目前已有一些针对路径跟踪控制中信号时滞问题的研究工作,但这些工作大多针对某种特定的控制方法,而在路径跟踪控制方法中,非线性模型预测控制(Nonlinear model predictive control,NMPC)具有能够显式处理系统约束、便于实现多目标优化...目前已有一些针对路径跟踪控制中信号时滞问题的研究工作,但这些工作大多针对某种特定的控制方法,而在路径跟踪控制方法中,非线性模型预测控制(Nonlinear model predictive control,NMPC)具有能够显式处理系统约束、便于实现多目标优化、能够有效利用被控对象前方参考路径信息等优势,但是针对NMPC路径跟踪控制系统中时滞问题的研究较不成熟,制约了这种控制方法的实际应用.为解决上述问题,开展了以下研究工作.首先构建了能够较好地孤立出时滞影响的类车机器人路径跟踪控制系统.接着分析了信号时滞对NMPC路径跟踪控制系统的影响机理,即时滞会导致控制器产生的控制信号不能适应类车机器人在执行控制信号时所处的位置.然后提出了基于增长NMPC预测时域的时滞影响消减方法,即在迭代周期不变的情况下,在无时滞系统较优预测步数的基础上增加二倍时滞周期比以上的整数.最后通过计算机仿真和实验验证了提出方法的有效性.仿真和实验结果表明,信号时滞对NMPC路径跟踪控制系统存在影响,未考虑时滞的NMPC控制算法能够在无时滞系统中实现高精确性路径跟踪,而在有时滞系统中控制失效.通过增长预测时域可以有效消减信号时滞的影响,在信号时滞约为0.2 s的仿真与实验系统中,基于该方法的NMPC控制器可以保证路径跟踪控制的位移误差幅值不超过0.1258 m,航向误差幅值不超过0.0583 rad.展开更多
目的:应用Walker-Avant经典概念分析法界定孤独症谱系障碍病人社交伪装的概念内涵。方法:使用关键词检索PubMed、Web of Science、Cochrane Library、OVID、EMbase、中国知网、维普中文期刊服务平台、万方数据知识服务平台、中国生物医...目的:应用Walker-Avant经典概念分析法界定孤独症谱系障碍病人社交伪装的概念内涵。方法:使用关键词检索PubMed、Web of Science、Cochrane Library、OVID、EMbase、中国知网、维普中文期刊服务平台、万方数据知识服务平台、中国生物医学数据库等中英文数据库,并进行手工检索相关文献,系统筛选了从建库至2025年3月1日公开发表的与孤独症谱系障碍社交伪装相关的文献,并采用Walker-Avant经典概念分析法进行分析。结果:共纳入58篇文献,其中孤独症谱系障碍病人社交伪装的定义属性包括掩饰特征、补偿策略、同化行为以及内化耻辱;前因包括社会文化因素、个体心理因素、人口学因素以及社会环境因素;后果包括对孤独症病人的积极影响和消极影响,分别是促进社会适应、损害心理健康以及阻碍社会支持和人际关系。结论:通过对孤独症谱系障碍社交伪装进行概念分析,有利于医护人员精准把握孤独症病人的相关病症、优化其诊疗方式,理解病人的社交策略和行为举止,为个性化干预提供相关依据。展开更多
Early life stress correlates with a higher prevalence of neurological disorders,including autism,attention-deficit/hyperactivity disorder,schizophrenia,depression,and Parkinson's disease.These conditions,primarily...Early life stress correlates with a higher prevalence of neurological disorders,including autism,attention-deficit/hyperactivity disorder,schizophrenia,depression,and Parkinson's disease.These conditions,primarily involving abnormal development and damage of the dopaminergic system,pose significant public health challenges.Microglia,as the primary immune cells in the brain,are crucial in regulating neuronal circuit development and survival.From the embryonic stage to adulthood,microglia exhibit stage-specific gene expression profiles,transcriptome characteristics,and functional phenotypes,enhancing the susceptibility to early life stress.However,the role of microglia in mediating dopaminergic system disorders under early life stress conditions remains poorly understood.This review presents an up-to-date overview of preclinical studies elucidating the impact of early life stress on microglia,leading to dopaminergic system disorders,along with the underlying mechanisms and therapeutic potential for neurodegenerative and neurodevelopmental conditions.Impaired microglial activity damages dopaminergic neurons by diminishing neurotrophic support(e.g.,insulin-like growth factor-1)and hinders dopaminergic axon growth through defective phagocytosis and synaptic pruning.Furthermore,blunted microglial immunoreactivity suppresses striatal dopaminergic circuit development and reduces neuronal transmission.Furthermore,inflammation and oxidative stress induced by activated microglia can directly damage dopaminergic neurons,inhibiting dopamine synthesis,reuptake,and receptor activity.Enhanced microglial phagocytosis inhibits dopamine axon extension.These long-lasting effects of microglial perturbations may be driven by early life stress–induced epigenetic reprogramming of microglia.Indirectly,early life stress may influence microglial function through various pathways,such as astrocytic activation,the hypothalamic–pituitary–adrenal axis,the gut–brain axis,and maternal immune signaling.Finally,various therapeutic strategies and molecular mechanisms for targeting microglia to restore the dopaminergic system were summarized and discussed.These strategies include classical antidepressants and antipsychotics,antibiotics and anti-inflammatory agents,and herbal-derived medicine.Further investigations combining pharmacological interventions and genetic strategies are essential to elucidate the causal role of microglial phenotypic and functional perturbations in the dopaminergic system disrupted by early life stress.展开更多
4-Nitrophenol(4-NP),a toxic and persistent pollutant in chemical wastewater,presents significant challenges in degradation and mineralization.Conventional ozone oxidation catalysts are hindered by low efficiency,mass ...4-Nitrophenol(4-NP),a toxic and persistent pollutant in chemical wastewater,presents significant challenges in degradation and mineralization.Conventional ozone oxidation catalysts are hindered by low efficiency,mass transfer constraints and metal leaching,necessitating the development of stable and efficient catalysts.Herein,BCn-H/MS,the derivative of Bi(Ce)-MOF,was prepared by in situ incorporation,thermal decomposition and acid etching.The resulting materials were characterized and employed in catalytic ozonation for the reduction of 4-NP.Under the specific experimental conditions of the O_(3)+BC0.3-H/MS system,the total organic carbon(TOC)and chemical oxygen demand(COD)removal rates of 4-NP were observed to reach 94.6%and 91.8%within 30 min,respectively.These two parameters were improved by raising the initial pH,reducing the pollutant concentration and increasing the catalyst dosage.The abundant oxygen vacancies(OVs)were regarded as the pivotal catalytic site of BC0.3-H/MS,which was conducive to the adsorption of O_(3) and the acceleration of the formation of reactive oxygen species(ROS).The regular hollow square structure effectively boosted the specific surface area,increased OVs exposure and accelerated the adsorption and mass transfer process.The electron paramagnetic resonance(EPR)results demonstrated that the primary ROS engaged in the degradation reaction were⋅OH and⋅O_(2)−.BC0.3-H/MS demonstrated excellent stability and reusability in cyclic experiments.Toxicity analysis revealed that the O_(3)+BC0.3-H/MS system exhibited an effective detoxification effect.Ultimately,the primary degradation pathway of 4-NP was proposed through liquid chromatography-mass spectroscopy(LC-MS)and in-situ diffuse reflectance infrared fourier-transform spectroscopy(DRIFTS)analyses at varying reaction times.展开更多
文摘目的探索加味蜈蚣败毒饮通过影响自噬上游信号通路腺苷酸活化蛋白激酶(adenosine monophosphate activated protein kinase,AMPK)—结节性硬化复合物1/2(tuberous sclerosiscomplex 1/2,TSC1/2)抑制银屑病复发的机制。方法选取30只小鼠,除空白对照组(5只)外,以咪喹莫特二次诱导的方法(每日咪喹莫特乳膏62.5 mg局部涂擦,连续8日后自然恢复30日,再在原皮损消退部位进行8日的二次涂擦)制备复发型银屑病模型小鼠,再将小鼠随机分为模型对照组、西药对照组、中药低、中、高剂量组,每组均为5只小鼠。对各组小鼠进行药物灌胃干预,中药低、中、高剂量组分别灌胃加味蜈蚣败毒饮药液(浓度分别为0.1 g/mL、0.2 g/mL、0.4 g/mL);西药对照组前4天灌胃甲氨蝶呤混悬液(浓度0.003 mg/mL),后4天灌胃生理盐水;模型对照组灌胃等体积生理盐水;空白对照组不做处理。灌胃剂量均为1 mL/20 g体质量,每日2次,连续8天(第47~54天)。灌胃结束后(第54天)取材,取小鼠背部典型皮损组织备用。采用鼠银屑病皮损面积和严重程度指数(mice psoriasis area and severity index,MPASI)对小鼠的皮损状态进行评价;采用脱氧核糖核苷酸末端转移酶介导的dUTP缺口末端标记法(terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling,TUNEL)染色小鼠皮损组织的凋亡细胞;分别采用蛋白印迹法(western blotting,WB)和免疫组化染色法对小鼠皮损组织中AMPKα、TSC1、TSC2蛋白的含量、表达及分布进行检测。结果(1)经咪喹莫特二次诱导,小鼠银屑病样皮损较一次诱导时的出现时间更早(2日<4日),造模完成时其皮损宏观表象更为严重。(2)复发模型药物干预前,其MPASI分值均在24分以上,各剂量中药均能显著改善复发型银屑病模型的MPASI分值,中药高剂量组疗效尤其显著(P<0.05)。(3)药物干预后,复发模型皮损中位于角质层、颗粒层中的凋亡细胞显著增多,细胞凋亡处于主导地位,从而改善皮损肥厚状态。(4)各剂量中药均能通过调控AMPK-TSC1/2信号通路,抑制AMPKα蛋白(P<0.05)和TSC1蛋白(P<0.05)的表达,并促进TSC2蛋白(P<0.05)在复发模型皮损组织中的含量、表达及分布,以此影响银屑病复发的相关机制通路水平,其中以中药高剂量组的作用最为显著(P<0.05),且WB法与免疫组化法检测上述各蛋白的含量及表达结果相互吻合。结论加味蜈蚣败毒饮可能通过调控自噬上游的关键信号通路AMPK-TSC1/2,影响自噬反应对组织驻留记忆T细胞的能量供给,从而抑制细胞在皮损组织中的再激活,降低银屑病的复发。
文摘目的:应用Walker-Avant经典概念分析法界定孤独症谱系障碍病人社交伪装的概念内涵。方法:使用关键词检索PubMed、Web of Science、Cochrane Library、OVID、EMbase、中国知网、维普中文期刊服务平台、万方数据知识服务平台、中国生物医学数据库等中英文数据库,并进行手工检索相关文献,系统筛选了从建库至2025年3月1日公开发表的与孤独症谱系障碍社交伪装相关的文献,并采用Walker-Avant经典概念分析法进行分析。结果:共纳入58篇文献,其中孤独症谱系障碍病人社交伪装的定义属性包括掩饰特征、补偿策略、同化行为以及内化耻辱;前因包括社会文化因素、个体心理因素、人口学因素以及社会环境因素;后果包括对孤独症病人的积极影响和消极影响,分别是促进社会适应、损害心理健康以及阻碍社会支持和人际关系。结论:通过对孤独症谱系障碍社交伪装进行概念分析,有利于医护人员精准把握孤独症病人的相关病症、优化其诊疗方式,理解病人的社交策略和行为举止,为个性化干预提供相关依据。
基金supported by the National Natural Science Foundation of China,Nos.82304990(to NY),81973748(to JC),82174278(to JC)the National Key R&D Program of China,No.2023YFE0209500(to JC)+4 种基金China Postdoctoral Science Foundation,No.2023M732380(to NY)Guangzhou Key Laboratory of Formula-Pattern of Traditional Chinese Medicine,No.202102010014(to JC)Huang Zhendong Research Fund for Traditional Chinese Medicine of Jinan University,No.201911(to JC)National Innovation and Entrepreneurship Training Program for Undergraduates in China,No.202310559128(to NY and QM)Innovation and Entrepreneurship Training Program for Undergraduates at Jinan University,Nos.CX24380,CX24381(both to NY and QM)。
文摘Early life stress correlates with a higher prevalence of neurological disorders,including autism,attention-deficit/hyperactivity disorder,schizophrenia,depression,and Parkinson's disease.These conditions,primarily involving abnormal development and damage of the dopaminergic system,pose significant public health challenges.Microglia,as the primary immune cells in the brain,are crucial in regulating neuronal circuit development and survival.From the embryonic stage to adulthood,microglia exhibit stage-specific gene expression profiles,transcriptome characteristics,and functional phenotypes,enhancing the susceptibility to early life stress.However,the role of microglia in mediating dopaminergic system disorders under early life stress conditions remains poorly understood.This review presents an up-to-date overview of preclinical studies elucidating the impact of early life stress on microglia,leading to dopaminergic system disorders,along with the underlying mechanisms and therapeutic potential for neurodegenerative and neurodevelopmental conditions.Impaired microglial activity damages dopaminergic neurons by diminishing neurotrophic support(e.g.,insulin-like growth factor-1)and hinders dopaminergic axon growth through defective phagocytosis and synaptic pruning.Furthermore,blunted microglial immunoreactivity suppresses striatal dopaminergic circuit development and reduces neuronal transmission.Furthermore,inflammation and oxidative stress induced by activated microglia can directly damage dopaminergic neurons,inhibiting dopamine synthesis,reuptake,and receptor activity.Enhanced microglial phagocytosis inhibits dopamine axon extension.These long-lasting effects of microglial perturbations may be driven by early life stress–induced epigenetic reprogramming of microglia.Indirectly,early life stress may influence microglial function through various pathways,such as astrocytic activation,the hypothalamic–pituitary–adrenal axis,the gut–brain axis,and maternal immune signaling.Finally,various therapeutic strategies and molecular mechanisms for targeting microglia to restore the dopaminergic system were summarized and discussed.These strategies include classical antidepressants and antipsychotics,antibiotics and anti-inflammatory agents,and herbal-derived medicine.Further investigations combining pharmacological interventions and genetic strategies are essential to elucidate the causal role of microglial phenotypic and functional perturbations in the dopaminergic system disrupted by early life stress.
基金supported by the National Natural Science Foundation of China(Regional Fund)(No.51868054)the Natural Science Foundation of Inner Mongolia of China(General Program)(No.2022MS05052).
文摘4-Nitrophenol(4-NP),a toxic and persistent pollutant in chemical wastewater,presents significant challenges in degradation and mineralization.Conventional ozone oxidation catalysts are hindered by low efficiency,mass transfer constraints and metal leaching,necessitating the development of stable and efficient catalysts.Herein,BCn-H/MS,the derivative of Bi(Ce)-MOF,was prepared by in situ incorporation,thermal decomposition and acid etching.The resulting materials were characterized and employed in catalytic ozonation for the reduction of 4-NP.Under the specific experimental conditions of the O_(3)+BC0.3-H/MS system,the total organic carbon(TOC)and chemical oxygen demand(COD)removal rates of 4-NP were observed to reach 94.6%and 91.8%within 30 min,respectively.These two parameters were improved by raising the initial pH,reducing the pollutant concentration and increasing the catalyst dosage.The abundant oxygen vacancies(OVs)were regarded as the pivotal catalytic site of BC0.3-H/MS,which was conducive to the adsorption of O_(3) and the acceleration of the formation of reactive oxygen species(ROS).The regular hollow square structure effectively boosted the specific surface area,increased OVs exposure and accelerated the adsorption and mass transfer process.The electron paramagnetic resonance(EPR)results demonstrated that the primary ROS engaged in the degradation reaction were⋅OH and⋅O_(2)−.BC0.3-H/MS demonstrated excellent stability and reusability in cyclic experiments.Toxicity analysis revealed that the O_(3)+BC0.3-H/MS system exhibited an effective detoxification effect.Ultimately,the primary degradation pathway of 4-NP was proposed through liquid chromatography-mass spectroscopy(LC-MS)and in-situ diffuse reflectance infrared fourier-transform spectroscopy(DRIFTS)analyses at varying reaction times.
