检索结果-南通市图书馆

uncoupling protein 2 deficiency of non-cancerous tissues inhibits the progression of pancreatic cancer in mice

Hepatobiliary & Pancreatic Diseases International 2023年第2期22卷 190-199页

作者： Denis Revskij Jakob Runst Camilla Umstätter Luise Ehlers Sarah Rohde Dietmar Zechner Manuela Bastian Brigitte Müller-Hilke Georg Fuellen Larissa Henze Hugo Murua Escobar Christian Junghanss Axel Kowald Uwe Walter Rüdiger Köhling Olaf Wolkenhauer Robert Jaster Department of Medicine Ⅱ Division of GastroenterologyRostock University Medical CenterRostockGermany Rudolf-Zenker-Institute of Experimental Surgery Rostock University Medical CenterRostockGermany Institute of Clinical Chemistry and Laboratory Medicine Rostock University Medical CenterRostockGermany Facility for Cell Sorting and Cell Analysis and Institute of Immunology Rostock University Medical CenterRostockGermany Institute for Biostatistics and Informatics in Medicine and Ageing Research Rostock University Medical CenterRostockGermany Department of Medicine Clinic ⅢHematologyOncologyPalliative MedicineRostock University Medical CenterRostockGermany Department of Neurology Rostock University Medical CenterRostockGermany Oscar LangendorffInstitute of Physiology Rostock University Medical CenterRostockGermany Department of Systems Biology and Bioinformatics University of RostockRostockGermany

Background: Pancreatic ductal adenocarcinoma(PDAC) is a disease of the elderly mostly because its development from preneoplastic lesions depends on the accumulation of gene mutations and epigenetic alterations over time. How aging of non-cancerous tissues of the host affects tumor progression, however, remains largely unknown. Methods: We took advantage of a model of accelerated aging, uncoupling protein 2-deficient( Ucp2 knockout, Ucp2 KO) mice, to investigate the growth of orthotopically transplanted Ucp2 wild-type(WT) PDAC cells(cell lines Panc02 and 6606PDA) in vivo and to study strain-dependent differences of the PDAC microenvironment. Results: Measurements of tumor weights and quantification of proliferating cells indicated a significant growth advantage of Panc02 and 6606PDA cells in WT mice compared to Ucp2 KO mice. In tumors in the knockout strain, higher levels of interferon-γ m RNA despite similar numbers of tumor-infiltrating T cells were observed. 6606PDA cells triggered a stronger stromal reaction in Ucp2 KO mice than in WT animals. Accordingly, pancreatic stellate cells from Ucp2 KO mice proliferated at a higher rate than cells of the WT strain when they were incubated with conditioned media from PDAC cells. Conclusions: Ucp2 modulates PDAC microenvironment in a way that favors tumor progression and implicates an altered stromal response as one of the underlying mechanisms.

关键词： Pancreatic cancer Orthotopic model uncoupling protein 2 Fibrosis

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

uncoupling protein 2 deficiency reduces proliferative capacity of murine pancreatic stellate cells

引用

Hepatobiliary & Pancreatic Diseases International 2016年第6期15卷 647-654页

作者： Sarah Muller Sandra Maria Klingbeil Andreea Sandica Robert Jaster Department of Medicine II Division of Gastroen-terologyRostock University Medical CenterE.-Heydemann-Str.618057 RostockGermany

BACKGROUND： uncoupling protein 2 （UCP2） has been suggested to inhibit mitochondrial production of reactive oxygen species （ROS） by decreasing the mitochondrial membrane potential. Experimental acute pancreatitis is associated with increased UCP2 expression, whereas UCP2 deficiency retards regeneration of aged mice from acute pancreatitis. Here, we have addressed biological and molecular functions of UCP2 in pancreatic stellate cells （PSCs）, which are involved in pancreatic wound repair and fibrogenesis. METHODS： PSCs were isolated from 12 months old （aged） UCP2^-/- mice and animals of the wild-type （WT） strain C57BL/6. Proliferation and cell death were assessed by em- ploying trypan blue staining and a 5-bromo-2＇-deoxyuridine incorporation assay. Intracellular fat droplets were visualized by oil red O staining. Levels of mRNA were determined by RT-PCR, while protein expression was analyzed by immunoblotting and immunofluorescence analysis. Intracellular ROS levels were measured with 2＇,7＇-dichlorofluorescin diacetate. Expression of senescence-associated β-galactosidase （SA β-Gal） was used as a surrogate marker of cellular senescence. RESULTS： PSCs derived from UCP2^-/- mice proliferated at a lower rate than cells from WT mice. In agreement with this observation, the UCP2 inhibitor genipin displayed dose- dependent inhibitory effects on WT PSC growth. Interestingly, ROS levels in PSCs did not differ between the two strains, and PSCs derived from UCP2^-/- mice did not senesce faster than those from corresponding WT cells. PSCs from UCP2^-/- mice and WT animals were also indistinguishable with respect to the activation-dependent loss of intracellular fat droplets, expression of the activation marker α-smooth muscle actin, type I collagen and the autocrine/paracrine mediators interleukin-6 and transforming growth factor-I~ 1. CONCLUSIONS： A reduced proliferative capacity of PSC from aged UCP2^-/- mice may contribute to the retarded regeneration after acute pancreatitis. Apart from their slower growth, PSC of UCP2^-/-

关键词： pancreatitis proliferation stellate cell biology uncoupling protein 2

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

Role and mechanism of uncoupling protein 2 on the fatty acid-induced dysfunction of pancreatic alpha cells in vitro

引用

Chinese Medical Journal 2010年第17期123卷 2416-2423页

作者： SU Jie-ying LI Hong-liang YANG Wen-ying XIAO Jian-zhong DU Rui-qin SHEN Xiao-xia CAI Zhe ZHANG Lan SHU Jun Graduate School Peking Union Medical College Tsinghua University Beijing 100730 China Department of Endocrinology China-Japan Friendship Hospital Beijing 100029 China Section of Diabetes and Endocrinology University of Oklahoma Health Sciences Center University of Oklahoma Oklahoma City OK 73104 USA Department of Endocrinology General Hospital of the Second Artilleryman of Chinese People's Liberation Army Beijing 100088 China Department of Immunology and Tissue Engineering Clinical Research Institute of China-Japan Friendship Hospital Beijing 100029 China

Background uncoupling protein （UCP） 2 is related to the dysfunction of beta cells induced by fatty acids. However,whether UCP2 has similar effects on alpha cell is still not clear. This study aimed to investigate the effects of UCP2 and its possible mechanisms in lipotoxicity-induced dysfunction of pancreatic alpha cells.Methods The alpha TC1-6 cells were used in this study to evaluate the effects of palmitate and/or UCP2 inhibit factors on the glucagon secretory function, glucagon content, the glucagon mRNA level and the nitrotyrosine level in the supernatant. Meantime, the expression levels of UCP2 and peroxisome proliferator-activated receptor-γ coactivator-1 alpha （PGC-1 alpha） were measured by real-time reverse transcription polymerase chain reaction （RT-PCR） and Western blotting. Furthermore, the possible relationship between UCP2 and insulin signal transduction pathway was analyzed.Results Palmitate stimulated alpha cell glucagon secretion and the expression of UCP2 and PGC-1 alpha, which could be partially decreased by the inhibition of UCP2. Palmitate increased nitrotyrosine level and suppressed insulin signal transduction pathway in alpha cells. Inhibition of UCP2 influenced the effects of free fatty acid on alpha cells and may relate to glucagon secretion.Conclusion UCP2 played an important role on alpha cell dysfunction induced by free fatty acid in vitro, which may be related to its effects on oxidative stress and insulin signal transduction pathway.

关键词： pancreatic alpha cells uncoupling protein 2 glucagon free fatty acids

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

Effect of Target-directed Regulation of uncoupling protein-2 Gene Expression on Ischemia-reperfusion Injury of Hepatocytes

引用

Journal of Huazhong University of Science and Technology(Medical Sciences) 2008年第5期28卷 558-563页

作者：万赤丹王宏博程锐勾善淼刘涛 Department of Hepatobiliary Surgery Union Hospital Tongji Medical College Huazhong University of Science and Technology

The effect of target-directed regulation of the uncoupling protein-2 （UCP-2） gene expression on the ischemia-reperfusion injury of hepatocytes under different conditions was investigated. The expression plasmid and RNAi plasmid targeting UCP-2 gene were constructed and trans- fected into normal hepatocytes and fatty liver cells, respectively. The expression of UCP-2 mRNA was detected by real time PCR. The cells were divided into normal cell group （NCG）, group of normal cells transfected with empty vector （EVNCG）, group of normal cells transfected with expression plasmid （EPNCG）, fatty liver cell group （FCG） and group of fatty liver cells transfected with RNAi plasmid （RPFCG）. The ischemia-reperfusion model in vitro was established. One, 6, 12 and 24 h after reperfusion, Annexin V/PI flow cytometry was used to measure cell necrosis rate, apoptosis rate and survival rate. Simultaneously, the intracellular ATP, ROS and MDA levels were determined. The re- sults showed that 1, 6, 12 and 24 h after ischemia-reperfusion, the intracellular ROS, MDA and ATP levels and cell survival rate in EPNCG were significantly lower, and cell necrosis rate significantly higher than in NCG and EVNCG, but there was no significant difference in apoptosis rate among NCG, EVNCG and EPNCG （P〉005）. Six, 12 and 24 h after reperfusion there was no significant dif- ference in ROS, MDA levels and apoptosis rate between FCG and RPFCG （P〉0.05）, but the ATP level and survival rate of cells in RPFCG were higher than in FCG （P〈0.05）. It was concluded that down-regulation of the UCP-2 gene expression in steatotic hepatocytes could alleviate the ische- mia-reperfusion injury of liver cells.

关键词： uncoupling protein 2 ischemia-reperfusion fatty liver cell siRNA

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 epidemiologic study of mitochondrial membrane transporter protein gene polymorphism and risk factors for neural tube defects in Shanxi, China

引用

Neural Regeneration Research 2012年第6期7卷 463-469页

作者： Zhizhen Liu Jun Xie Tian＇e Luo Tao Zhang Xia Zhao Hong Zhao Peizhen Li Department of Biochemistry and Molecular Biology Shanxi Medical University Taiyuan 030001 Shanxi Province China Department of Epidemiology and Statistics Shanxi Medical University Taiyuan 030001 Shanxi Province China Shanghai Yangpu District Center for Disease Control and Prevention Shanghai 200093 China Department of Physical and Chemical Detection Shanxi Centre for Disease Control and Prevention Taiyuan 030001 Shanxi Province China Department of Epidemiology Zhuhai Campus of Zunyi Medical College Zhuhai 519041 Guangdong Province China

The present study involved a questionnaire survey of 156 mothers that gave birth to children with neural tube defects or had a history of pregnancy resulting in children with neural tube defects （case group） and 156 control mothers with concurrent healthy children （control group） as well as detection of mitochondrial membrane transporter protein gene [uncoupling protein 2 （UCP2）] polymorphism. The maternal UCP2 3＇ untranslated region （UTR） D/D genotype and D allele frequency were significantly higher in the case group compared with the control group （odds ratio （OR） 3.233; 95% confidence interval （C/） 1.103 9.476; P= 0.040; OR： 3.484; 95% CI： for neural tube defects 2.109 5.753; P 〈 0.001）. Univariate and multivariate logistic regression analysis of risk factors for neural tube defects showed that a matemal UCP2 3＇ UTR D/D genotype was negatively interacted with the mothers＇ consumption of frequent fresh fruit and vegetables （S = 0.007）, positively interacted with the mothers＇ frequency of germinated potato consumption （S = 2.15） and positively interacted with the mothers＇ body mass index （S = 3.50）. These findings suggest that maternal UCP2 3＇ UTR gene polymorphism, pregnancy time, consumption of germinated potatoes and body mass index are associated with an increased risk for neural tube defects in children from mothers living in Shanxi province, China. Moreover, there is an apparent gene-environment interaction involved in the development of neural tube defects in offspring.

关键词： neural tube defects uncoupling protein 2 genetic polymorphisms risk factors interaction

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

Role and mechanism of rosiglitazone on the impairment of insulin secretion induced by free fatty acids on isolated rat islets

引用

Chinese Medical Journal 2006年第7期119卷 574-580页

作者： TIAN Jing-yan LI Guo GU Yan-yun ZHANG Hong-li ZHOU Wen-zhong WANG Xiao ZHU Hong-da LUO Tian-hong LUO Min Shanghai Institute of Endocrinology and Metabolism ShanghaiClinical Center of Endocrine and Metabolic Diseases RuijinHospital Shanghai Second Medical University Shanghai 200025China

Background Prolonged exposure of pancreatic β-cells to fatty acids increases basal insulin secretion but inhibits glucose-stimulated insulin secretion. Rosiglitazone is a new antidiabetic agent of the thiazolidinediones. However, the relationship between thiazolidinediones and insulin secretion is highly controversial. The aim of this study is to explore the effect and mechanism of rosiglitazone on insulin secretion of islets under chronic exposure to free fatty acids （FFA）.Methods Pancreatic islets were isolated from the pancreata of male Sprague-Dawley rats by the collagenase digestion and by the dextran gradient centrifugation method. The purified islets were cultured in the presence or absence of rosiglitazone and palmitate for 48 hours. The insulin secretion was measured by radioimmunoassay. The mRNA level of peroxisome proliferator-activated receptor y, uncoupling protein 2 0dCP-2） and insulin were determined by real-time polymerase chain reaction （PCR）. The cell cytotoxicity assay was measured by cell counting kit-8.Results Islets exposed to elevated palmitate for 48 hours showed an increased basal and a decreased glucose-stimulated insulin secretion （P〈0.01）. The mRNA level of UCP-2 was increased by 3.7 fold in the 0.5 mmol/L concentration of palmitate. When islets were cultured with palmitate （0.5 mmol/L） in the presence of rosiglitazone （1.0 pmol/L）, both basal and glucose-stimulated insulin secretion reversed to a pattern of control islets （P〈0.05, P〈0.0 1）. The addition of rosiglitazone in the culture medium decreased the mRNA level of UCP-2 by 2.2 fold, having a statistically significant difference （P〈0.05） as compared with islets cultured with palmitate alone. The cell viability was not affected.Conclusion The protective effects of rosiglitazone on insulin secretion of isolated pancreatic islets under chronic exposure to palmitate might be mediated through the downregulation of UCP-2 expression.

关键词： rosiglitazone fatty acids uncoupling protein 2

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

Antifibrotic Effect of Total Flavonoids of Astmgali Radix on Dimethylnitrosamine-lnduced Liver Cirrhosis in Rats

引用

Chinese Journal of Integrative Medicine 2017年第1期23卷 48-54页

作者： CHENG Yang MAI Jing-yin WANG Mei-feng CHEN Gao-feng PING Jian Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine Shanghai 201203China Shanghai Pudong New Area Hospital of Traditional Chinese Medicine Shanghai 201299China

Objective：To study the effect of total flavonoids of Astmgali Radix（TFA）on liver cirrhosis induced with dimethylnitrosamine（DMN）in rats,and the effect on peroxisome proliferator-activated receptorγ（PPARγ）,uncoupling protein 2（UCP2）and farnesoid X receptor（FXR）.Methods：Fifty-three Sprague-Dawley rats were randomly divided into a control group（10 rats）and a DMN group（43 rats）.Rats in the DMN group were given DMN for 4 weeks and divided randomly into a model group（14 rats）,a low-dosage TFA group（14 rats）and a high-dosage TFA group（15 rats）in the 3rd week.Rats were given TFA for 4 weeks at the dosage of 15 and 30 mg/kg in the low-and high-TFA groups,respectively.At the end of the experiment blood and liver samples were collected.Serum liver function and liver tissue hydroxyproline content were determined.hematoxylin-eosin（HE）,Sirus red and immunohistochemical stainings of collagenⅠ,smooth muscle actin（α-SMA）was conducted in paraffinembedded liver tissue slices.Real time polymerase chain reaction（PCR）was adopted to determine PPARγ,UCP2 and FXR m RNA levels.Western blot was adopted to determine protein levels of collagenⅠ,α-SMA,PPARγ,UCP2 and FXR.Results：Compared with the model group,TFA increased the ratio of liver/body weight（low-TFA group P〈0.05,high-TFA group P〈0.01）,improved liver biochemical indices（P〈0.01 for ALT,AST,GGT in both groups,P〈0.05 for albumin and TBil in the high-TFA group）and reduced liver tissue hydroxproline content（P〈0.01 in both groups）in treatment groups significantly.HE staining showed that TFA alleviated liver pathological changes markedly and Sirus red staining showed that TFA reduced collagen deposition,alleviated formation and extent of liver pseudolobule.CollagenⅠandα-SMA immunohistochemical staining showed that staining area and extent markedly decreased in TFA groups compared with the model group.TFA could increase PPARγ,it regulated target UCP2,and FXR levels significantly compared with the model group（in the low-TFA group all P〈0.05,in the high group all P〈0.01）.Conclusions：TFA could

关键词： total flavonoids of Astmgali Radix dimethylnitrosamine liver cirrhosis peroxisome proliferator-activated receptor γ uncoupling protein 2 farnesoid X receptor rat

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

NADPH Oxidase-dependent Oxidative Stress and Mitochondrial Damage in Hippocampus of D-galactose-induced Aging Rats

引用

Journal of Huazhong University of Science and Technology(Medical Sciences) 2012年第4期32卷 466-472页

作者：杜政德胡钰娟杨阳孙宇张甦琳周涛曾玲玲张文娟黄翔孔维佳张红莲 Department of Otorhinolaryngology Department of Otorhinolaryngology Shenzhen Sixth People's Hospital(Nanshan Hospital)Huazhong University of Science and Technology Department of Public Health Union HospitalTongji Medical CollegeHuazhong University of Science and Technology

Mitochondrial DNA(mtDNA) common deletion(CD) plays a significant role in aging and age-related diseases.In this study,we used D-galactose(D-gal) to generate an animal model of aging and the involvement and causative mechanisms of mitochondrial damage in such a model were investigated.Twenty 5-week-old male Sprague-Dawley rats were randomly divided into two groups:D-gal group(n=10) and control group(n=10).The quantity of the mtDNA CD in the hippocampus was determined using a TaqMan real-time PCR assay.Transmission electron microscopy was used to observe the mitochondrial ultrastructure in the hippocampus.Western blot was used to detect the protein levels of NADPH oxidase(NOX) and uncoupling protein 2(UCP2).We found that the level of mtDNA CD was significantly higher in the hippocampus of D-gal-induced aging rats than in control rats.In comparison with the control group,the mitochondrial ultrastructure in the hippocampus of D-gal-treated rats was damaged,and the protein levels of NOX and UCP2 were significantly increased in the hippocampus of D-gal-induced aging rats.This study demonstrated that the levels of mtDNA CD and NOX protein expression were significantly increased in the hippocampus of D-gal-induced aging rats.These findings indicate that NOX-dependent reactive oxygen species generation may contribute to D-gal-induced mitochondrial damage.

关键词： D-galactose common deletion oxidative stress NADPH oxidase uncoupling protein 2

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

The study on neural stem cells by Lentivirus mediated UCP2 lower expression

The study on neural stem cells by Lentivirus mediated UCP2 l...

引用

第八届泛环渤海生物化学与分子生物学会2018年学术交流...

作者： Kai-li Zhang Hujun Jin-rong Suo Zhi-zhen Liu Department of Biochemistry and Molecular Biology Shanxi Medical University

Objectives:1. Isolation, cultivation and identify C57 mice primary neural stem cells, providing a cell model to study the mechanism of neural tube defects caused by low expression of UCP2. 2. Construct an effective UCP2 RNA interference vector, and establish an efficient method to transfect neural stem cells, to support the study of gene function latter.3. Testing the change of ROS level and cell apoptosis after UCP2 experssion decrease in NSCs, exploring the pathogenesis of NTDs caused by UCP2 lower expression. Methods:1. Neural stem cells extraction, cultivation and identification: Through mechanical method, isolating neural stem cells from 14.5 days fetal rat’s brain tissue, Neural stem cells were identified by characteristic protein nestin immunofluorescence staining. DMEM/F12 culture medium containing 10% fetal calf serum was used to induce NSCs to differentiate, neuron, astrocyte and oligodendroglia were identified through characteristic proteins NF-H, GFAP and GALC immunofluorescence staining. 2. Construct UCP2 RNA interfere lentiviral vector and virus packing: Targeting UCP2 gene specific sequence were designed to link with p Magic4.1 lentiviral vector(p NL-EGFP/CMV/WPREdU 3-sh mU CP2). Then virus packing recombinant lentiviral vectors were harvested from 293 T cells with recombinant lentiviral vector, second generation virus packing plasmid p CD/NL-BH*DDD and membrane protein expression plasmid p LTR-G co-transfection.3. Construct electroporation UCP2 RNA interfere vector: The same as UCP2 RNA interfere lentiviral vector p NL-EGFP/CMV/WPREdU 3-sh mU CP2 above.4. Compare lentiviral transfection and electroporation: NSCs were transfected by lentiviral transfection and electroporation, transfection efficiency was compared By observing the green fluorescent protein expression of NSCs;The interference maintenance time was compared by green fluorescent intensity of NSCs after transfection 48 h and 72 h. Western Blot and QPCR were used to test NSCs UCP2 expression after lentiviral transfection. 5. ROS level det

关键词： neural stem cells uncoupling protein 2 lentiviral transfection reactive oxygen species cell apoptosis

来源： cnki会议评论

在线全文

cnki会议

学校读者我要写书评

暂无评论

Study on Neural stem cells by Lentivirus mediated UCP2 lower expression

Study on Neural stem cells by Lentivirus mediated UCP2 lower...

引用

2017第七届泛环渤海生物化学与分子生物学会学术交流会

作者： Kai-li Zhang San-san Jia Jin-rong Suo Zhi-zhen Liu Jun Xie Department of Biochemistry and Molecular Biology Shanxi Medical University

Objectives:1.Isolation,cultivation and identify C57 mice primary neural stem cells,providing a cell model to study the mechanism of neural tube defects caused by low expression of UCP2.2.Construct an effective UCP2 RNA interference vector,and establish an efficient method to transfect neural stem cells,to support the study of gene function latter.3.Testing the change of ROS level and cell apoptosis after UCP2 experssion decrease in NSCs,exploring the pathogenesis of NTDs caused by UCP2 lower expression.4.Testing the change of ROS level and cell apoptosis after UCP2 experssion decrease in NSCs,exploring the pathogenesis of NTDs caused by UCP2 lower expression.Methods:1.Neural stem cells extraction,cultivation and identification.2.Construct UCP2 RNA interfere lentiviral vector and virus packing.***.lentiviral transfection:Western Blot and QPCR were used to test NSCs UCP2expression after lentiviral transfection.4.ROS level detection:Testing NSCs ROS level of blank group,negative control group and UCP2 low expression vector transfection experimental group by DCFH-DA respectively,Comparing ROS level of each group.5.Cells apoptosis detection:Dividing NSCs into three groups:blank group,negative control group and UCP2 low expression vector transfection experimental group.Caspase3 activation fluorescent staining was used to test the rate of caspase3 activation NSCs,Western Blot was used to test caspase3 expression.6.The mechanism of UCP2 and ROS production and apoptosis was further explored.

关键词： neural stem cells uncoupling protein 2 lentiviral transfection reactive oxygen species cell apoptosis

来源： cnki会议评论

在线全文

cnki会议

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：