检索结果-南通市图书馆

inducible nitric oxide synthase contributes to intermittent hypoxia against ischemia/reperfusion injury

Acta Pharmacologica Sinica 2005年第3期26卷 315-322页

作者： Hai-lei DING~2 Hai-feng ZHU~2 Jian-wen DONG~2 Wei-zhong ZHU~2 Wei-wei YANG~3 Huang-tian YANG~3 Zhao-nian ZHOU~(2,4)2 Physiological Laboratory of Hypoxia,Shanghai Institutes for Biological Sciences,Chinese Academy of Sciences,Shanghai 200031,China 3 Laboratory of Molecular Cardiology,Health Science Center,Shanghai Institutes for Biological Sciences,Chinese Academy of Sciences and Shanghai Second Medical University,Shanghai 200025,China Physiological Laboratory of Hypoxia Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai China Laboratory of Molecular Cardiology Health Science Center Shanghai Institutes for Biological Sciences Chinese Academy of Sciences and Shanghai Second Medical University Shanghai China

Aim:To investigate the role of inducible nitric oxide synthase (iNOS)-derivednitric oxide (NO) in the cardioprotection of intermittent hypoxia (IH) against is-chemia/reperfusion (I/R) injury.Methods:Langendorff-perfused isolated rathearts were used to measure variables of left ventricular function during baselineperfusion,ischemia,and reperfusion period.Nitrate plus nitrite (NOx) content inmyocardium was measured using a biochemical method,iNOS mRNA and pro-tein expression in rat left ventricles were detected using reverse transcription poly-merase chain reaction (RT-PCR) and Western blot,respectively.Results:Myo-cardial function recovered better in IH rat hearts than in normoxic control hearts.The iNOS-selective inhibitor aminoguanidine (AG) (100μmol/L) significantlyinhibited the protective effects of IH,but had no influence on normoxic rat hearts.The baseline content of NOx in IH hearts was higher than that in normoxic hearts.After 30 min ischemia,the NOx level in normoxic hearts increased compared tothe corresponding baseline level,whereas there was no significant change in IHhearts.However,the NOx level in IH hearts was still higher than that of normoxichearts during ischemia and reperfusion period.AG 100μmol/L significantly di-minished the NOx content in IH and normoxic hearts during ischemia and reperfusignperiod.The baseline levels of iNOS mRNA and protein in IH hearts were higherthan those of normoxic hearts.Compared to the corresponding baseline level,iNOS mRNA and protein levels in normoxic rat hearts increased and those in IH rathearts decreased after reperfusion.The addition of AG 100μmol/L significantlydecreased iNOS mRNA and protein expression in IH rat hearts after I/R.Conclusion:IH upregulated the baseline level of iNOS mRNA and protein expres-sion leading to an increase in NO production,which may play an important role inthe cardiac protection of IH against I/R injury.

关键词： intermittent hypoxia ischemia/reperfusion inducible nitric oxide synthase aminoguanidine: rats

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Dynamic changes of inducible nitric oxide synthase expression in rat's retina and its role on blood-retinal barrier injury after acute high intraocular pressure

引用

International Journal of Ophthalmology(English edition) 2022年第7期15卷 1053-1061页

作者： Min Li Ju-Fang Huang Yi Li Jing Shen Lu-Jia Yang Qian Chen Quan-Peng Zhang Xi-Nan Yi College of Basic Medicine and Life Sciences Hainan Medical UniversityKey Laboratory of Tropical Brain Research and Translation of Hainan ProvinceHaikou 571199Hainan ProvinceChina Department of Human Anatomy and Neurobiology School of Basic Medical SciencesCentral South UniversityChangsha 410013Hunan ProvinceChina Grade 18 Clinical Bachelor of Clinical College of Hainan Medical University Haikou 571199Hainan ProvinceChina Department of Ophthalmology the First Affiliated Hospital of Hainan Medical UniversityHaikou 571199Hainan ProvinceChina

AIM: To clarify the role of inducible nitric oxide synthase(i NOS) in blood-retinal barrier(BRB) injury after acute high intraocular pressure(IOP) in rats.METHODS: Forty-two Sprague-Dawley(SD) rats were randomized into 7 groups [control(Cont), 3, 6, 12, 24, 48, and 72 h, n=6]. Except Cont group, other groups’ retina tissue was obtained at corresponding time points after a model of acute high IOP have been established in rats. The expression of i NOS and tight junction protein zonula occludens(ZO)-1 was detected by Western blotting. Evans blue(EB;3%) was injected into the great saphenous vein to detect the leakage of EB by spectrophotometer. Nine rats were divided into Cont, 6 h, 12 h groups, the expression of i NOS was localized by immunofluorescence. In order to verify the role of i NOS in the damage to BRB, thirty-six rats were randomly divided into 4 groups [Cont, Cont+inhibitor(Inh), 6 h and 6 h+Inh, n=9]. After treatment with the i NOSspecific inhibitor 1400 W, the expression of i NOS and ZO-1 and the leakage of BRB were detected again.RESULTS: The immunofluorescence results showed that the expression of i NOS was observed in the Cont group and 6 h group, but not in the 12 h group. i NOS was mainly expressed in the retinal nerve fiber layer, ganglion cell layer and inner nuclear layer and that it did not colocalize with the retinal ganglion cell marker Neu N but was co-expressed with the vascular endothelial cell marker CD31. Western blotting showed that in the early period(3 h, 6 h) after acute high IOP, the expression of i NOS was upregulated, then the down-regulation of i NOS were tested in the follow-up timing spots. ZO-1 expression showed a continuous downregulation after 6 h. The quantitative results for EB showed that the amount of EB leakage began to increase at 3 h after acute high IOP. At 6 h, the leakage of EB was lower, but at 12 h, the leakage of EB was highest, after which it gradually recovered but remained higher than that in the Cont group. The expression of i NOS was down-regulated after 14

关键词： inducible nitric oxide synthase acute high intraocular pressure blood-retinal barrier ZO-1

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

inducible nitric oxide synthase is involved in the oxidation stress induced by HIV-1 gp120 in human retina pigment epithelial cells

引用

Chinese Medical Journal 2008年第24期121卷 2578-2583页

作者： YU Qiu-rong ZHANG Zhen-ping ZHANG Hui LIN Hao-tian LI Xiu-mei BAI Ling CAI Wei-bin State Key Laboratory of Ophthalmology Zhongshan Ophthalmic Center Sun Yat-sen University Guangzhou Guangdong 510060 China Department of Medicine Division of Infectious Diseases Center for Human Virology Thomas Jefferson University Philadelphia USA Department of Biochemistry Sun Yat-sen University Guangzhou Guangdong 510060 China

Background The human immunodeficiency virus-1 （HIV-1） envelope glycoprotein gp120 has been implicated in the development of AIDS-associated retinopathy. The present study tested the hypothesis that gp120 may induce oxidative stress including up regulation of inducible nitric oxide synthase （iNOS） and production of malondialdehyde （MDA） and nitric oxide （NO） to mediate retinopathy in retinal pigment epithelial （RPE） cells. Methods Human RPE cell line D407 was cultured and treated with gp120. HIV-1 gp120 protein induced lipid peroxidation product MDA. NO production and iNOS expression were examined in vitro by spectrophomtometry, real-time PCR, Western blotting, and confocal microscope. Results Addition of gp120 was able to induce RPE cells to produce NO and MDA in time- and dose-dependent manners （P 〈0.05）. Similarly, gp120 was also capable of up-regulating iNOS mRNA and protein in D407 cells in time- and dose-dependent manners. Conclusions Gp120 induces oxidative stress in D407 cell by stimulating MDA and NO production, which is mediated by up-regulating iNOS expression. Gp120 may mediate oxidation stress in AIDS-associated retinopathy.

关键词： inducible nitric oxide synthase HIV-1 gp120 human retina pigment epithelium 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

Triptolide Inhibits Cyclooxygenase-2 and inducible nitric oxide synthase Expression in Human Colon Cancer and Leukemia Cells

引用

Acta Biochimica et Biophysica Sinica 2007年第2期39卷 89-95页

作者： Xiangmin TONG~# Shui'er ZHENG~# Jie JIN Lifen ZHU Yinjun LOU and Hangping YAO Institute of Hematologic Disease,Department of Hematology,First Affiliated Hospital,Medical School,Zhejiang University,Hangzhou 310003,China Institute of Hematologic Disease Department of Hematology First Affiliated HospitalMedical School Zhejiang University Hangzhou 310003 China

Triptolide （TP）,a traditional Chinese medicine,has been reported to be effective in thetreatment of autoimmune diseases and exerting antineoplastic activity in several human tumor cell lines.Thisstudy investigates the antitumor effect of TP in human colon cancer cells （SW114） and myelocytic leukemia（K562）,and elucidates the possible molecular mechanism involved.SW114 and K562 cells were treatedwith different doses of TP （0,5,10,20,or 50 ng/ml）.The cell viability was assessed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide （MTT）. Results demonstrated that TP inhibited the proliferation ofboth tumor cell lines in a dose-dependent manner.To further investigate its mechanisms,the productsprostaglandin E2（PGE2） and nitric oxide （NO） were measured by enzyme-linked immunosorbent assay（ELISA）.Our data showed that TP strongly inhibited the production of NO and PGE2. Consistent with theseresults,the expression of inducible NO synthase （iNOS） and cyclooxygenase-2 （COX-2） was up-regulatedboth at the mRNA level and the protein expression level,as shown by real-time RT-PCR and Westernblotting.These results indicated that the inhibition of the inflammatory factor COX-2 and iNOS activitycould be involved in the antitumor mechanisms of TP.

关键词： triptolide leukemia colon cancer cyclooxygenase-2 inducible nitric oxide synthase

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Tongxinluo Inhibits Cyclooxygenase-2, inducible nitric oxide synthase, Hypoxia-inducible Factor-2α/Vascular Endothelial Growth Factor to Antagonize Injury in Hypoxia-stimulated Cardiac Microvascular Endothelial Cells

引用

Chinese Medical Journal 2015年第8期128卷 1114-1120页

作者： Yan-Ning Li Xiu-Juan Wang Bin Li Kun Liu Jin-Sheng Qi Bing-Hui Liu Ye Tian Department of Biochemistry Hebei Key Laboratory of Medical Biotechnology Hebei Medical University Shijiazhuang Hebei 050017 China Department of Molecular Biology Hebei Key Laboratory of Laboratory Animal Hebei Medical University Shijiazhuang Hebei 050017 China

Background： Endothelial dysflinction is considered as the initiating process and pathological basis of cardiovascnlar disease. Cyclooxygenase-2 （COX-2） and prostacyclin synthase （PGIS）, inducible nitric oxide synthase （iNOS） and endothelial NOS （eNOS） are key enzymes with opposing actions in inflammation and oxidative stress, which are believed to be the major driver of endothelial dysfunction. And in hypoxia （Hx）, Hx-inducible factor （HIF）-1α and HIF-2α are predominantly induced to activate vascular endothelial growth factor （VEGF）, restllting in abnormal proliferation. Whether and how Tongxinluo （TXL） modulates COX-2, PGIS, iNOS, eNOS, HIF-1α, HIF-2α, and VEGF in Hx-stimulated human cardiac microvascular endothelial cells （HCM ECs） have not been clarified. Methods： HCMEC were treated with CoCl2 to mimic Hx and the mRNA expressions of COX-2, PGIS, iNOS, eNOS, HIF-1α, HIF-2α. and VEGF were first confirmed, and then their mRNA expression and protein content as well as the cell pathological alterations were evaluated for TXL treatment with different concentrations, In addition, the effector molecular of inflammation prostaglandin E2 （PGE2） and the oxidative marker nitrotyrosine （NT） was adopted to reflect HCMEC in.jury. Results： Hx could induce time-dependent increase of COX-2, iNOS, HIF-2α, and VEGF in HCMEC. Based on the Hx-induced increase, TXL could mainly decrease COX-2, iNOS, HIF-2α, and VEGF in a concentration-dependent manner, with limited effect on the increase of PGIS and eNOS. Their protein contents verified the mRNA expression changes, which was consistent with the cell morphological alterations. Furthermore, high dose TXL could inhibit the Hx-induced increase of PG E, and NT contents, attenuating the inflammatory and oxidative injury. Conclusions： TXL could inhibit inflammation-related COX-2, oxidative stress-related iNOS, and H IF-2α/VEGF to antagonize Hx-induced HCMEC injury.

关键词： Cyclooxygenase-2 Hypoxia-inducible Factor-2α Hypoxia inducible nitric oxide synthase Tongxinluo Vascular Endothelial Growth Factor

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

Effects of Naoxintong on atherosclerosis and inducible nitric oxide synthase expression in atherosclerotic rabbit

引用

Chinese Medical Journal 2013年第6期126卷 1166-1170页

作者： ZHONG Xiao-nan WANG Hong-hao LU Zheng-qi DAI Yong-qiang HUANG Jian-hua QIU Wei SHU Ya-qing XU Wen CHENG Chen HU Xue-qiang Department of Neurology Third Affiliated Hospital of Sun Yat-sen University Guangzhou Guangdong 510630 China Department of Clinical Laboratory Third Affiliated Hospital of Sun Yat-sen University Guangzhou Guangdong 510630 China

Background High levels of nitric oxide （NO） produced by inducible NO synthase （iNOS） have been associated with atherosclerosis processes. Naoxintong is a traditional Chinese medicine for treatment of cerebrovascular and cardiovascular disease. The aim of the present study was to detect and quantify changes of iNOS mRNA and NO levels in the vessel wall after the administration of Naoxintong in an atherosclerotic rabbit model. Methods Forty New Zealand white rabbits were randomly divided into five groups （n=8）. Rabbits were fed a standard diet （group A）, an atherogenic diet consisting of 79% standard feed＋l% cholesterol＋5% lard＋15% egg yolk powder （group B）, an atherogenic diet with Naoxintong 0.25 mg.kg^-l.d^-1 （group C）, an atherogenic diet with Naoxintong 0.5 mg.kg^-l.d^-1 （group D）, or atherogenic diet with Naoxintong 1.***.kg^-l.d^-1 （group E） for 12 weeks. Results Supplemented administration of Naoxintong led to a down-regulation of cholesterol （CHOL）（P 〈0.001） and low-density lipoprotein （LDL）（P 〈0.001）. The trend became more notable as the dose of Naoxintong increased; group C vs. group B （CHOL, P=0.568; LDL-cholesterol （LDL-C）, P=0.119）, group D vs. group B （CHOL, P=0.264; LDL-C, P=0.027）, group E vs. group B （CHOL, P=0.028; LDL-C, P=0.002）. Atherosclerotic lesions in aorta were reduced in Naoxintong groups （groups C, D, E） compared to group B. Group B had higher iNOS mRNA （P=0.001） and NO level （P 〈0.001） than group A. Compared with the atherogenic diet fed-rabbits, Naoxintong supplements decreased the expression of iNOS mRNA （P 〈0.001） and the NO level （P 〈0.001） in the vessel wall. Groups given a higher Naoxintong dose exhibited greater benefits, iNOS mRNA and NO levels seemed to be reduced in group C, although the difference did not quite reach statistical significance （iNOS mRNA, P=0.130; NO, P=0.038）. iNOS mRNA and NO levels significantly decreased in group D （iNOS mRNA, P=0.019; NO, P=0.018） and group E （iNOS mRNA, P=0.004; NO, P 〈0.001）. Conclusion Naoxintong has beneficial effects on atheroscler

关键词： Naoxintong atherosclerosis rabbit inducible nitric oxide synthase

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

Clinical Significance of a Myeloperoxidase Gene Polymorphism and inducible nitric oxide synthase Expression in Cirrhotic Patients with Hepatopulmonary Syndrome

引用

Journal of Huazhong University of Science and Technology(Medical Sciences) 2010年第4期30卷 437-442页

作者：王燕颖王文多张艳霞赵欣杨东亮 Department of Gastroenterology Heilongjiang Provincial Hospital Department of Infectious Disease Tongji Hospital Tongji Medical College Huazhong University of Science and Technology

The clinical significance of a myeloperoxidase (MPO) gene polymorphism and inducible nitric oxide synthase (iNOS) expression in cirrhotic patients with hepatopulmonary syndrome (HPS) was explored. Enrolled subjects were divided into three groups according to their disease/health conditions: the HPS group (cirrhotic patients with HPS; n=63), the non-HPS group (cirrhotic patients without HPS; n=182), and the control group (healthy subjects without liver disease; n=35). The distribution of the MPO–463 G/A genotype and its relationship with iNOS expression in a typical cell block from ascitic fluid were detected by immunohistochemistry and polymerase chain reaction-restricted fragment length polymorphism analysis (PCR-RFLP). In the HPS group, the partial pressure of oxygen in blood and ascitic fluid was significantly decreased (8.95±1.58 kPa and 6.81±0.95 kPa, respectively; both Poxide significantly increased (4.62±0.20 kPa and 5.92±0.45 kPa, respectively; P<0.01). MPO and iNOS levels were significantly increased in the HPS group as compared with the non-HPS group. These increases were even more remarkable in ascitic fluid (41.36±11.62 and 13.23±4.81 μg/L; 10.27± 3.20 and 4.95±1.12 μg/L) than in blood (16.66±5.24 and 4.87±1.73 μg/L; 5.79±2.31 and 2.35±0.84 μg/L). The distribution of the MPO genotypes GG, GA, and AA were 76.2%, 22.2% and 1.6% in the HPS group, and 57.7%, 37.9% and 4.4% in the non-HPS group (P<0.05). The expression of iNOS was significantly higher in patients with the G alleles (G/G and G/A) (61.54%, 48/78) than in patients with A alleles (G/A and A/A) (38.46%, 30/78) (P<0.01). It was suggested that the expression levels of iNOS and MPO were correlated with HPS-induced hypoxemia. The MPO-463 G/A mutation might be a protective factor that prevents the development of HPS. The MPO might be involved in the regulation of iNOS expression. In humans, MPO pathways, the iNOS/NO system, and their interaction might have an impact on the occurrence and development of

关键词： hepatopulmonary syndrome myeloperoxidase inducible nitric oxide synthase polymorphism

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

Potential involvement of nitric oxide synthase but not inducible nitric oxide synthase in the development of experimental corneal neovascularization

引用

International Journal of Ophthalmology(English edition) 2011年第4期4卷 343-348页

作者： Yuan Chen Gao-Qin Liu and Pei-Rong Lu Department of Ophthalmology the First Affiliated Hospital of Soochow University Suzhou 215006 Jiangsu Province China

AIM: To investigate the effect of nitric oxide and its synthetase on experimental corneal neovascularization (CRNV). METHODS: CRNV was induced by alkali injury in mice, nitric oxide synthetase (NOS) was inhibited by NG-nitro-L-arginine (L-NAME) and inducible nitric oxide synthetase (iNOS) was inhibited by aminoguanidine hemisulfate salt (AG). The inhibitory effect was detected at day 2 and 4 after corneal alkali injury by reverse transcription polymerase chain reaction (RT-PCR). CRNV was compared between the control and the treated mice by microscopic observation and corneal whole mount CD31 immunostaining. RESULTS: The inhibition of L-NAME to NOS and AG to iNOS after corneal injury was confirmed by RT-PCR (P 0.05). CONCLUSION: Our findings suggest that NOS but not iNOS plays a critical role in alkali injury induced CRNV.

关键词： corneal neovascularization nitric oxide synthase inducible nitric oxide synthase

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

Lanthanum Chloride Inhibiting Expression of inducible nitric oxide synthase in RAW264.7 Macrophages Induced by Lipopolysaccharide

引用

Journal of Rare Earths 2007年第3期25卷 359-363页

作者：郭菲娄远蕾汪泱谢安李国辉 Burns Institute Nanchang UniversityNanchang 330006ChinaPostgraduate DepartmentNanchang UniversityNanchang 330006China Institute of Urology Nanchang University Burns Institute Nanchang University

nitric oxide（NO）and its reaction products were key players in the pathophysiology of sepsis and shock.The present study was designed to explore the effects of lanthanum chloride（LaCl3）on inducible nitric oxide synthase（iNOS）expression,at both gene and protein levels,in RAW264.7 macrophages induced by Lipopolysaccharide（LPS）.Reverse transcription polymerase chain reaction（RT-PCR）,immunofluorescence,and western blot were employed to measure iNOS gene expression,localization,and protein expression respectively.NO production in culture supernatants was detected by the nitrate reductase method.The results showed that LaCl3 significantly attenuated the iNOS gene and protein expression,as well as NO production in RAW264.7cells induced by LPS.

关键词： lanthanum chloride lipopolysaccharide nitric oxide inducible nitric oxide synthase rare earths

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

Ginkgo biloba leaf extract effects on inducible nitric oxide synthase, Bcl-2, and Bax expression in rat models of spinal cord injury

引用

Neural Regeneration Research 2008年第8期3卷 875-880页

作者： Jiejun Jiao Bin Du Seventh Area Department of Orthopaedics Yixing People＇s Hospital Yixing 214200 Jiangsu Province China

BACKGROUND：Ginkgo biloba leaf extract exhibits neuroprotective effects in spinal cord injury. However, the mechanisms of action remain unclear. OBJECTIVE： To investigate inducible nitric oxide synthase （iNOS） and Bcl-2/Bax expression in the injured spinal cord, and to explore the neuroprotective mechanisms of ginkgo biloba leaf extract in rats with spinal cord injury. DESIGN, TIME AND SETTING： The randomized, controlled, cell molecular biology experiment was performed at Soochow University, China from March 2007 to March 2008. MATERIALS： A total of 120 healthy, adult Sprague Dawley rats were selected for this study. Rat models of moderate acute thoracic （T9） spinal cord injury were established using the modified Allen method. Shuxuening injection was obtained from Zhenbaodao Pharmaceutical Co., Ltd., China. Methylprednisolone was purchased from North China Pharmaceutical Co., Ltd. METHODS： All rats were equally and randomly divided into four groups. Only the spinal cord was exposed in the sham operation group rats. In the trauma group, rats were not treated with drugs following spinal cord injury. Rats in the hormone group were intraperitoneally injected with 30 mg/kg methylprednisolone following spinal cord injury. Rats in the ginkgo biloba leaf extract group were intraperitoneally infused with a 1.0 mL/kg Shuxuening injection per day. MAIN OUTCOME MEASURES： At 1 hour, as well as 1, 3, 5, 7, and 14 days after spinal cord injury, iNOS- and Bcl-2/Bax-positive cells were quantified with immunohistochemistry. Pathological changes were detected using hematoxylineosin staining under an optical microscope. RESULTS： Spinal cord injury in the ginkgo biloba leaf extract and hormone groups was milder compared with the trauma group. Demyelination was significantly ameliorated and the necrotic cavity was obviously reduced in the injured spinal cord of rats in the ginkgo biloba leaf extract and hormone groups at each time point. iNOS expression was increased in the injured spinal cord, and reached a peak at 5 days. The number

关键词： apoptosis Bcl-2/Bax ginkgo biloba leaf extract inducible nitric oxide synthase methylprednisolone neuroprotection spinal cord injury

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：