Facile preparation and efficient MnxCoy porous nanosheets for the sustainable catalytic process of soot

The pursuit of high-performance is worth considerable effort in catalysis for energy efficiency and environmental sustainability. To develop redox catalysts with superior performance for soot combustion, a series of Mn_(x)Co_(y) oxides were synthesized using MgO template substitution.This method greatly improves the preparation and catalytic efficiency and is more in line with the current theme of green catalysts and sustainable development. The resulting Mn_(1)Co_(2.3) has a strong activation capability of gaseous oxygen due to a high concentration of Co^(3+) and Mn^(3+). The Mn doping enhanced the intrinsic activity by prompting oxygen vacancy formation and gaseous oxygen adsorption. The nanosheet morphology with abundant mesoporous significantly increased the solid–solid contact efficiency and improved the adsorption capability of gaseous reactants. The novel design of Mn_(1)Co_(2.3)oxide enhanced its catalytic performance through a synergistic effect of Mn doping and the porous nanosheet morphology, showing significant potential for the preparation of high-performance soot combustion catalysts.

Artificial neural network-based one-equation model for simulation of laminar-turbulent transitional flow

A mapping function between the Reynolds-averaged Navier-Stokes mean flow variables and transition intermittency factor is constructed by fully connected artificial neural network(ANN),which replaces the governing equation of the intermittency factor in transition-predictive Spalart-Allmaras(SA)-γmodel.By taking SA-γmodel as the benchmark,the present ANN model is trained at two airfoils with various angles of attack,Mach numbers and Reynolds numbers,and tested with unseen airfoils in different flow states.The a posteriori tests manifest that the mean pressure coefficient,skin friction coefficient,size of laminar separation bubble,mean streamwise velocity,Reynolds shear stress and lift/drag/moment coefficient from the present two-way coupling ANN model almost coincide with those from the benchmark SA-γmodel.Furthermore,the ANN model proves to exhibit a higher calculation efficiency and better convergence quality than traditional SA-γmodel.

清洗刷材质与刷洗速度对内镜导光软管内吸引管道清洗质量的影响

目的富士胃镜EG-450WR5与富士结肠镜EC-600WM导光软管内吸引管道的长度一致,选取1.70 m的导光软管内的吸引管道,分析不同刷洗速度与不同材质清洗刷对相同长度的胃镜和结肠镜导光软管内吸引管道清洗质量的影响,探讨内镜导光软管内吸引管道最佳的刷洗速度与清洗刷材质.方法选取该院内镜室2017年3月-2017年9月应用的160条内镜,胃镜EG-450WR5和结肠镜EC-600WM各80条,随机分为4组(A、B、C和D组),每组又分为两组(Ⅰ组,Ⅱ组),塑料材质海绵刷头清洗刷(Ⅰ组)和钢丝材质塑料刷头清洗刷(Ⅱ组),每组中均包括20条胃镜和20条肠镜.应用不同材质的清洗刷对4组(A、B、C和D组)采取速度分别为0.57、0.34、0.21和0.17 m/s,耗时分别用3、5、8和10 s,每条均进行100人次的清洗之后,对吸引管道进行菌落数监测,从而得出最佳的刷洗速度.对自购的8条导光软管内的吸引管道采用的速度分别为0.57、0.34、0.21和0.17 m/s,应用不同材质(塑料材质海绵刷头清洗刷;钢丝材质塑料刷头清洗刷)对吸引管道进行100次的清洗,之后用手术剪刀纵向抛开吸引管道用放大内镜进行观察,查看管道损害程度.结果 C组中钢丝材质塑料刷头速度在0.21 m/s清洗胃镜和结肠镜导光软管内的吸引管道时,细菌采样菌落数明显优于其他3组的清洗效果,差异有统计学意义(P<0.05).对自购的8条导管软管内的吸引管道以4个速度、两种材质的刷子模拟进行100人次刷洗,C组管道内壁损坏程度优于其他3组.结论采用钢丝材质塑料刷头的清洗刷、刷洗速度在0.21 m/s(清洗时间为8 s),对胃镜和结肠镜导光软管内吸引管道清洗质量最佳.

Activation of paternally expressed imprinted genes in newly derived germline-competent mouse parthenogenetic embryonic stem cell lines

单性生殖的胚胎的茎(足) 细胞为学习位于印的 genomic 下面的分子的机制提供一个珍贵试管内模型系统。然而，足房间的 thepluripotency 和父亲一般地表示的印的基因的表示侧面一直不是充分探索了。在这研究，三根老鼠足房间线被建立，在扩大文化的这些房间的区别潜力被评估。无差别的房间有正常核型和同型结合的染色体，并且表示了 ES-cell-specific 分子的标记。房间在超过 50 个段落以后仍然保持无差别并且展出了 pluripotentdifferentiation 能力。确定的 ES 房间的所有三根线生产了 teratomas；ES 房间的二根线生产了怪物和细菌线传播。而且，在这些房间的父亲一般地表示的印的基因 Snrpn， U2af1-rs1， Peg3，影响， Zfp127， Dlk1 和 Mest 的激活被检测。父亲一般地表示的印的基因被发现在单性生殖的联盟者的胚囊阶段被表示的一些激活胚胎试管内，他们的表示水平与扩大的足细胞培养增加了。而且，我们在足房间的这些父亲一般地表示的印的基因的激活在 ther 的甲基化与一个变化被联系的数据表演鼓舞了差别 methylated 区域。这些调查结果为足房间的 thepluripotency 提供直接证据并且在足房间表明在脱氧核糖核酸甲基化模式和父亲一般地表示的印的基因的激活之间的协会。因此，确定的 ES 房间线为在哺乳动物的开发学习 epigenetic 规定提供一个珍贵模型。

TRIB3 promotes pulmonary fibrosis through inhibiting SLUG degradation by physically interacting with MDM2

Pulmonary fibrosis(PF)is the pathological structure of incurable fibroproliferative lung diseases that are attributed to the repeated lung injury-caused failure of lung alveolar regeneration(LAR).Here,we report that repetitive lung damage results in a progressive accumulation of the transcriptional repressor SLUG in alveolar epithelial type II cells(AEC2s).The abnormal increased SLUG inhibits AEC2s from self-renewal and differentiation into alveolar epithelial type I cells(AEC1s).We found that the elevated SLUG represses the expression of the phosphate transporter SLC34A2 in AEC2s,which reduces intracellular phosphate and represses the phosphorylation of JNK and P38 MAPK,two critical kinases supporting LAR,leading to LAR failure.TRIB3,a stress sensor,interacts with the E3 ligase MDM2 to suppress SLUG degradation in AEC2s by impeding MDM2-catalyzed SLUG ubiquitination.Targeting SLUG degradation by disturbing the TRIB3/MDM2 interaction using a new synthetic staple peptide restores LAR capacity and exhibits potent therapeutic efficacy against experimental PF.Our study reveals a mechanism of the TRIB3—MDM2—SLUG—SLC34A2 axis causing the LAR failure in PF,which confers a potential strategy for treating patients with fibroproliferative lung diseases.

(Ca,Ta)共掺杂Ti O_(2)陶瓷巨介电性能及机理

随着社会的飞速发展,微电子器件的功能不断向一体化方向发展,使开发具有高介电常数、低介电损耗、良好频率和温度稳定性的高介电陶瓷受到越来越多的关注。本工作通过固相反应烧结法制备了(Ca,Ta)共掺杂的TiO_(2)陶瓷。采用X射线衍射仪(XRD)、扫描电镜(SEM)及能谱分析仪(EDS)、阻抗分析仪、X射线光电子能谱(XPS)等对(Ca,Ta)共掺杂的TiO_(2)陶瓷性能进行分析研究。结果表明,不同掺杂量的(Ca1/3Ta2/3)_(x )Ti_(O_(1-x))O_(2)陶瓷表面形貌致密度良好,且随掺杂量增加TiO_(2)的(110)主峰逐渐向小角度移动。当x≥7%时,(Ca1/3Ta2/3)_(x) Ti_(O_(1-x))O_(2)陶瓷样品出现CaTi4O9和CaTa4O11。与纯TiO_(2)相比,不同掺杂量的(Ca1/3Ta2/3)_(x) Ti_(O_(1-x))O_(2)陶瓷皆具有巨介电常数;随掺杂量的不断增加,介电常数先升高后降低,但介电损耗变化趋势相反。当掺杂量x=3%时,(Ca1/3Ta2/3)_(x )Ti_(O_(1-x))O_(2)陶瓷获得相对较优异的性能,在1 kHz下,非线性系数高达7.3,这主要是由于Ta5+掺杂使材料内部产生电子,Ca2+掺杂提高了材料内部空位的产生,产成的缺陷偶极子簇可以提高介电性能。

1,25-Dihydroxyvitamin D3 protects obese rats from metabolic syndrome via promoting regulatory T cell-mediated resolution of inflammation

Vitamin D_3 has been found to produce therapeutic effects on obesity-associated insulin resistance and dyslipidemia through its potent anti-inflammatory activity, but the precise immunomodulatory mechanism remains poorly understood. In the present study we found that 1,25-dihydroxyvitamin D_3[1,25(OH)_2D_3], the biologically active form of vitamin D_3, significantly attenuated monosodium glutamate(MSG)-induced obesity and insulin resistance as indicated by body weight reduction, oral glucose tolerance improvement, and a glucose infusion rate increase as detected with hyperinsulinemiceuglycemic clamp. Moreover, 1,25(OH)_2D_3 not only restored pancreatic islet functions but also improved lipid metabolism in insulin-targeted tissues. The protective effects of 1,25(OH)_2D_3 on glycolipid metabolism were attributed to its ability to inhibit an obesity-activated inflammatory response in insulin secretory and targeted tissues, as indicated by reduced infiltration of macrophages in pancreas islets and adipose tissue while enhancing the expression of Tgf-β1 in liver tissue, which was accompanied byincreased infiltration of Treg cells in immune organs such as spleen and lymph node as well as in insulintargeted tissues such as liver, adipose, and muscle. Together, our findings suggest that 1,25(OH)_2D_3 serves as a beneficial immunomodulator for the prevention and treatment of obesity or metabolic syndrome through its anti-inflammatory effects.

Antagonism of toll-like receptor 2 attenuates the formation and progression of abdominal aortic aneurysm

Abdominal aortic aneurysm(AAA) is an inflammatory vascular disorder with high mortality.Accumulating evidence shows that toll-like receptor 2(TLR2) plays a critical role in the regulation of wound-repairing process after tissue injury.We wondered if TLR2 signaling contributed to the pathogenesis of AAA and that targeting TLR2 would attenuate AAA development and progression.In this study,enhanced expression of TLR2 and its ligands were observed in human AAA tissue.Neutralization of TLR2 protected against AAA development and caused established AAA to regress in mouse models of AAA.In addition,TLR2-deficient mice also failed to develop AAA.The prophylactic and therapeutic effects of blocking TLR2 were accompanied by a significant resolution of inflammation and vascular remodeling,as indicated by the decreased expression or activity of MMP-2/9,α-SMA,inflammatory cytokines,and transcription factors NF-κB,AP-1 and STAT1/3 in AAA tissue.Mechanistically,blocking TLR2 decreased the expression and interaction of TLR2 and several endogenousligands,which diminished chronic inflammation and vascular remodeling in the vascular tissue of AAA.Our studies indicate that the interactions between TLR2 and its endogenous ligands contribute to the pathogenesis of AAA and that targeting TLR2 offers great potential toward the development of therapeutic agents against AAA.

TRIB3-GSK-3β interaction promotes lung fibrosis and serves as a potential therapeutic target

Pulmonary fibrosis(PF)is a chronic,progressive,fatal interstitial lung disease with limited available therapeutic strategies.We recently reported that the protein kinase glycogen synthase kinase-3β(GSK-3β)interacts with and inactivates the ubiquitin-editing enzyme A20 to suppress the degradation of the transcription factor CCAAT/enhancer-binding protein beta(C/EBPβ)in alveolar macrophages(AMs),resulting in a profibrotic phenotype of AMs and promoting the development of PF.Here,we showed that chronic lung injury upregulated the stress response protein tribbles homolog 3(TRIB3),which interacted with GSK-3βand stabilized GSK-3βfrom ubiquitination and degradation.Elevated GSK-3βexpression phosphorylated A20 to inhibit its ubiquitin-editing activity,causing the accumulation of C/EBPβand the production of several profibrotic factors in AMs and promoting PF development.Activated C/EBPβ,in turn,increased the transcription of TRIB3 and GSK-3β,thereby establishing a positive feedback loop in AMs.The knockdown of TRIB3 expression or the pharmacologic disruption of the TRIB3-GSK-3βinteraction was an effective PF treatment.Our study reveals an intact profibrotic axis of TRIB3-GSK-3β-A20-C/EBPβin AMs,which represents a target that may provide a promising treatment strategy for PF.

Highlights of the 2nd International Symposium on Tribbles and Diseases: tribbles tremble in therapeutics for immunity, metabolism, fundamental cell biology and cancer

The Tribbles(TRIB) family of pseudokinase proteins has been shown to play key roles in cell cycle, metabolic diseases, chronic inflammatory disease, and cancer development. A better understanding of the mechanisms of TRIB pseudokinases could provide new insights for disease development and help promote TRIB proteins as novel therapeutic targets for drug discovery. At the 2 nd International Symposium on Tribbles and Diseases held on May 7–9, 2018 in Beijing, China, a group of leading Tribbles scientists reported their findings and ongoing studies about the effects of the different TRIB proteins in the areas of immunity, metabolism, fundamental cell biology and cancer. Here, we summarize important and insightful overviews from 4 keynote lectures, 13 plenary lectures and 8 short talks that took place during this meeting. These findings may offer new insights for the understanding of the roles of TRIB pseudokinases in the development of various diseases.

Regulation of immune-related diseases by multiple factors: a meeting report of 2017 International Workshop of the Chinese Academy of Medical Sciences Initiative for Innovative Medicine on Tumor Immunology

Immune cells play key roles in cancer and chronic inflammatory disease. A better understanding of the mechanisms and risks will help develop novel target therapies. At the 2017 International Workshop of the Chinese Academy of Medical Sciences Initiative for Innovative Medicine on Tumor Immunology held in Beijing, China, on May 12, 2017, a number of speakers reported new findings and ongoing studies on immune-related diseases such as cancer, fibrotic disease, diabetes, and others. A considerably insightful overview was provided on cancer immunity, tumor microenvironments,and new immunotherapy for cancer. In addition, chronic inflammatory diseases were discussed. These findings may offer new insights into targeted immunotherapy.

The cell cycle inhibitor P21 promotes the development of pulmonary fibrosis by suppressing lung alveolar regeneration

The cell cycle inhibitor P21 has been implicated in cell senescence and plays an important role in the injury-repair process following lung injury.Pulmonary fibrosis(PF)is a fibrotic lung disorder characterized by cell senescence in lung alveolar epithelial cells.In this study,we report that P21 expression was increased in alveolar epithelial type 2 cells(AEC2 s)in a time-dependent manner following multiple bleomycin-induced PF.Repeated injury of AEC2 s resulted in telomere shortening and triggered P21-dependent cell senescence.AEC2 s with elevated expression of P21 lost their self-renewal and differentiation abilities.In particular,elevated P21 not only induced cell cycle arrest in AEC2 s but also bound to P300 andβ-catenin and inhibited AEC2 differentiation by disturbing the P300-β-catenin interaction.Meanwhile,senescent AEC2 s triggered myofibroblast activation by releasing profibrotic cytokines.Knockdown of P21 restored AEC2-mediated lung alveolar regeneration in mice with chronic PF.The results of our study reveal a mechanism of P21-mediated lung regeneration failure during PF development,which suggests a potential strategy for the treatment of fibrotic lung diseases.

Crosstalk between ferroptosis and stress—Implications in cancer therapeutic responses

Ferroptosis is a newly discovered form of cell death that is characterized by the accumulation of iron‐dependent lipid peroxidation.Research on ferroptosis has seen exponential growth over the past few years.Tumor cells are strongly dependent on iron for their growth,which makes them develop mechanisms to increase iron uptake and inhibit iron output,thereby completing iron accumulation.Ferroptosis can be induced or inhibited by various stresses through multiple mechanisms,making it stands at the crossroads of stresses related cancer cell fate determination.In this review,we give a brief summary of ferroptosis hallmarks and provide a systematic analysis of the current molecular mechanisms and regulatory networks of diverse stress conditions on ferroptosis.We also discuss the relationships between ferroptosis and cancer therapy responses to further understand potential targets and therapeutic strategies for cancer treatment.

Hot working process optimization of Fe-20Mn-19Cr-0.5C-0.6N steel by activation energy, power dissipation and microstructural evolution

Hot deformation behavior of an Fe-20Mn-19Cr-0.5C-0.6N high-nitrogen austenitic steel has been studied by isothermal compression tests in deformation temperature range of 800-1200℃ and strain rate range of 0.01-10 s^-1. Results indicate that the Fe-20Mn-19Cr-0.5C-0.6N steel has high deformation resistance due to strong hindering effect on dislocation moving by nitrogen-induced lattice misfit. The twinning-induced plasticity effect is gradually suppressed with the increase in deformation temperature, and high-temperature plastic deformation mechanism by twinning is gradually replaced by dislocation planar slip. The deformation resistance is up to 343 MPa at deformation conditions of (1000 ℃, 0.01 s^-1), which is over 100 MPa higher than that in martensitic steel and 50 MPa higher than that in austenitic steel. Besides, value of deformation activation energy for the Fe-20Mn-19Cr-0.6N steel is up to 784 kJ mol^-1. Power dissipation efficiency is lower than 0.13, while hot processing map exhibits a very wide range of working area. The optimum hot working process obtains at deformation temperature range of 950-1200℃ and strain rate range of 0.01-10 s^-1, when deformation acti-vation energy is less than 662.6 kJ mol^-1, power dissipation efficiency exceeds 0.22, dynamic recrystallization fraction is over 46.1% and microstructures are without instable characteristics.

A review on DFACS(II):Modeling and analysis of disturbances and noises

This paper presents Part II of a review on DFACS,which specifically focuses on the modeling and analysis of disturbances and noises in DFACSs.In Part I,the system composition and dynamics model of the DFACS were presented.In this paper,we discuss the effects of disturbance forces and noises on the system,and summarize various analysis and modeling methods for these interferences,including the integral method,frequency domain analysis method,and magnitude evaluation method.By analyzing the impact of disturbances and noises on the system,the paper also summarizes the system’s performance under slight interferences.Additionally,we highlight current research difficulties in the field of DFACS noise analysis.Overall,this paper provides valuable insights into the modeling and analysis of disturbances and noises in DFACSs,and identifies key areas for future research.

A review on DFACS(I):System design and dynamics modeling

The Drag-Free and Attitude Control System(DFACS)is a critical platform for various space missions,including high precision satellite navigation,geoscience and gravity field measurement,and space scientific experiments.This paper presents a comprehensive review of over sixty years of research on the design and dynamics model of DFACS.Firstly,we examine the open literature on DFACS and its applications in Drag-Free missions,providing readers with necessary background information on the field.Secondly,we analyze the system configurations and main characteristics of different DFACSs,paying particular attention to the coupling mechanism between the system configuration and dynamics model.Thirdly,we summarize the dynamics modeling methods and main dynamics models of DFACS from multiple perspectives,including common fundamentals and specific applications.Lastly,we identify current challenges and technological difficulties in the system design and dynamics modeling of DFACS,while suggesting potential avenues for future research.This paper aims to provide readers with a comprehensive understanding of the state-of-the-art in DFACS research,as well as the future prospects and challenges in this field.