Trimetallic NiFeCr-LDH/MoS2composites as novel electrocatalyst for OER

The development of efficient and stable oxygen evolution reaction (OER) catalysts is an ongoing challenge. In order to solve the problem of low oxygen evolution efficiency of the current OER catalysts, a novel material was synthesized by the incorporation of NiFeCr-LDH and MoS₂, and its structural and electrochemical properties were also investigated. The introduction of MoS₂ improves the electrochemical performance of NiFeCr-LDH. The polarization curve shows that the potential of composite material is only 1.50 V at a current density of 10 mA cm^?2, which is far superior to commercial precious metal catalysts. In addition, the stability experiment shows that the composite material has excellent stability, and the current density has little change after 500 cycles. Furthermore, we found that some metal ions, such as Ni, Cr and Mo, exist in the form of high valence on the surface of NiFeCr-LDH@MoS₂, which is also conducive to the occurrence of oxygen evolution reaction.     

Targeting S1PRs as a Therapeutic Strategy for Inflammatory Bone Loss Diseases—Beyond Regulating S1P Signaling

As G protein coupled receptors, sphingosine-1-phosphate receptors (S1PRs) have recently gained attention for their role in modulating inflammatory bone loss diseases. Notably, in murine studies inhibiting S1PR2 by its specific inhibitor, JTE013, alleviated osteoporosis induced by RANKL and attenuated periodontal alveolar bone loss induced by oral bacterial inflammation. Treatment with a multiple S1PRs modulator, FTY720, also suppressed ovariectomy-induced osteoporosis, collagen or adjuvant-induced arthritis, and apical periodontitis in mice. However, most previous studies and reviews have focused mainly on how S1PRs manipulate S1P signaling pathways, subsequently affecting various diseases. In this review, we summarize the underlying mechanisms associated with JTE013 and FTY720 in modulating inflammatory cytokine release, cell chemotaxis, and osteoclastogenesis, subsequently influencing inflammatory bone loss diseases. Studies from our group and from other labs indicate that S1PRs not only control S1P signaling, they also regulate signaling pathways induced by other stimuli, including bacteria, lipopolysaccharide (LPS), bile acid, receptor activator of nuclear factor κB ligand (RANKL), IL-6, and vitamin D. JTE013 and FTY720 alleviate inflammatory bone loss by decreasing the production of inflammatory cytokines and chemokines, reducing chemotaxis of inflammatory cells from blood circulation to bone and soft tissues, and suppressing RANKL-induced osteoclast formation.     

Ablative Radiotherapy Reprograms the Tumor Microenvironment of a Pancreatic Tumor in Favoring the Immune Checkpoint Blockade Therapy

The low overall survival rate of patients with pancreatic cancer has driven research to seek a new therapeutic protocol. Radiotherapy (RT) is frequently an option in the neoadjuvant or palliative settings for pancreatic cancer treatment. This study explored the effect of RT protocols on the tumor microenvironment (TME) and their consequent impact on anti-programmed cell death ligand-1 (PD-L1) therapy. Using a murine orthotopic pancreatic tumor model, UN-KC-6141, RT-disturbed TME was examined by immunohistochemical staining. The results showed that ablative RT is more effective than fractionated RT at recruiting T cells. On the other hand, fractionated RT induces more myeloid-derived suppressor cell infiltration than ablative RT. The RT-disturbed TME presents a higher perfusion rate per vessel. The increase in vessel perfusion is associated with a higher amount of anti-PD-L1 antibody being delivered to the tumor. Animal survival is increased by anti-PD-L1 therapy after ablative RT, with 67% of treated animals surviving more than 30 days after tumor inoculation compared to a median survival time of 16.5 days for the control group. Splenocytes isolated from surviving animals were specifically cytotoxic for UN-KC-6141 cells. We conclude that the ablative RT-induced TME is more suited than conventional RT-induced TME to combination therapy with immune checkpoint blockade.     

电动汽车用动力电池振动疲劳测试方法开发

动力电池是当前新能源汽车中的核心零件,其性能,安全,可靠与耐久性直接影响整个车辆安全耐久性能,而电池系统的抗振动冲击特性是产品开发设计过程中需要满足的重要指标.文中着重阐述动力电池振动疲劳的测试验证策略与具体实施指导,为电池系统研发和测试工作提供重要参考.     

多式联运对航空客运量的影响分析

多式联运是一种新兴的运输方式,通过整合多种交通资源形成一套完善的体系来提高运输效率.航空客运量可以用来评估民航业的发展状况,根据分析出的影响客运量变化的因素,可以为民航系统的发展提供方向.本文利用多元回归分析法,根据现阶段多式联运发展程度较高的上海虹桥机场数据,分析铁路、轨道、公路和水运的客运量对航空客运量产生的影响.     

水杨酸处理诱导采后甜瓜抗坏血酸-还原型谷胱甘肽循环代谢清除过氧化氢的作用及机制

目的：研究抗坏血酸（ascorbic acid，AsA）-还原型谷胱甘肽（reduced glutathione，GSH）循环代谢在水杨酸处理采后甜瓜诱导的过量H2O2清除过程中的作用。方法：用4 mmol/L水杨酸浸泡‘玉金香’厚皮甜瓜10 min，测定处理后果实常温贮藏过程中丙二醛（malondialdehyde，MDA）含量，分析活性氧的积累水平、超氧化物歧化酶（superoxide dismutase，SOD）和过氧化氢酶（catalase，CAT）活力，以及AsA-GSH循环过程相关酶活力及产物和底物含量。结果：水杨酸处理降低了果实MDA含量，第10天处理组MDA含量较对照组降低14.6%；显著提高了果实O2－·的产生速率和H2O2含量（P＜0.05），其中处理后第2天O2－·的产生速率高出同期对照组的1.9 倍，第6天H2O2含量高出对照组果实29.7%；提高了果实SOD活力，但抑制了CAT活力，说明H2O2的清除可能是依赖于除酶促系统外的其他系统。此外，水杨酸处理提高了果实抗坏血酸过氧化物酶、单脱氢抗坏血酸过氧化物酶、脱氢抗坏血酸还原酶和谷胱甘肽还原酶的活力，增加了AsA和氧化型谷胱甘肽的含量，降低了脱氢抗坏血酸和GSH的含量。结论：水杨酸处理诱导了厚皮甜瓜果实的氧爆，抑制了MDA产生，由水杨酸诱导产生的过量H2O2主要依靠AsA-GSH循环系统清除。     

Inconel 690传热管GTAW对接焊接头组织及力学性能研究

对Inconel 690传热管材进行钨极气体保护焊(GTAW)对接焊,采用拉伸试验机、压扁试验机和光学显微镜测试和分析传热管焊接接头,同时利用ANSYS软件开展焊接接头在设计工况失压时的一次应力强度校核。研究结果表明:焊缝中心为树枝胞状晶,熔合线附近为粗大柱状晶。室温时接头的平均抗拉强度为619 MPa,平均屈服强度为292 MPa,350℃时接头平均抗拉强度为475 MPa,平均屈服强度为206 MPa,拉伸接头断裂从熔合区开始贯穿整个焊缝组织,呈塑性断裂。压扁试验和反向压扁试验结果表明管接头完好。通过ANSYS分析可知,设计工况下传热管接头350℃许用应力强度150 MPa限值可满足其一次应力强度要求,且裕量较大。     

毫米波三维异质异构集成技术的进展与应用

三维异质异构集成技术是实现电子信息系统向着微型化、高效能、高整合、低功耗及低成本方向发展的最重要方法,也是决定信息化平台中微电子和微纳系统领域未来发展的一项核心高技术。文章详细介绍了毫米波频段三维异质异构集成技术的优势、近年来的发展趋势以及面临的挑战。利用硅基MEMS 光敏复合薄膜多层布线工艺可实现异质芯片的低损耗互连,同时三维集成高性能封装滤波器、高辐射效率封装天线等无源元件,还能很好地处理布线间的电磁兼容和芯片间的屏蔽问题。最后介绍了一款新型毫米波三维异质异构集成雷达及其在远距离生命体征探测方面的应用。     

小型无线场强探测传感器研究

近年来,微波加热因其高效性和清洁无污染等优点广泛应用于各个领域。然而,微波加热的不均匀性限制了微波作为高效加热能源的应用。通过测量和分析加热腔中的电场分布情况可以帮助设计人员改进微波加热腔体设计,提高微波加热的均匀性。现有的场强测量设备均为有线设备,应用场景极为有限。因此,本文提出了一种由探头、接收机和上位机三部分组成的无线场强探测传感器。介绍了无线场强探测传感器的结构和原理,采用横电磁波小室进行校准。通过一系列测量实验表明实测值与标准场强仪测量值一致性较好,可满足工程测量需求。