Research on motor rotation anomaly detection based on improved VMD algorithm

Purpose–The electromechanical brake system is leading the latest development trend in railway braking technology.The tolerance stack-up generated during the assembly and production process catalyzes the slight geometric dimensioning and tolerancing between the motor stator and rotor inside the electromechanical cylinder.The tolerance leads to imprecise brake control,so it is necessary to diagnose the fault of the motor in the fully assembled electromechanical brake system.This paper aims to present improved variational mode decomposition(VMD)algorithm,which endeavors to elucidate and push the boundaries of mechanical synchronicity problems within the realm of the electromechanical brake system.Design/methodology/approach–The VMD algorithm plays a pivotal role in the preliminary phase,employing mode decomposition techniques to decompose the motor speed signals.Afterward,the error energy algorithm precision is utilized to extract abnormal features,leveraging the practical intrinsic mode functions,eliminating extraneous noise and enhancing the signal’s fidelity.This refined signal then becomes the basis for fault analysis.In the analytical step,the cepstrum is employed to calculate the formant and envelope of the reconstructed signal.By scrutinizing the formant and envelope,the fault point within the electromechanical brake system is precisely identified,contributing to a sophisticated and accurate fault diagnosis.Findings–This paper innovatively uses the VMD algorithm for the modal decomposition of electromechanical brake(EMB)motor speed signals and combines it with the error energy algorithm to achieve abnormal feature extraction.The signal is reconstructed according to the effective intrinsic mode functions(IMFS)component of removing noise,and the formant and envelope are calculated by cepstrum to locate the fault point.Experiments show that the empirical mode decomposition(EMD)algorithm can effectively decompose the original speed signal.After feature extraction,signal enhancement and fault identification,the motor mechanical fault point can be accurately located.This fault diagnosis method is an effective fault diagnosis algorithm suitable for EMB systems.Originality/value–By using this improved VMD algorithm,the electromechanical brake system can precisely identify the rotational anomaly of the motor.This method can offer an online diagnosis analysis function during operation and contribute to an automated factory inspection strategy while parts are assembled.Compared with the conventional motor diagnosis method,this improved VMD algorithm can eliminate the need for additional acceleration sensors and save hardware costs.Moreover,the accumulation of online detection functions helps improve the reliability of train electromechanical braking systems.

液相色谱-四极杆-飞行时间质谱法快速筛查化妆品中8种亚硝胺

建立了液相色谱-四极杆-飞行时间质谱(LC-QTOF-MS)快速筛查和定量测定化妆品中8种亚硝胺的方法。化妆品经饱和氯化钠分散均匀后,加二氯甲烷涡旋提取,在室温下用氮气吹干二氯甲烷并以甲醇复溶后进样分析;待测物以甲醇和水作为流动相进行梯度洗脱,在Agilent Poroshell 120 SB-C_(18)色谱柱上分离,采用大气压化学离子源,正离子信息依赖扫描(IDA)模式采集,同时获得了目标化合物的一级和二级质谱信息,采用Library view软件构建了8种亚硝胺的高分辨质谱数据库,将采集的结果与数据库比对实现了化妆品中8种亚硝胺的快速筛查。实验优化了样品前处理方法,经方法学考察,建立了化妆品中8种亚硝胺的含量测定方法。结果表明,与其他方法相比,该前处理方法既能达到净化目的,回收率还较高;在优化的条件下,8种亚硝胺在5~100 ng/m L范围内线性关系均良好(r≥0.999);在高(0.50 mg/kg)、中(0.10 mg/kg)、低(0.03 mg/kg)3个加标水平下,平均回收率在85.1%~113.1%之间,相对标准偏差(RSD)为1.4%~6.6%;检出限在0.0010~0.0200 mg/kg之间,定量限在0.0030~0.0600 mg/kg之间。该法前处理方式简便,分析时间短,可实现缺乏标准品的情况下对目标化合物的快速筛查,方法灵敏度和准确度均较高,适用于化妆品中痕量亚硝胺的检测。

Extremely low friction on gold surface with surfactant molecules induced by surface potential

An extremely low friction state was observed on the gold surface induced by applying a specific negative potential in cationic surfactant solution.The friction force showed a remarkable reduction from 8.3 to 3.5×10−2 nN(reduced by 99.6%)with increasing the period of negative applied potential,and the final friction coefficient could reduce down to 3×10−4.The extremely low friction state was robust,and it also exhibited an excellent load bearing capacity,which cannot be damaged by a high load.Moreover,the extremely low friction state achieved under negative applied potential could keep stable even after the removal of potential,but failed in a short time,once a specific positive potential was applied.It was demonstrated that there was a stable electro-adsorption of surfactant molecules on the gold surface induced by applying a negative potential,leading to the formation of a bilayer structure on the gold surface.The hydration layers of the bilayer on the gold surface and micelles on the silica probe provided a shear plane with an extremely low shear strength,leading to the extremely low friction state on the gold surface.This study provides a method to achieve extremely low friction state by applied potential.

JARID2 coordinates with the NuRD complex to facilitate breast tumorigenesis through response to adipocyte-derived leptin

Background Proteins containing the Jumonji C(JmjC)domain participated in tumorigenesis and cancer progression.However,the mechanisms underlying this effect are still poorly understood.Our objective was to investigate the role of Jumonji and the AT-rich interaction domain-containing 2(JARID2)—a JmjC family protein—in breast cancer,as well as its latent association with obesity.Methods Immunohistochemistry,The Cancer Genome Atlas,Gene Expression Omnibus,and other databases were used to analyze the expression of JARID2 in breast cancer cells.Growth curve,5-ethynyl-2-deoxyuridine(EdU),colony formation,and cell invasion experiments were used to detect whether JARID2 affected breast cancer cell proliferation and invasion.Spheroidization-based experiments and xenotumor transplantation in NOD/SCID mice were used to examine the association between JARID2 and breast cancer stemness.RNA-sequencing,Kyoto Encyclopedia of Genes and Genomes,and Gene Set Enrichment Analysis were used to identify the cell processes in which JARID2 participates.Immunoaffinity purification and silver staining mass spectrometry were conducted to search for proteins that might interact with JARID2.The results were further verified using co-immunoprecipitation and glutathione S-transferase(GST)pull-down experiments.Using chromatin immunoprecipitation(ChIP)sequencing,we sought the target genes that JARID2 and metastasis-associated protein 1(MTA1)jointly regulated;the results were validated by ChIP-PCR,quantitative ChIP(qChIP)and ChIP-reChIP assays.A coculture experiment was used to explore the interactions between breast cancer cells and adipocytes.Results In this study,we found that JARID2 was highly expressed in multiple types of cancer including breast cancer.JARID2 promoted glycolysis,lipid metabolism,proliferation,invasion,and stemness of breast cancer cells.Furthermore,JARID2 physically interacted with the nucleosome remodeling and deacetylase(NuRD)complex,transcriptionally repressing a series of tumor suppressor genes such as BRCA2 DNA repair associated(BRCA2),RB transcriptional corepressor 1(RB1),and inositol polyphosphate-4-phosphatase type II B(INPP4B).Additionally,JARID2 expression was regulated by the obesity-associated adipokine leptin via Janus kinase 2/signal transducer and activator of transcription 3(JAK2/STAT3)pathway in the breast cancer microenvironment.Analysis of various online databases also indicated that JARID2/MTA1 was associated with a poor prognosis of breast cancer.Conclusion Our data indicated that JARID2 promoted breast tumorigenesis and development,confirming JARID2 as a target for cancer treatment.