. The detected QTL regions and candidate genes could be further used for gene clone and marker-assisted selection in foxtail millet breeding.     

The Protective Effect of Zebularine,an Inhibitor of DNA Methyltransferase,on Renal Tubulointerstitial Inflammation and Fibrosis

Renal fibrosis, the final pathway of chronic kidney disease, is caused by genetic and epigenetic mechanisms. Although DNA methylation has drawn attention as a developing mechanism of renal fibrosis, its contribution to renal fibrosis has not been clarified. To address this issue, the effect of zebularine, a DNA methyltransferase inhibitor, on renal inflammation and fibrosis in the murine unilateral ureteral obstruction (UUO) model was analyzed. Zebularine significantly attenuated renal tubulointerstitial fibrosis and inflammation. Zebularine decreased trichrome, α-smooth muscle actin, collagen IV, and transforming growth factor-β1 staining by 56.2%. 21.3%, 30.3%, and 29.9%, respectively, at 3 days, and by 54.6%, 41.9%, 45.9%, and 61.7%, respectively, at 7 days after UUO. Zebularine downregulated mRNA expression levels of matrix metalloproteinase (MMP)-2, MMP-9, fibronectin, and Snail1 by 48.6%. 71.4%, 31.8%, and 42.4%, respectively, at 7 days after UUO. Zebularine also suppressed the activation of nuclear factor-κB (NF-κB) and the expression of pro-inflammatory cytokines, including tumor necrosis factor-α, interleukin (IL)-1β, and IL-6, by 69.8%, 74.9%, and 69.6%, respectively, in obstructed kidneys. Furthermore, inhibiting DNA methyltransferase buttressed the nuclear expression of nuclear factor (erythroid-derived 2)-like factor 2, which upregulated downstream effectors such as catalase (1.838-fold increase at 7 days, p < 0.01), superoxide dismutase 1 (1.494-fold increase at 7 days, p < 0.05), and NAD(P)H: quinone oxidoreduate-1 (1.376-fold increase at 7 days, p < 0.05) in obstructed kidneys. Collectively, these findings suggest that inhibiting DNA methylation restores the disrupted balance between pro-inflammatory and anti-inflammatory pathways to alleviate renal inflammation and fibrosis. Therefore, these results highlight the possibility of DNA methyltransferases as therapeutic targets for treating renal inflammation and fibrosis.     

4-O-Methylascochlorin-Mediated BNIP-3 Expression Controls the Balance of Apoptosis and Autophagy in Cervical Carcinoma Cells

4-O-methylascochlorin (MAC) is a 4-fourth carbon-substituted derivative of ascochlorin, a compound extracted from a phytopathogenic fungus Ascochyta viciae. MAC induces apoptosis and autophagy in various cancer cells, but the effects of MAC on apoptosis and autophagy in cervical cancer cells, as well as how the interaction between apoptosis and autophagy mediates the cellular anticancer effects are not known. Here, we investigated that MAC induced apoptotic cell death of cervical cancer cells without regulating the cell cycle and promoted autophagy by inhibiting the phosphorylation of serine-threonine kinase B (Akt), mammalian target of rapamycin (mTOR), and 70-kDa ribosomal protein S6 kinase (p70S6K). Additional investigations suggested that Bcl-2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP-3), but not Hypoxia-inducible factor 1 alpha (HIF-1α), is a key regulator of MAC-induced apoptosis and autophagy. BNIP-3 siRNA suppressed MAC-induced increases in cleaved- poly (ADP-ribose) polymerase (PARP) and LC3II expression. The pan-caspase inhibitor Z-VAD-FMK suppressed MAC-induced cell death and enhanced MAC-induced autophagy. The autophagy inhibitor chloroquine (CQ) enhanced MAC-mediated cell death by increasing BNIP-3 expression. These results indicate that MAC induces apoptosis to promote cell death and stimulates autophagy to promote cell survival by increasing BNIP-3 expression. This study also showed that co-treatment of cells with MAC and CQ further enhanced the death of cervical cancer cells.