检索结果-南通市图书馆

Ultrasensitive and point-of-care detection of plasma phosphorylated tau in Alzheimer’s disease using colorimetric and surface-enhanced Raman scattering dual-readout lateral flow assay

引用

Nano Research 2023年第5期16卷 7459-7469页

作者： Liding Zhang Ying su Xiaohan Liang Kai Cao Qingming Luo Haiming Luo Britton Chance Center for Biomedical Photonics Wuhan National Laboratory for OptoelectronicsHuazhong University of Science and Technology(HUST)Wuhan 430074China MoE Key Laboratory for Biomedical Photonics School of Engineering SciencesHuazhong University of Science and TechnologyWuhan 430074China Department of Neurology Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430074China Key Laboratory of Biomedical Engineering of Hainan Province School of Biomedical EngineeringHainan UniversityHaikou 570228China Research Unit of Multimodal Cross scale Neural signal Detection and Imaging Chinese Academy of Medical SciencesHUST-Suzhou Institute for BrainsmaticsJiangsu Industrial Technology Research Institute(JITRI)Suzhou 215123China

Phosphorylation of tau at ser(396,404)(p-tau^(396,404))is one of the earliest phosphorylation events,plasma p-tau^(396,404) level appears to be a potentially promising biomarker of Alzheimer’s disease(AD).The low abundance and easy degradation of p-tau in the plasma make the lateral flow assay(LFA)a suitable choice for point-of-care detection of plasma p-tau^(396,404) levels.Herein,based on our screening of a pair of p-tau^(396,404)-specific antibodies,we developed a colorimetric and surface-enhanced Raman scattering(sERs)dual-readout LFA for the rapid,highly sensitive,robust detection of plasma p-tau^(396,404) levels.This LFA realized a detection limit of 60 pg/mL by the naked eye or 3.8 pg/mL by sERs without cross-reacting with other tau species.More importantly,LFA rapidly and accurately differentiated AD patients from healthy controls,suggesting that it has the potential for clinical point-of-care application in AD diagnosis.This dual-readout LFA has the advantages of simple operation,rapid,ultra-sensitive detection,providing a new way for early AD diagnosis and intervention,especially in primary and community AD screening.

关键词： Alzheimer’s disease p-tau^(396,404) plasma detection surface-enhanced Raman scattering lateral flow assay

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Inhibiting 5-hydroxytryptamine receptor 3 alleviates pathological changes of a mouse model of alzheimer's disease

引用

Neural Regeneration Research 2023年第9期18卷 2019-2028页

作者： Li-Fen Liu Yu-Tong Liu Dan-Dan Wu Jie Cheng Na-Na Li Ya-Ni Zheng Liang Huang Qiong-Lan Yuan Department of Neurology Shanghai Tongji HospitalTongji University School of MedicineShanghaiChina Department of Radiology University of Nebraska Medical CenterOmahaNEUSA Department of Human Anatomy Histology&EmbryologyTongji University School of MedicineShanghaiChina

Extracellular amyloid beta(Aβ) plaques are main pathological feature of Alzheimer’s disease.However,the specific type of neuro ns that produce Aβ peptides in the initial stage of Alzheimer’s disease are unknown.In this study,we found that 5-hydroxytryptamin receptor 3A subunit(HTR3A) was highly expressed in the brain tissue of transgenic amyloid precursor protein and presenilin-1 mice(an Alzheimer’s disease model) and patients with Alzheimer’s disease.To investigate whether HTR3A-positive interneurons are associated with the production of Aβ plaques,we performed double immunostaining and found that HTR3A-positive interneurons were clustered around Aβ plaques in the mouse model.some amyloid precursor protein-positive or β-site amyloid precursor protein cleaving enzyme-1-positive neurites near Aβ plaques were co-localized with HTR3A interneurons.These results suggest that HTR3A-positive interneurons may partially contribute to the generation of Aβ peptides.We treated 5.0-5.5-month-old model mice with tro pisetron,a HTR3 antagonist,for 8 consecutive weeks.We found that the cognitive deficit of mice was partially reversed,Aβ plaques and neuroinflammation we re remarkably reduced,the expression of HTR3 was remarkably decreased and the calcineurin/nuclear factor of activated T-cell 4 signaling pathway was inhibited in treated model mice.These findings suggest that HTR3A interneurons partly contribute to generation of Aβ peptide at the initial stage of Alzheimer’s disease and inhibiting HTR3 partly reve rses the pathological changes of Alzheimer’s disease.

关键词： 5-hydroxytryptamin receptor 3 Alzheimer’s disease amyloid beta plaques calcineurin cognitive deficits HTR3 interneurons iCa2+ nuclear factor of activated T-cells transgenic amyloid precursor protein and presenilin-1 mice tropisetron

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

TMEM16F may be a new therapeutic target for alzheimer's disease

引用

Neural Regeneration Research 2023年第3期18卷 643-651页

作者： Zhi-Qiang Cui Xiao-Ying Hu Tuo Yang Jing-Wei Guan Ying Gu Hui-Yuan Li Hui-Yu Zhang Qing-Huan Xiao Xiao-Hong sun Department of Neurology The Fourth Affiliated Hospital of China Medical UniversityShenyangLiaoning ProvinceChina Department of Ion Channel Pharmacology School of PharmacyChina Medical UniversityShenyangLiaoning ProvinceChina

TMEM16F is involved in many physiological processes such as blood coagulation,cell membrane fusion and bone mineralization.Activation of TMEM16F has been studied in various central nervous system diseases.High TMEM16F level has been also found to participate in microglial phagocytosis and transformation.Microglia-mediated neuroinflammation is a key factor in promoting the progression of Alzheimer’s disease.However,few studies have examined the effects of TMEM16F on neuroinflammation in Alzheimer’s disease.In this study,we established TMEM16F-knockdown AD model in vitro and in vivo to investigate the underlying regulatory mechanism about TMEM16F-mediated neuroinflammation in AD.We performed a Morris water maze test to evaluate the spatial memory ability of animals and detected markers for the microglia M1/M2 phenotype and NLRP3 inflammasome.Our results showed that TMEM16F was elevated in 9-month-old APP/Ps1 mice.After TMEM16F knockdown in mice,spatial memory ability was improved,microglia polarization to the M2 phenotype was promoted,NLRP3 inflammasome activation was inhibited,cell apoptosis and Aβplaque deposition in brain tissue were reduced,and brain injury was alleviated.We used amyloid-beta(Aβ_(25-35))to stimulate human microglia to construct microglia models of Alzheimer’s disease.The levels of TMEM16F,inducible nitric oxide synthase(iNOs),proinflammatory cytokines and NLRP3 inflammasome-associated biomarkers were higher in Aβ_(25-35) treated group compared with that in the control group.TMEM16F knockdown enhanced the expression of the M2 phenotype biomarkers Arg1 and socs3,reduced the release of proinflammatory factors interleukin-1,interleukin-6 and tumor necrosis factor-α,and inhibited NLRP3 inflammasome activation through reducing downstream proinflammatory factors interleukin-1βand interleukin-18.This inhibitory effect of TMEM16F knockdown on M1 microglia was partially reversed by the NLRP3 agonist Nigericin.Our findings suggest that TMEM16F participates in neuroinflammation in Alzheimer’s disease throu

关键词： Alzheimer’s disease Aβplaque inflammatory cytokines M1 phenotype M2 phenotype microglia polarization neuroinflammation NLRP3 inflammasome siRNA TMEM16F

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

An integrative analysis of miRNA and mRNA expression in the brains of alzheimer's disease transgenic mice after real-world PM_(2.5)exposure

引用

Journal of Environmental sciences 2022年第12期34卷 25-40页

作者： Pengfei Fu Yufei Zhao Chuan Dong Zongwei Cai Ruijin Li Ken Kin Lam Yung Department of Biology Hong Kong Baptist UniversityHong Kong SARChina Golden Meditech Center for NeuroRegeneration sciences Hong Kong Baptist UniversityHong Kong SARChina Institute of Environmental science Shanxi UniversityTaiyuan 237016China state Key Laboratory of Environmental and Biological Analysis Hong Kong Baptist UniversityHong Kong SARChina

Fine particulate matter(PM_(2.5))is associated with increased risks of alzheimer's disease(AD),yet the toxicological mechanisms of PM_(2.5)promoting AD remain unclear.In this study,wildtype and APP/Ps1 transgenic mice(AD mice)were exposed to either filtered air(FA)or PM_(2.5)for eight weeks with a real-world exposure system in Taiyuan,China(mean PM_(2.5)concentration in the cage was 61μg/m~3).We found that PM_(2.5)exposure could remarkably aggravate AD mice's ethological and brain ultrastructural damage,along with the elevation of the pro-inflammatory cytokines(IL-6 and TNF-α),Aβ-42 and ACh E levels and the decline of Ch AT levels in the brains.Based on high-throughput sequencing results,some differentially expressed(DE)m RNAs and DE mi RNAs in the brains of AD mice after PM_(2.5)exposure were screened.Using RT-q PCR,seven DE mi RNAs(mmu-mi R-193b-5p,122b-5p,466h-3p,10b-5p,1895,384–5p,and 6412)and six genes(Pcdhgb8,Unc13b,Robo3,Prph,Pter,and Tbata)were evidenced the and verified.Two mi RNA-target gene pairs(mi R-125b-Pcdhgb8 pair and mi R-466h-3p-IL-17Rα/TGF-βR2/Aβ-42/ACh E pairs)were demonstrated that they were more related to PM_(2.5)-induced brain injury.Results of Gene Ontology(GO)pathways and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways predicted that synaptic and postsynaptic regulation,axon guidance,Wnt,MAPK,and m TOR pathways might be the possible regulatory mechanisms associated with pathological response.These revealed that PM_(2.5)-elevated pro-inflammatory cytokine levels and PM_(2.5)-altered neurotransmitter levels in AD mice could be the important causes of brain damage and proposed the promising mi RNA and m RNA biomarkers and potential mi RNA-m RNA interaction networks of PM_(2.5)-promoted AD.

关键词： Fine particulate matter mRNAs miRNAs Brain Alzheimer’s disease APP/Ps1 transgenic mice

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Converging links between adult-onset neurodegenerative Alzheimer’s disease and early life neurodegenerative neuronal ceroid lipofuscinosis?

引用

Neural Regeneration Research 2023年第7期18卷 1463-1471页

作者： Marcel Klein Guido Hermey Institute for Molecular and Cellular Cognition Center for Molecular Neurobiology HamburgUniversity Medical Center Hamburg-EppendorfHamburgGermany

Evidence from genetics and from analyzing cellular and animal models have converged to suggest links between neurodegenerative disorders of early and late life.Here,we summarize emerging links between the most common late life neurodegenerative disease,Alzheimer’s disease,and the most common early life neurodegenerative diseases,neuronal ceroid lipofuscinoses.Genetic studies reported an overlap of clinically diagnosed Alzheimer’s disease and mutations in genes known to cause neuronal ceroid lipofuscinoses.Accumulating data strongly suggest dysfunction of intracellular trafficking mechanisms and the autophagy-endolysosome system in both types of neurodegenerative disorders.This suggests shared cytopathological processes underlying these different types of neurodegenerative diseases.A better understanding of the common mechanisms underlying the different diseases is important as this might lead to the identification of novel targets for therapeutic concepts,the transfer of therapeutic strategies from one disease to the other and therapeutic approaches tailored to patients with specific mutations.Here,we review dysfunctions of the endolysosomal autophagy pathway in Alzheimer’s disease and neuronal ceroid lipofuscinoses and summarize emerging etiologic and genetic overlaps.

关键词： Alzheimer’s disease autophagy Batten disease CLN3 disease dementia endosome lysosome neurodegeneration neuronal ceroid lipofuscinosis presenilin

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Engineered macrophage-biomimetic versatile nanoantidotes for inflammation-targeted therapy against Alzheimer’s disease by neurotoxin neutralization and immune recognition suppression

引用

Bioactive Materials 2023年第8期26卷 337-352页

作者： Meng Cheng Caihua Ye Chunxiao Tian Dongju Zhao Haonan Li Zuhao sun Yuyang Miao Qiang Zhang Junping Wang Yan Dou Department of Radiology and Tianjin Key Laboratory of Functional Imaging Tianjin Medical University General HospitalTianjin300052PR China school of Biomedical Engineering and Technology Tianjin Medical UniversityTianjin300070PR China school of Life sciences Tianjin UniversityTianjin300072PR China Department of Geriatrics Tianjin Medical University General HospitalTianjin Geriatrics InstituteTianjin300052PR China

Immune recognition of excessive neurotoxins by microglia is a trigger for the onset of neuroinflammation in the brain,leading to neurodegeneration in Alzheimer’s disease(AD).Blocking active recognition of microglia while removing neurotoxins holds promise for fundamentally alleviating neurotoxin-induced immune responses,but is very challenging.Herein,an engineered macrophage-biomimetic versatile nanoantidote(OT-Lipo@M)is developed for inflammation-targeted therapy against AD by neurotoxin neutralization and immune recognition suppression.Coating macrophage membranes can not only endow OT-Lipo@M with anti-phagocytic and inflammation-tropism capabilities to target inflammatory lesions in AD brain,but also efficiently reduce neurotoxin levels to prevent them from activating microglia.The loaded oxytocin(OT)can be slowly released to downregulate the expression of immune recognition site Toll-like receptor 4(TLR4)on microglia,inhibiting TLR4-mediated pro-inflammatory signalling cascade.Benefiting from this two-pronged immunosuppressive strategy,OT-Lipo@M exhibits outstanding therapeutic effects on ameliorating cognitive deficits,inhibiting neuronal apoptosis,and enhancing synaptic plasticity in AD mice,accompanied by the delayed hippocampal atrophy and brain microstructural disruption by in vivo 9.4T MR imaging.This work provides new insights into potential AD therapeutics targeting microglia-mediated neuroinflammation at the source.

关键词： Alzheimer’s disease Biomimetic nanomedicine Biological neutralization Immune recognition and response Neuroinflammation-targeted therapy 9.4T MR imaging

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

signaling interactions among neurons impact cell fitness and death in alzheimer's disease

引用

Neural Regeneration Research 2023年第4期18卷 784-789页

作者： Catherine Yeates Prajakta Deshpande Madhuri Kango-singh Amit singh Department of Biology University of DaytonDaytonOHUSA Premedical Program University of DaytonDaytonOHUSA Center for Tissue Regeneration and Engineering at Dayton(TREND) University of DaytonDaytonOHUSA The Integrative science and Engineering Center University of DaytonDaytonOHUSA Center for Genomic Advocacy(TCGA) Indiana State UniversityTerre HauteINUSA

The pathology of Alzheimer’s disease involves a long preclinical period,where the characteristic clinical symptoms of the changes in the brain are undetectable.During the preclinical period,homeostatic mechanisms may help prevent widespread cell death.Evidence has pointed towards selective cell death of diseased neurons playing a potentially protective role.As the disease progresses,dysregulation of signaling pathways that govern cell death contributes to neurodegeneration.Aberrant activation of the c-Jun N-terminal kinase pathway has been established in human and animal models of Alzheimer’s disease caused by amyloid-beta 42-or tau-mediated neurodegeneration.Clonal mosaic studies in Drosophila that examine amyloid-beta 42 in a subset of neurons suggest complex interplay between amyloid-beta 42-expressing and wild-type cells.This review examines the role of c-Jun N-terminal kinase signaling in the context of cell competition and short-range signaling interactions between amyloid-beta 42-expressing and wild-type neurons.Cell competition is a conserved phenomenon regulating tissue integrity by assessing the fitness of cells relative to their neighbors and eliminating suboptimal cells.somatic clones of amyloid-beta 42 that juxtapose genetically distinct neuronal cell populations show promise for studying neurodegeneration.Generating genetic mosaics with labeled clones of amyloid-beta 42-or tau-expressing and wild-type neurons will allow us to understand how short-range signaling alterations trigger cell death in neurons and thereby contribute to the progression of Alzheimer’s disease.These approaches have the potential to uncover biomarkers for early Alzheimer’s disease detection and new therapeutic targets for intervention.

关键词： Alzheimer’s disease amyloid-beta 42 mediated neurodegeneration cell competition Drosophila c-Jun N-terminal kinase signaling suboptimal cell super competition super competitor cell two clone-approach wild type cell

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Intelligent lesion blood–brain barrier targeting nano-missiles for alzheimer's disease treatment by anti-neuroinflammation and neuroprotection

引用

Acta Pharmaceutica sinica B 2022年第4期12卷 1987-1999页

作者： Xueqin He Xiaorong Wang Lianyi Yang Zhihang Yang Wenqi Yu Yazhen Wang Rui Liu Meiwan Chen Huile Gao Key Laboratory of Drug-Targeting and Drug Delivery system of the Education Ministry and sichuan Province Sichuan Engineering Laboratory for Plant-Sourced Drug and Sichuan Research Center for Drug Precision Industrial TechnologyWest China School of PharmacySichuan UniversityChengdu 610041China state Key Laboratory of Quality Research in Chinese Medicine Institute of Chinese Medical SciencesUniversity of MacaoMacao 999078China

The treatment of alzheimer's disease(AD)is one of the most difficult challenges in neurodegenerative diseases due to the insufficient blood‒brain barrier(BBB)permeability and unsatisfactory intra-brain distribution of drugs.Therefore,we established an ibuprofen and FK506 encapsulated drug co-delivery system(Ibu&FK@RNPs),which can target the receptor of advanced glycation endproducts(RAGE)and response to the high level of reactive oxygen species(ROs)in AD.RAGE is highly and specifically expressed on the lesion neurovascular unit of AD,this property helps to improve targeting specificity of the system and reduce unselective distribution in normal brain.Meanwhile,these two drugs can be specifically released in astrocytes of AD lesion in response to high levels of ROs.As a result,the cognition of AD mice was significantly improved and the quantity of Aβplaques was decreased.Neurotoxicity was also alleviated with structural regeneration and functional recovery of neurons.Besides,the neuroinflammation dominated by NF-κB pathway was significantly inhibited with decreased NF-κB and IL-1βin the brain.Overall,Ibu&FK@RNPs can efficiently and successively target diseased BBB and astrocytes in AD lesion.Thus it significantly enhances intracephalic accumulation of drugs and efficiently treats AD by anti-neuroinflammation and neuroprotection.

关键词： Receptor for advanced glycation end products ROs-responsive Blood‒brain barrier transcytosis Alzheimer’s disease Drug combination Anti-neuroinflammation Neuroprotection Nano drug delivery system

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Emerging roles of astrocytes in blood-brain barrier disruption upon amyloid-beta insults in alzheimer's disease

引用

Neural Regeneration Research 2023年第9期18卷 1890-1902页

作者： Qian Yue Maggie Pui Man Hoi state Key Laboratory of Quality Research in Chinese Medicine Institute of Chinese Medical SciencesUniversity of MacaoMacao Special Administrative RegionChina Department of Pharmaceutical sciences Faculty of Health SciencesUniversity of MacaoMacao Special Administrative RegionChina

Blood-brain barrier disruption occurs in the early stages of Alzheimer’s disease.Recent studies indicate a link between blood-brain barrier dysfunction and cognitive decline and might accelerate Alzheimer’s disease progression.Astrocytes are the most abundant glial cells in the central nervous system with important roles in the structural and functional maintenance of the blood-brain barrier.For example,astrocytic cove rage around endothelial cells with perivascular endfeet and secretion of homeostatic soluble factors are two major underlying mechanisms of astrocytic physiological functions.Astrocyte activation is often observed in Alzheimer’s disease patients,with astrocytes expressing a high level of glial fibrillary acid protein detected around amyloid-beta plaque with the elevated phagocytic ability for amyloid-beta.structural alte rations in Alzheimer’s disease astrocytes including swollen endfeet,somata shrinkage and possess loss contribute to disruption in vascular integrity at capillary and arte rioles levels.In addition,Alzheimer’s disease astrocytes are skewed into proinflammatory and oxidative profiles with increased secretions of vasoactive mediators inducing endothelial junction disruption and immune cell infiltration.In this review,we summarize the findings of existing literature on the relevance of astrocyte alte ration in response to amyloid pathology in the context of blood-brain barrier dysfunction.First,we briefly describe the physiological roles of astrocytes in blood-brain barrier maintenance.Then,we review the clinical evidence of astrocyte pathology in Alzheimer’s disease patients and the preclinical evidence in animal and cellular models.We further discuss the structural changes of blood-brain barrier that correlates with Alzheimer’s disease astrocyte.Finally,we evaluate the roles of soluble factors secreted by Alzheimer’s disease astrocytes,providing potential molecular mechanisms underlying blood-brain barrier modulation.We conclude with a perspective on investigating the therapeutic pot

关键词： Alzheimer’s disease amyloid-beta astrocyte(astroglial)-endothelial interaction astrocyte pathology blood-brain barrier blood-brain barrier disruption brain endothelial cell neuroinflammation reactive astrocyte

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Progress in blood biomarkers of subjective cognitive decline in preclinical Alzheimer’s disease

引用

Chinese Medical Journal 2023年第5期136卷 505-521页

作者： Xianfeng Yu Kai shao Ke Wan Taoran Li Yuxia Li Xiaoqun Zhu Ying Han Department of Neurology Xuanwu Hospital of Capital Medical UniversityBeijing 100053China Department of Neurology The First Affiliated Hospital of Anhui Medical UniversityHefeiAnhui 230022China Department of Neurology Tangshan Central HospitalTangshanHebei 063000China school of Biomedical Engineering Hainan UniversityHaikouHainan 570228China Center of Alzheimer’s disease Beijing Institute for Brain DisordersBeijing 100053China National Clinical Research Center for Geriatric diseases Beijing 100053China.

alzheimer's disease(AD)is a neurodegenerative disease that gradually impairs cognitive functions.Recently,there has been a conceptual shift toward AD to view the disease as a continuum.since AD is currently incurable,effective intervention to delay or prevent pathological cognitive decline may best target the early stages of symptomatic disease,such as subjective cognitive decline(sCD),in which cognitive function remains relatively intact.Diagnostic methods for identifying AD,such as cerebrospinal fluid biomarkers and positron emission tomography,are invasive and expensive.Therefore,it is imperative to develop blood biomarkers that are sensitive,less invasive,easier to access,and more cost effective for AD diagnosis.This review aimed to summarize the current data on whether individuals with sCD differ reliably and effectively in subjective and objective performances compared to cognitively normal elderly individuals,and to find one or more convenient and accessible blood biomarkers so that researchers can identify sCD patients with preclinical AD in the population as soon as possible.Owing to the heterogeneity and complicated pathogenesis of AD,it is difficult to make reliable diagnoses using only a single blood marker.This review provides an overview of the progress achieved to date with the use of sCD blood biomarkers in patients with preclinical AD,highlighting the key areas of application and current challenges.

关键词： Alzheimer’s disease Biomarker Blood Evolving technologies subjective cognitive decline

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：