针对无公网覆盖区输电线路故障快速上报的需求,设计一种集成北斗短报文与通用分组无线服务(General Packet Radio Service,GPRS)的双模通信故障上报终端。采用双模通信网络自适应冗余接入、输电故障特征数据自适应分包传输及基于事件触...针对无公网覆盖区输电线路故障快速上报的需求,设计一种集成北斗短报文与通用分组无线服务(General Packet Radio Service,GPRS)的双模通信故障上报终端。采用双模通信网络自适应冗余接入、输电故障特征数据自适应分包传输及基于事件触发的终端间歇低功耗运行等关键技术,解决了偏远地区通信网络可接入能力不足、故障数据上报时效性差及终端功耗高等问题。研究结果表明,该终端能够保障无公网覆盖区故障信息的可靠传输,显著提高电网故障处置效率。展开更多
Detecting internal defects,particularly voids behind linings,is critical for ensuring the structural integrity of aging high-speed rail(HSR)tunnel networks.While ground-penetrating radar(GPR)is widely employed,systema...Detecting internal defects,particularly voids behind linings,is critical for ensuring the structural integrity of aging high-speed rail(HSR)tunnel networks.While ground-penetrating radar(GPR)is widely employed,systematic quantification of performance boundaries for air-coupled(A-CGPR)and ground-coupled(G-CGPR)systems within the complex electromagnetic environment of multilayer reinforced HSR tunnels remains limited.This study establishes physics-based quantitative performance limits for A-CGPR and G-CGPR through rigorously validated GPRMax finite-difference time-domain(FDTD)simulations and comprehensive field validation over a 300 m operational HSR tunnel section.Key performance metrics were quantified as functions of:(a)detection distance(A-CGPR:2.0–4.5 m;G-CGPR:≤0.1 m),(b)antenna frequency(A-CGPR:300 MHz;G-CGPR:400/900 MHz),(c)reinforcement configuration(unreinforced,single-layer,multilayer rebar),and(d)void geometry(axial length:0.1–1.0 m;radial depth:0.1–0.5 m).Key findings demonstrate:a.A-CGPR(300 MHz):Reliably detects axial voids≥0.3 m at distances≤3 m in minimally reinforced(single-layer rebar)linings(field R2=0.89).Performance degrades significantly at distances>3 m(>60%signal attenuation at 4.5 m)or under multilayer rebar interference,causing 25%–40%accuracy loss for voids<0.3 m.Optimal distance:2.0–2.5 m.b.G-CGPR(900 MHz):Achieves<5%size measurement error for axial voids≥0.1 m and radial voids≥0.2 m in unreinforced linings.Resolution degrades under multilayer reinforcement due to severe signal attenuation,increasing axial void detection error to 10%–20%for voids≥0.3 m and constraining radial size measurement.c.Synergistic Framework:A hybrid inspection protocol is proposed,integrating A-CGPR(20 km/h)for rapid large-area screening and targeted G-CGPR(3 km/h)for high-resolution verification of identified anomalies.This framework enhances NDT efficiency while reducing estimated lifecycle inspection costs by 34%compared to G-CGPR alone.This research provides the first physics-derived quantitative detection thresholds for A-CGPR and G-CGPR in multi-rebar HSR tunnels,validated through field-correlated simulations.Future work will focus on multi-frequency antenna arrays and deep learning algorithms to mitigate reinforcement interference.The established performance boundaries and hybrid framework offer critical guidance for optimizing tunnel lining inspection strategies in extensive HSR networks.展开更多
从示范中学习(Learning from Demonstration,LfD),是指机器人学习人类的操作工作,相比传统的脚本指令操作机器人更简单,而机器人需要学习人类示范来快速适应环境的变化。对于机器人运动轨迹学习之后进行技能泛化,GMR-GPR生成的轨迹无法...从示范中学习(Learning from Demonstration,LfD),是指机器人学习人类的操作工作,相比传统的脚本指令操作机器人更简单,而机器人需要学习人类示范来快速适应环境的变化。对于机器人运动轨迹学习之后进行技能泛化,GMR-GPR生成的轨迹无法精确通过每个部分起始约束点,基于GMR-GPR算法进行改进,进行增量GMR-GPR技能泛化,在尽可能保持教学动作的真实意图的同时,也能够同时经过约束点,生成的轨迹进一步提高在约束点区域的泛化性,此外,通过执行字母仿真和UR5e机器人实验,验证和分析了所提方法的可用性。结果表明,所改进的方法能够提供可靠的解决方案,在尽可能保留真实演示意图的同时,挽回示教者纠正意愿的损失。展开更多
目的观察GPR120基因对脓毒症进展的作用,探索GPR120基因对胞内多蛋白复合物—NLRP3(NOD-,LRR-and pyrin domain-containing protein 3)及巨噬细胞极化的调控作用。方法收集临床脓毒症患者血液及胸水样本后,采用流式及ELISA实验检测炎症...目的观察GPR120基因对脓毒症进展的作用,探索GPR120基因对胞内多蛋白复合物—NLRP3(NOD-,LRR-and pyrin domain-containing protein 3)及巨噬细胞极化的调控作用。方法收集临床脓毒症患者血液及胸水样本后,采用流式及ELISA实验检测炎症因子及炎症小体相关蛋白表达。利用细菌脂多糖(lipopolysaccharide,LPS)处理C57BL/6小鼠及单核-巨噬细胞株Raw264.7构建体内外脓毒症模型,并通过GPR120基因激动剂TUG891的干预,观察对照组和脓毒症组间GPR120基因、NLRP3炎症小体蛋白及巨噬细胞极化蛋白的表达差异。结果在临床标本中检测发现,与对照组相比脓毒症患者血清中IL-1β等炎症因子表达明显升高(P<0.001),胸水中NLRP3、Caspase-1及IL-1β等炎症小体蛋白的表达水平也明显升高(P均<0.05)。体内实验发现LPS诱导的急性肺损伤动物模型中肺组织内重度炎症表现,肺组织内GPR120基因表达下降,小鼠血清中炎症因子表达上调(P<0.01),炎症小体激活相关蛋白的表达增强,巨噬细胞M1型极化增强。通过TUG891激活GPR120基因,可减轻小鼠及细胞的炎症反应,抑制NLRP3炎症小体激活,促进巨噬细胞M2极化(P<0.01)。体外实验证实了LPS可抑制细胞内GPR120蛋白的表达并促进炎症蛋白的分泌,而TUG891促进GPR120蛋白水平的上调表达并对炎症因子的分泌具有缓解作用(P<0.05)。结论在脓毒症中,GPR120基因激活可抑制NLRP3炎症小体的活化,促进巨噬细胞修复型极化,减轻组织炎症损伤,从而延缓脓毒症的快速进展。展开更多
GPR126也称ADGRG6,是研究较为深入的黏附类G蛋白偶联受体(adhesion G protein-coupled receptors,aGPCRs)成员之一。最初,GPR126被认为是一种与肌肉发育相关的受体,主要在肌肉和骨骼系统中表达;随着研究的深入,人们发现GPR126在哺乳动...GPR126也称ADGRG6,是研究较为深入的黏附类G蛋白偶联受体(adhesion G protein-coupled receptors,aGPCRs)成员之一。最初,GPR126被认为是一种与肌肉发育相关的受体,主要在肌肉和骨骼系统中表达;随着研究的深入,人们发现GPR126在哺乳动物多个组织和器官中表达,并参与胚胎发育、神经系统发育和细胞外基质相互作用等多种生物学过程。GPR126具有典型的aGPCRs的七次跨膜螺旋结构,可介导跨膜信号转导,参与调控细胞增殖、分化和迁移等多种细胞过程。近年来,GPR126新配体的发现为探索其生理功能提供了有价值的工具。然而,目前GPR126在各类疾病中的生物学功能及其作为治疗靶点的潜力仍待进一步研究。该文重点描述GPR126的结构、物种间差异性与保守性、信号转导及其生物学功能,为未来GPR126的研究提供思路和参考。展开更多
本文旨在对3个影响猪达100 kg体重日龄(Age at 100 kg,AGE)和达100 kg体重平均日增重(Average Daily Gain at 100 kg,ADG)的候选基因进行生物信息学分析。运用生物信息学数据库及其软件,分别分析了肉碱O-乙酰转移酶(Carnitine O-acetylt...本文旨在对3个影响猪达100 kg体重日龄(Age at 100 kg,AGE)和达100 kg体重平均日增重(Average Daily Gain at 100 kg,ADG)的候选基因进行生物信息学分析。运用生物信息学数据库及其软件,分别分析了肉碱O-乙酰转移酶(Carnitine O-acetyltransferase,CRAT)、G蛋白偶联受体107(G Protein-Coupled Receptor 107,GPR107)和泛素特异性肽酶20(Ubiquitin Specific Peptidase 20,USP20)3个基因与其编码的产物。结果发现:CRAT基因位于猪的1号染色体,具有15个外显子、14个内含子,共编码626个氨基酸;USP20基因位于猪的1号染色体,具有26个外显子,25个内含子,共编码915个氨基酸;GPR107基因位于猪的1号染色体,具有19个外显子、18个内含子,共编码597个氨基酸;3个蛋白的二级结构主要组成均为无规则卷曲,且均表现出疏水特征,含有磷酸化位点,仅GPR107蛋白检测到信号肽和跨膜结构;猪CRAT、USP20、GPR107在进化过程中与其他哺乳动物之间均具有高度保守性以及序列同源性;CRAT与羟基类固醇17-β脱氢酶4(Hydroxysteroid 17-Beta Dehydrogenase 4,HSD17B4)、囊泡乙酰胆碱转运蛋白(Solute Carrier Family 18 Member A3,SLC18A3)、脂肪酶(Patatin Like Phospholipase Domain Containing 2,PNPLA2)等蛋白互作;USP20与STAM结合蛋白样1(STAM Binding Protein Like 1,STAMBPL1)、β2-肾上腺素能受体(Adrenoceptor Beta 2,ADRB2)、泛素特异性肽酶14(Ubiquitin Specific Peptidase 14,USP14)等蛋白互作;GPR107与LIN52(Lin-52 Homolog,LIN52)、P-选择素(Selectin P,SELP)、G蛋白偶联受体137C(G Protein-Coupled Receptor 137C,GPR137C)等蛋白互作;GO富集分析发现CRAT、USP20、GPR107主要参与脂肪酸的分解代谢、蛋白质稳定性和降解、配子生成过程;CRAT基因在肌肉组织中高表达,USP20基因在下丘脑中高表达,GPR107基因在血管和下丘脑中高表达。本文结果为进一步研究猪生长性状相关的功能基因提供了数据与理论参考。展开更多
In a recent work published in Neuron,Xu et al.identified a novel contribution of G protein-coupled receptor 37-like 1(GPR37L1),which is identified to be expressed by spinal astrocytes,to the regulation of neuropathic ...In a recent work published in Neuron,Xu et al.identified a novel contribution of G protein-coupled receptor 37-like 1(GPR37L1),which is identified to be expressed by spinal astrocytes,to the regulation of neuropathic pain[1].By interacting and enhancing the activity of glutamate transporter-1(GLT-1)in spinal astrocytes,GPR37L1 promotes glutamate uptake by spinal astrocytes and reduces excitatory synaptic transmission in the spinal dorsal horn,all of which contribute to the resolution of chronic neuropathic pain.展开更多
文摘针对无公网覆盖区输电线路故障快速上报的需求,设计一种集成北斗短报文与通用分组无线服务(General Packet Radio Service,GPRS)的双模通信故障上报终端。采用双模通信网络自适应冗余接入、输电故障特征数据自适应分包传输及基于事件触发的终端间歇低功耗运行等关键技术,解决了偏远地区通信网络可接入能力不足、故障数据上报时效性差及终端功耗高等问题。研究结果表明,该终端能够保障无公网覆盖区故障信息的可靠传输,显著提高电网故障处置效率。
基金funded by the Key Project of Science&Technology Research ofChina Academy of Railway Sciences,grant number 2023YJ022.
文摘Detecting internal defects,particularly voids behind linings,is critical for ensuring the structural integrity of aging high-speed rail(HSR)tunnel networks.While ground-penetrating radar(GPR)is widely employed,systematic quantification of performance boundaries for air-coupled(A-CGPR)and ground-coupled(G-CGPR)systems within the complex electromagnetic environment of multilayer reinforced HSR tunnels remains limited.This study establishes physics-based quantitative performance limits for A-CGPR and G-CGPR through rigorously validated GPRMax finite-difference time-domain(FDTD)simulations and comprehensive field validation over a 300 m operational HSR tunnel section.Key performance metrics were quantified as functions of:(a)detection distance(A-CGPR:2.0–4.5 m;G-CGPR:≤0.1 m),(b)antenna frequency(A-CGPR:300 MHz;G-CGPR:400/900 MHz),(c)reinforcement configuration(unreinforced,single-layer,multilayer rebar),and(d)void geometry(axial length:0.1–1.0 m;radial depth:0.1–0.5 m).Key findings demonstrate:a.A-CGPR(300 MHz):Reliably detects axial voids≥0.3 m at distances≤3 m in minimally reinforced(single-layer rebar)linings(field R2=0.89).Performance degrades significantly at distances>3 m(>60%signal attenuation at 4.5 m)or under multilayer rebar interference,causing 25%–40%accuracy loss for voids<0.3 m.Optimal distance:2.0–2.5 m.b.G-CGPR(900 MHz):Achieves<5%size measurement error for axial voids≥0.1 m and radial voids≥0.2 m in unreinforced linings.Resolution degrades under multilayer reinforcement due to severe signal attenuation,increasing axial void detection error to 10%–20%for voids≥0.3 m and constraining radial size measurement.c.Synergistic Framework:A hybrid inspection protocol is proposed,integrating A-CGPR(20 km/h)for rapid large-area screening and targeted G-CGPR(3 km/h)for high-resolution verification of identified anomalies.This framework enhances NDT efficiency while reducing estimated lifecycle inspection costs by 34%compared to G-CGPR alone.This research provides the first physics-derived quantitative detection thresholds for A-CGPR and G-CGPR in multi-rebar HSR tunnels,validated through field-correlated simulations.Future work will focus on multi-frequency antenna arrays and deep learning algorithms to mitigate reinforcement interference.The established performance boundaries and hybrid framework offer critical guidance for optimizing tunnel lining inspection strategies in extensive HSR networks.
文摘从示范中学习(Learning from Demonstration,LfD),是指机器人学习人类的操作工作,相比传统的脚本指令操作机器人更简单,而机器人需要学习人类示范来快速适应环境的变化。对于机器人运动轨迹学习之后进行技能泛化,GMR-GPR生成的轨迹无法精确通过每个部分起始约束点,基于GMR-GPR算法进行改进,进行增量GMR-GPR技能泛化,在尽可能保持教学动作的真实意图的同时,也能够同时经过约束点,生成的轨迹进一步提高在约束点区域的泛化性,此外,通过执行字母仿真和UR5e机器人实验,验证和分析了所提方法的可用性。结果表明,所改进的方法能够提供可靠的解决方案,在尽可能保留真实演示意图的同时,挽回示教者纠正意愿的损失。
文摘目的观察GPR120基因对脓毒症进展的作用,探索GPR120基因对胞内多蛋白复合物—NLRP3(NOD-,LRR-and pyrin domain-containing protein 3)及巨噬细胞极化的调控作用。方法收集临床脓毒症患者血液及胸水样本后,采用流式及ELISA实验检测炎症因子及炎症小体相关蛋白表达。利用细菌脂多糖(lipopolysaccharide,LPS)处理C57BL/6小鼠及单核-巨噬细胞株Raw264.7构建体内外脓毒症模型,并通过GPR120基因激动剂TUG891的干预,观察对照组和脓毒症组间GPR120基因、NLRP3炎症小体蛋白及巨噬细胞极化蛋白的表达差异。结果在临床标本中检测发现,与对照组相比脓毒症患者血清中IL-1β等炎症因子表达明显升高(P<0.001),胸水中NLRP3、Caspase-1及IL-1β等炎症小体蛋白的表达水平也明显升高(P均<0.05)。体内实验发现LPS诱导的急性肺损伤动物模型中肺组织内重度炎症表现,肺组织内GPR120基因表达下降,小鼠血清中炎症因子表达上调(P<0.01),炎症小体激活相关蛋白的表达增强,巨噬细胞M1型极化增强。通过TUG891激活GPR120基因,可减轻小鼠及细胞的炎症反应,抑制NLRP3炎症小体激活,促进巨噬细胞M2极化(P<0.01)。体外实验证实了LPS可抑制细胞内GPR120蛋白的表达并促进炎症蛋白的分泌,而TUG891促进GPR120蛋白水平的上调表达并对炎症因子的分泌具有缓解作用(P<0.05)。结论在脓毒症中,GPR120基因激活可抑制NLRP3炎症小体的活化,促进巨噬细胞修复型极化,减轻组织炎症损伤,从而延缓脓毒症的快速进展。
文摘GPR126也称ADGRG6,是研究较为深入的黏附类G蛋白偶联受体(adhesion G protein-coupled receptors,aGPCRs)成员之一。最初,GPR126被认为是一种与肌肉发育相关的受体,主要在肌肉和骨骼系统中表达;随着研究的深入,人们发现GPR126在哺乳动物多个组织和器官中表达,并参与胚胎发育、神经系统发育和细胞外基质相互作用等多种生物学过程。GPR126具有典型的aGPCRs的七次跨膜螺旋结构,可介导跨膜信号转导,参与调控细胞增殖、分化和迁移等多种细胞过程。近年来,GPR126新配体的发现为探索其生理功能提供了有价值的工具。然而,目前GPR126在各类疾病中的生物学功能及其作为治疗靶点的潜力仍待进一步研究。该文重点描述GPR126的结构、物种间差异性与保守性、信号转导及其生物学功能,为未来GPR126的研究提供思路和参考。
文摘本文旨在对3个影响猪达100 kg体重日龄(Age at 100 kg,AGE)和达100 kg体重平均日增重(Average Daily Gain at 100 kg,ADG)的候选基因进行生物信息学分析。运用生物信息学数据库及其软件,分别分析了肉碱O-乙酰转移酶(Carnitine O-acetyltransferase,CRAT)、G蛋白偶联受体107(G Protein-Coupled Receptor 107,GPR107)和泛素特异性肽酶20(Ubiquitin Specific Peptidase 20,USP20)3个基因与其编码的产物。结果发现:CRAT基因位于猪的1号染色体,具有15个外显子、14个内含子,共编码626个氨基酸;USP20基因位于猪的1号染色体,具有26个外显子,25个内含子,共编码915个氨基酸;GPR107基因位于猪的1号染色体,具有19个外显子、18个内含子,共编码597个氨基酸;3个蛋白的二级结构主要组成均为无规则卷曲,且均表现出疏水特征,含有磷酸化位点,仅GPR107蛋白检测到信号肽和跨膜结构;猪CRAT、USP20、GPR107在进化过程中与其他哺乳动物之间均具有高度保守性以及序列同源性;CRAT与羟基类固醇17-β脱氢酶4(Hydroxysteroid 17-Beta Dehydrogenase 4,HSD17B4)、囊泡乙酰胆碱转运蛋白(Solute Carrier Family 18 Member A3,SLC18A3)、脂肪酶(Patatin Like Phospholipase Domain Containing 2,PNPLA2)等蛋白互作;USP20与STAM结合蛋白样1(STAM Binding Protein Like 1,STAMBPL1)、β2-肾上腺素能受体(Adrenoceptor Beta 2,ADRB2)、泛素特异性肽酶14(Ubiquitin Specific Peptidase 14,USP14)等蛋白互作;GPR107与LIN52(Lin-52 Homolog,LIN52)、P-选择素(Selectin P,SELP)、G蛋白偶联受体137C(G Protein-Coupled Receptor 137C,GPR137C)等蛋白互作;GO富集分析发现CRAT、USP20、GPR107主要参与脂肪酸的分解代谢、蛋白质稳定性和降解、配子生成过程;CRAT基因在肌肉组织中高表达,USP20基因在下丘脑中高表达,GPR107基因在血管和下丘脑中高表达。本文结果为进一步研究猪生长性状相关的功能基因提供了数据与理论参考。
基金supported by the National Natural Science Foundation of China(82474625)Zhejiang Provincial Natural Science Funds(LZ23H270001).
文摘In a recent work published in Neuron,Xu et al.identified a novel contribution of G protein-coupled receptor 37-like 1(GPR37L1),which is identified to be expressed by spinal astrocytes,to the regulation of neuropathic pain[1].By interacting and enhancing the activity of glutamate transporter-1(GLT-1)in spinal astrocytes,GPR37L1 promotes glutamate uptake by spinal astrocytes and reduces excitatory synaptic transmission in the spinal dorsal horn,all of which contribute to the resolution of chronic neuropathic pain.
