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浙江大学学报（医学版） 2004年第2期33卷 151-154页

作者：蔡思宇俞锋施育平浙江大学医学院附属第二医院浙江杭州310009

目的 :探讨浙江汉族人群中血管紧张素原 (AGT)基因 M2 35 T变异与原发性高血压的关系。方法 :对116例高血压病患者与 114名正常血压者进行对照研究。采用聚合酶链式反应 (PCR)与限制性片段长度多态性(RFLP)技术检测 AGT基因 M2 35 T变... 详细信息

目的 :探讨浙江汉族人群中血管紧张素原 (AGT)基因 M2 35 T变异与原发性高血压的关系。方法 :对116例高血压病患者与 114名正常血压者进行对照研究。采用聚合酶链式反应 (PCR)与限制性片段长度多态性(RFLP)技术检测 AGT基因 M2 35 T变异。同时测量血压、身高、体重、空腹血糖与血脂。结果 :1高血压组收缩压与舒张压水平显著高于对照组 (P<0 .0 1) ;而两组间年龄、性别、体重指数、血糖与血脂差异无显著性 (P>0 .0 5 )。2经 PCR扩增及 Tth 111I酶切 ,AGT基因型有三种形式 :MM、TT与 MT基因型。两组 AGT基因型的分布均符合 Hardy- Weinberg平衡。 3AGT基因 M2 35 T基因型在高血压组与对照组的分布差异有显著性 (χ2 =6 .96 6 ,P<0 .0 5 )。高血压组 TT基因型与 T2 35等位基因的频率高于对照组 (TT基因型 :0 .4 7vs 0 .33,χ2 =5 .36 ,P<0 .0 5 ;T2 35等位基因 :0 .71vs 0 .6 0 ,χ2 =6 .179,P<0 .0 5 )。结论 :在浙江汉族人群中 ,AGT基因 M2 35 T变异与原发性高血压的发病显著相关 ,TT基因型或 T2 35等位基因可能是高血压的一个遗传方面的危险因素。

关键词：血管紧张素原/遗传学基因多态性原发性高血压

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Human-chimpanzee DNA sequence variation in the four major genes of the renin angiotensin system

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GENOMICS 2000年第1期69卷 14-26页

作者： Dufour, C Casane, D Denton, D Wickings, J Corvol, P Jeunemaitre, X Coll France INSERM U36 Chaire Med Expt & Endocrinol Renale F-75005 Paris France Univ Paris 11 UPRESA CNRS 8080 Equipe Phylogenie & Evolut Mol F-91405 Orsay France Univ Melbourne Howard Florey Inst Expt Physiol & Med Parkville Vic 3052 Australia Ctr Int Rech Med Franceville Gabon

The renin angiotensin system (RAS) is involved in blood pressure control and water/sodium metabolism. The genes encoding the proteins of this system are candidate genes for essential hypertension. The RAS involves four main molecules: angiotensinogen, renin, angiotensin I-converting enzyme, and the angiotensin II type 1 receptor (encoded by the genes AGT, REN, DCP1, and AGTR1, respectively). We performed a molecular screening over 17,037 bp of the coding and 5' and 3' untranslated regions of these genes, from three to six common chimpanzees. We identified 44 single-nucleotide polymorphisms (SNPs) in chimpanzee samples, including 18 coding-region SNPs, 5 of which led to an amino acid replacement. We observed common and different features at various sites (synonymous, nonsynonymous, and noncoding) within and between the four chimpanzee genes: (1) the nucleotide diversity at noncoding sites was similar;(2) the nucleotide diversity at nonsynonymous sites was low, probably reflecting purifying selection, except for the AGT gene;(3) the nucleotide diversity at synonymous sites, which was dependent on the G+C content at the third position of the codon, was high, except for the AGTR1 gene. Comparison of the chimpanzee SNPs with those previously reported for humans identified 119 sites with fixed differences (including 62 coding sites, 17 of which resulted in amino acid differences between the species). Analysis of polymorphism within species and divergence between species shed light on the evolutionary constraints on these genes. In particular, comparison of the pattern of mutation at polymorphic and fixed sites between humans and chimpanzees suggested that the high G+C content of the DCP1 gene was maintained by positive selection at its silent sites. Finally, we propose 68 ancestral alleles for the human RAS genes and discuss the implications for their use in future hypertension-susceptibility association studies. (C) 2000 Academic Press.

关键词：血管紧张素原/遗传学 DNA/化学 DNA/遗传学进化分子外显子基因/遗传学内含子分子序列数据突变黑猩猩属肽基二肽酶A/遗传学多态性单核苷酸受体血管紧张素 1型受体血管紧张素 2型受体血管紧张素/遗传学肾素/遗传学肾素-血管紧张素系统/遗传学序列分析 DNA 变异(遗传学) 动物人类

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Associations between angiotensinogen gene variants and left ventricular mass and function in the HyperGEN study

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AMERICAN HEART JOURNAL 2002年第5期143卷 854-860页

作者： Tang, W Devereux, RB Rao, DC Oberman, A Hopkins, PN Kitzman, DW Arnett, DK Univ Minnesota Div Epidemiol Sch Publ Hlth Minneapolis MN 55455 USA Cornell Univ Weill Med Coll Dept Med Div Cardiol Ithaca NY 14853 USA Univ Washington Sch Med Div Biostat Seattle WA 98195 USA Univ Alabama Div Prevent Med Tuscaloosa AL 35487 USA Univ Utah Salt Lake City UT 84112 USA Wake Forest Univ Sch Med Winston Salem NC 27109 USA

Background The angiotensinogen M235T polymorphism is positively associated with plasma angiotensinogen, hypertension, and coronary heart disease. However, the association of M235T polymorphism with left ventricular (LV) mass and function is not well defined at the population level. We investigated whether 2 tightly linked polymorphisms of angiotensinogen gene, M235T and G-6A, are associated with LV mass and function in a large population-based sample, composed mostly of patients with hypertension. Methods Two-dimensional guided M-mode and pulsed Doppler scan echocardiograms were performed in 605 participants. The angiotensinogen M235T was analyzed with a standard polymerase chain reaction test, and the G-6A variant was measured with mass spectrophotometry. Results The association of angiotensinogen gene to LV mass and LV mass indexed to body surface area (LVMi) differed significantly between subjects with normotensive and hypertensive conditions with respect to the direction of association (P < .005). The methionine-threonine/threonine-threonine genotype was negatively associated with LV mass and LVM1 in patients with hypertension after adjustment for blood pressure, antihypertensive medication use, weight, and other covariates (P < .001), and patients with normotensive conditions with the methionine-threonine/threonine-threonine genotype had higher LV mass and LVM1 (P = .04, for LV mass;P = .14, for LVM1). The association in patients with normotensive conditions was not influenced by blood pressure but was partly confounded by weight. Conclusion Variation in the angiotensinogen gene was modestly associated with LV mass independently of covariates in patients with hypertensive conditions. The direction of the association was opposite to that observed in patients with normotensive conditions, probably because of the influence of other risk factors or antihypertensive medication use or both.

关键词：方差分析血管紧张素原/遗传学横断面研究高血压/并发症肥大左心室/遗传学肥大左心室/病理学肥大左心室/病理生理学多态现象遗传/遗传学心室功能障碍左/遗传学心室功能障碍左/病理生理学女(雌)性人类男(雄)性中年人

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Genetic control of fertility and embryonic waste in the mouse: A role for angiotensinogen

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BIOLOGY OF REPRODUCTION 2000年第2期62卷 457-462页

作者： Tempfer, CB Moreno, RM Gregg, AR Baylor Coll Med Dept Gynecol & Obstet Houston TX 77030 USA Baylor Coll Med Dept Human & Mol Genet Houston TX 77030 USA

The purpose of this study was to evaluate the impact of angiotensinogen gene (Agt) deficiency on reproductive fitness in a rodent model. Mice with 0 (Agt(-/-)), 1 (Agt(-/+)), and 2 (Agt(+/+)) copies of Agt were bred according to the following schemes: 1) Agt(-/-) X Agt(-/-), 2) Agt(-/+) X Agt(-/+), 3) Agt(+/+) X Agt(+/+), and 4) Agt(+/+) female X Ag-/+ male. There were 4 breeding pairs per scheme. Breedings were time mated. Mice and litters were weighed daily. Southern blotting was used for genotyping. We found that Agt(-/-) breeding pairs had fewer litters (2 [range 1-2] vs. 4 [range 3-5];P = 0.01), fewer pups per litter (4 [range 1-7] vs. 6 [range 1-10];P = 0.006), and longer interpregnancy intervals (43 days [range 31-44] vs. 35.5 days [range 22-58];P = 0.04) compared to wild-type controls. The ratio of postcoital plugs to subsequent litters was 4.0 and 1.2 for Agt(-/-) and Agt(+/+) breedings, respectively (P = 0.03). Median maternal weights during all trimesters of pregnancy were significantly lower for Agt-deficient mice compared to wild-type controls. Among Agt(-/+) X Agt(-/+) breedings, the proportions of Agt(+/+) (n = 17), Agt(-/+) (n = 38), and Agt(-/-) (n = 4) offspring differed significantly from the expected 1:2:1 Mendelian inheritance pattern (P = 0.03). Neonatal survival among the offspring derived from the Agt(-/-) X Agt(-/-) breeding scheme was significantly reduced (P = 0.001). We conclude that Agt deficiency is associated with an in utero lethal effect, decreased fertility, and impaired neonatal survival.

关键词：流产自然/遗传学血管紧张素原/遗传学动物新生胚胎丢失/遗传学生育力/遗传学生殖器女(雌)性/解剖学和组织学生殖器男(雄)性/解剖学和组织学基因型生长/遗传学生长/生理学小鼠基因敲除妊娠动物/遗传学生殖/遗传学生殖/生理学存活率分析动物女(雌)性男(雄)性小鼠妊娠

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Angiotensinogen M235T polymorphism is associated with plasma angiotensinogen and cardiovascular disease

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AMERICAN HEART JOURNAL 1999年第4期137卷 698-705页

作者： Winkelmann, BR Russ, AP Nauck, M Klein, B Böhm, BO Maier, V Zotz, R Matheis, G Wolf, A Wieland, H Gross, W Galton, DJ März, W Ludwigshafen Heart Ctr Dept Cardiol Ludwigshafen Germany Univ Frankfurt Dept Med D-6000 Frankfurt Germany Univ Frankfurt Dept Heart Surg D-6000 Frankfurt Germany Univ Frankfurt Dept Biochem D-6000 Frankfurt Germany Univ Freiburg Dept Med Div Clin Chem D-7800 Freiburg Germany Univ Ulm Dept Med Ulm Germany Univ Dusseldorf Inst Blood Transfus & Hemostasiol D-4000 Dusseldorf Germany St Bartholomews Hosp Dept Metab & Genet London England

Background Genes encoding components of the renin-angiotensin system have been associated with elevated blood pressure (BP) and an increased risk of coronary artery disease. To explore the role of the angiotensinogen (AGT) gene in coronary atherosclerosis and thrombosis, we studied the effect of the AGT M235T gene variant on plasma AGT levels and BP in patients with coronary artery disease and in the subgroup of survivors of myocardial infarction as compared with angiographically defined control subjects. Methods and Results This was a case-control study of 301 white male subjects examined at Frankfurt University medical center. Plasma AGT levels increased stepwise according to the number of T235 alleles present (no T235 allele, 14.8 +/- 3.9 nmol/L;1 allele, 15.7 +/- 5.1 nmol/L;2 alleles, 17.3 +/- 4.7 nmol/L;P = .006). In a multivariate model, circulating AGT emerged as the most important predictor of diastolic pressure (P = .001). In addition, AGT M235T gene polymorphism remained a significant predictor of diastolic BP in a multivariate model adjusted for age, body mass index, fasting glucose, apolipoprotein B, presence of coronary artery disease, and treatment with antihypertensive agents (P < .05). Finally, homozygosity for T235 was associated with increased univariate risk of coronary artery disease and myocardial infarction (odds ratio estimates 1.5;95% confidence intervals 1.1 to 2.1, P = .03, and 1.0 to 2,1, P = .05, respectively). Conclusions The significant relations observed between the AGT M235T variant, its protein product, and the cardiovascular disease phenotypes provide evidence for a possible role of elevated circulating AGT in the pathogenesis of coronary artery disease.

关键词：等位基因血管紧张素原/血液血管紧张素原/遗传学血压/遗传学心血管疾病/遗传学病例对照研究冠状动脉血栓形成/遗传学基因频率基因型多元分析心肌梗死/遗传学比值比肽基二肽酶A/血液多态现象遗传肾素-血管紧张素系统/遗传学危险因素人类男(雄)性中年人

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Genetics of hypertension

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CURRENT OPINION IN GENETICS & DEVELOPMENT 2000年第3期10卷 325-329页

作者： Munroe, PB Caulfield, MJ St Bartholomews & Royal London Sch Med & Dent Dept Clin Pharmacol London EC1M 6BQ England

In the past year, substantial progress has been made in both mapping and fine mapping the genes involved in blood pressure regulation. Genome scans have been carried out in humans and mice and these reveal many new potential chromosomal locations for blood pressure susceptibility loci. The chromosomal regions containing blood pressure genes for many of the inbred hypertensive rat models have been refined using new congenic strains. Further genetic studies support a role for angiotensinogen, aldosterone synthase and a region close to the epithelial sodium channel in blood pressure regulation. Finally, comprehensive single-nucleotide polymorphism analysis of cardiovascular genes has been undertaken using chip technology.

关键词：血管紧张素原/遗传学基因组人高血压/遗传学大鼠近交SHR 钠通道/遗传学动物人类小鼠大鼠

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Evidence of a major gene effect for angiotensinogen among Nigerians

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ANNALS OF HUMAN GENETICS 1999年第4期63卷 293-300页

作者： Guo, X Rotimi, C Cooper, R Luke, A Elston, RC Ogunbiyi, O Ward, R Loyola Univ Dept Epidemiol & Prevent Med Stritch Sch Med Ctr Genet Epidemiol Maywood IL 60153 USA Loyola Univ Dept Epidemiol & Prevent Med Stritch Sch Med Maywood IL 60153 USA Case Western Reserve Univ Dept Epidemiol & Biostat Cleveland OH 44106 USA Univ Ibadan Univ Coll HOsp Ibadan Nigeria Univ Oxford Dept Biol Anthropol Oxford England

To dissect the genetic pathway of hypertension, we measured angiotensinogen in 685 members of 186 families recruited from a rural community in southwest Nigeria. Commingling and segregation analyses were carried out. A mixture of two and/or three distributions fits the data significantly better than a single distribution in commingling analysis, suggesting a major gene effect. Segregation analysis confirmed that a recessive major gene model for low values of angiotensinogen provides the best fit to the data and about 13% of the variance was due to the recessive gene segregation.

关键词：血管紧张素原/血液血管紧张素原/遗传学血压/遗传学基因隐性高血压/血液高血压/流行病学高血压/遗传学模型遗传学尼日利亚/流行病学农村人口青少年成年人女(雌)性人类男(雄)性中年人

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DNA-Polymorphisms and plasma levels of vascular disease risk factors in Greenland Inuit - Is there a relation with the low risk of cardiovascular disease in the Inuit?

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THROMBOSIS AND HAEMOSTASIS 1999年第4期81卷 547-552页

作者： de Maat, MPM Bladbjerg, EM Johansen, LG de Knijff, P Gram, J Kluft, C Jespersen, J TNO PG Gaubius Lab NL-2301 CE Leiden Netherlands Ribe Cty Hosp Dept Clin Biochem Esbjerg Denmark Univ So Denmark Dept Thrombosis Res Esbjerg Denmark

Greenland Inuit are a population with a low risk of cardiovascular disease. Recently, we stated that frequencies of potentially high risk alleles of the apolipoproteins, fibrinogen, factor V, glycoprotein IIIa and factor VII (FVII) genes have different allele frequencies in the Inuit when compared with Caucasian populations. We have extended this study and evaluated whether or not this was also true for the genetic polymorphisms of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), angiotensin-converting enzyme (ACE) and angiotensinogen in a group of 133 Greenland Inuit, aged 30-34 y. In addition, we compared the plasma levels of these factors and those of C-reactive protein (CRP) and D-Dimer in Inuit and in Danes, comparable for age and gender. Frequencies (f) were assessed of the alleles that are known as the potential high risk alleles in Caucasians. In the Inuit, the f(insertion allele) of the t-PA intron8ins311 polymorphism was 0.37 (CI 0.32-0.43), the f(4G allele) of the PAI-1 promoter polymorphism was 0.88 (CI 0.83-0.91), the f(deletion allele) of the ACE intron16ins287 polymorphism was 0.40 (CI 0.33-0.47) and the f(M-allele) of the angiotensinogen M/T353 polymorphism was 0.30 (CI 0.25-0.38). As for fibrinogen and FVII polymorphisms, these frequencies are all significantly different from what is reported for Caucasian populations. In the Inuit, plasma levels of fibrinogen and D-Dimer were higher than in the Danes, the PAI-1 levels were lower and FVII, t-PA and CRP levels were comparable. The observed allele frequencies of the polymorphisms of t-PA, fibrinogen, FVII, ACE, angiotensinogen and the plasma levels of PAI-1 and D-Dimer were in accordance with the low CVD risk in the Inuit, considering the observed associations between these measures and CVD risk in Caucasian populations, but for other measures this was not the case (allele frequencies of the PAI-1 polymorphism, and plasma levels of fibrinogen, FVII and t-PA). In con

关键词：等位基因血管紧张素原/遗传学抗纤维蛋白溶解药/药理学心血管疾病/流行病学 DNA/血液 DNA/遗传学丹麦/流行病学纤维蛋白纤维蛋白原降解物/遗传学格陵兰/流行病学伊努/遗传学多态现象遗传危险因素血管疾病/血液血管疾病/人种学血管疾病/遗传学成年人女(雌)性人类男(雄)性

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Maternal and fetal angiotensinogen gene allele sharing in pre-eclampsia

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BRITISH JOURNAL OF OBSTETRICS AND GYNAECOLOGY 1999年第3期106卷 244-251页

作者： Morgan, L Crawshaw, S Baker, PN Pipkin, FB Kalsheker, N Univ Nottingham Hosp Dept Clin Lab Sci Div Clin Chem Nottingham NG7 2UH England Univ Nottingham Hosp Dept Obstet Midwifery & Gynaceol Nottingham NG7 2UH England

Objective To compare the angiotensinogen genotypes in normotensive and pre-eclamptic pregnancies in maternal and fetal samples. Design Prospective observational study. Setting University Hospital, Queen's Medical Centre Nottingham. Population Forty-three women with pre-eclampsia and 84 normotensive pregnant women. Fetal samples were available for genotyping from 96% of the pregnancies. Methods Maternal and fetal DNA was genotyped at angiotensinogen codon 235 and at a dinuclcotide repeat polymorphism in the 3' flanking region of the gene. Angiotensinogen and renin concentrations were measured in maternal plasma by radioimmunoassay. Results In contrast to earlier studies, no association was demonstrated between the angiotensinogen 235 and variant and pre-eclampsia. Normotensive pregnant women homozygous for this variant had significantly lower plasma angiotensinogen concentrations (median 2.2 ng Al/mL;IQR 1.8-3.0) than women homozygous for the 235 Met allele (3.6 ng Al/mL: IQR 2.5-4.1;P = 0.04). In pre-eclamptic pregnancies, 79% (11/14) of mothers heterozygous for the dinucleotide repeat allele designated A9 transmitted this allele to the fetus, more frequently than would be expected by chance (P = 0.02). The A9 allele was associated with low plasma angiotensinogen concentrations (P = 0.001) and high renin concentrations (P = 0.02) in normotensive women. Conclusions There is no evidence that the angiotensinogen 235 Thr allele is associated with pre-eclampsia in the Nottingham population. The angiotensinogen 235 Thr allele is associated with low plasma angiotensinogen concentrations in normotensive pregnant women, in contrast to the high levels associated with this variant in non-pregnant women suggesting that regulation of angiotensinogen expression in normal pregnancy may differ significantly from that in the non-pregnant state. There is preliminary evidence that maternal-fetal transmission of an angiotensinogen allele associated with low plasma angiotensinogen conce

关键词：等位基因血管紧张素原/血液血管紧张素原/遗传学胎血/代谢基因型多态现象遗传先兆子痫/血液先兆子痫/遗传学前瞻性研究肾素/血液成年人女(雌)性人类妊娠

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Apoptosis of lung epithelial cells in response to TNF-α requires angiotensin II generation de novo

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JOURNAL OF CELLULAR PHYSIOLOGY 2000年第2期185卷 253-259页

作者： Wang, RQ Alam, G Zagariya, A Gidea, C Pinillos, H Lalude, O Choudhary, G Oezatalay, D Uhal, BD Michigan State Univ Dept Physiol E Lansing MI 48824 USA Michael Reese Hosp & Med Ctr Dept Med Chicago IL 60616 USA Michael Reese Hosp & Med Ctr Div Neonatol Chicago IL 60616 USA Michael Reese Hosp & Med Ctr Cardiovasc Inst Chicago IL 60616 USA

Recent work from this laboratory demonstrated that apoptosis of pulmonary alveolar epithelial cells (AEC) in response to fas requires angiotensin II (ANGII) generation de novo and binding to its receptor (Wang et at., 1999b, Am I Physiol Lung Cell Mol Physiol 277:L1245-L1250). These findings led us to hypothesize that a similar mechanism might be involved in the induction of AEC apoptosis by TNF-alpha. Apoptosis was detected by assessment of nuclear and chromatin morphology, increased activity of caspase 3, binding of annexin V, and by net cell loss inhibitable by the caspase inhibitor ZVAD-fmk. Purified human TNF-alpha induced dose-dependent apoptosis in primary type II pneumocytes isolated from rats or in the AEC-derived human lung carcinoma cell line A549. Apoptosis in response to TNF-alpha was inhibited in a dose-dependent manner by the nonselective ANGII receptor antagonist saralasin or by the nonthiol ACE inhibitor lisinopril;the inhibition of TNF-induced apoptosis was maximal at 50 mu g/ml saralasin (101% inhibition) and at 0.5 mu g/ml lisinopril (86% inhibition). in both cell culture models, purified TNF-alpha caused a significant increase in the mRNA for angiotensinogen (ANGEN), which was not expressed in unactivated cells. Transfection of primary cultures of rat AEC with antisense oligonucleotides against ANGEN mRNA inhibited the subsequent induction of TNF-stimulated apoptosis by 72% (P < 0.01). Exposure to TNF-alpha increased the concentration of ANGII in the serum-free extracellular medium by fivefold in A549 cell cultures and by 40-fold in primary AEC preparations;further, exposure to TNF-alpha for 40 h caused a net eel I loss of 70%, which was completely abrogated by either the caspase inhibitor ZVAD-fmk, lisinopril, or saralasin. Apoptosis in response to TNF-alpha was also completely inhibited by neutralizing antibodies specific for ANGII (P < 0.01), but isotype-matched nonimmune immunoglobulins had no significant effect. These data indicate that the

关键词：血管紧张素Ⅱ/生物合成血管紧张素Ⅱ/代谢血管紧张素转换酶抑制药/药理学血管紧张素原/遗传学血管紧张素原/代谢细胞凋亡/药物作用细胞凋亡/生理学细胞系剂量效应关系药物上皮细胞/药物作用上皮细胞/生理学基因表达/生理学赖诺普利/药理学肺/细胞学肺/药物作用肺/生理学蛋白质加工转译后/生理学 RNA 信使/代谢受体血管紧张素/拮抗剂和抑制剂受体血管紧张素/代谢沙拉新/药理学肿瘤坏死因子α/药理学人类

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