检索结果-内蒙古大学图书馆

The renin-angiotensin system influences ocular endothelial cell proliferation in diabetes - Transgenic and interventional studies

引用

AMERICAN JOURNAL OF PATHOLOGY 2003年第1期162卷 151-160页

作者： Moravski, CJ Skinner, SL Stubbs, AJ Sarlos, S Kelly, DJ Cooper, ME Gilbert, RE Wilkinson-Berka, JL Univ Melbourne Dept Physiol Parkville Vic 3010 Australia St Vincents Hosp Dept Med Fitzroy Vic 3065 Australia Austin & Repatriat Med Ctr Dept Med Heidelberg West Australia

Neovascularization in the retina and iris of diabetic patients is a major cause of severe visual loss. However, study of these lesions is compromised by the lack of a comparable diabetic rodent model. Because the vasoactive and angiogenic agent, angiotensin H, is involved in diabetic microvascular disease, we aimed to determine whether endothelial cell proliferation could be induced in the retinae and irides of hypertensive transgenic (mRen-2)27 rats that display an enhanced extra-renal renin-angiotensin system (RAS), including the eye. Six-week-old Ren-2, spontaneously hypertensive, and Sprague-Dawley rats received either streptozotocin or control vehicle and were studied for 36 weeks. Additional nondiabetic and diabetic Ren-2 rats were treated throughout with the angiotensin-converting enzyme inhibitor lisinopril (LIS) (10 mg/kg/day in drinking water). Endothelial cell proliferation was only observed in retinae and irides of diabetic Ren-2 rats and was reduced with LIS. In diabetic Ren-2, vascular endothelial growth factor (VEGF) and VEGFR-2 mRNA were increased in retinae and irides and reduced with US. Diabetes activated ocular renin in Ren-2 but not Sprague-Dawley rats. The diabetic Ren-2 rat is a model of intraocular endothelial cell proliferation that can be attenuated by RAS blockade via VEGF-dependent pathways. RAS blockade is a potential treatment for vision-threatening diabetic microvascular complications.

关键词：血管紧张素转换酶抑制药/药理学动物基因修饰慢性病糖尿病实验性/化学诱导糖尿病实验性/并发症糖尿病实验性/病理学糖尿病视网膜病变/病因学糖尿病视网膜病变/病理学疾病模型动物内皮生长因子/遗传学内皮生长因子/代谢内皮血管/药物作用内皮血管/代谢内皮血管/病理学眼/代谢眼/病理学杂合子原位杂交胞间信号肽类和蛋白质类/遗传学胞间信号肽类和蛋白质类/代谢虹膜/血液供给虹膜/药物作用虹膜/病理学赖诺普利/药理学淋巴因子/遗传学淋巴因子/代谢 RNA 信使/代谢大鼠近交SHR 大鼠 Sprague-Dawley 肾素/遗传学肾素/代谢肾素-血管紧张素系统/药物作用肾素-血管紧张素系统/生理学视网膜/药物作用视网膜/病理学链脲菌素血管内皮生长因子A 血管内皮生长因子受体2/遗传学血管内皮生长因子受体2/代谢血管内皮生长因子类动物女(雌)性大鼠

来源：评论

学校读者我要写书评

暂无评论

A comparison of primary endothelial cells and endothelial cell lines for studies of immune interactions

引用

TRANSPLANT IMMUNOLOGY 1999年第4期7卷 239-246页

作者： Lidington, EA Moyes, DL McCormack, AM Rose, ML Harefield Hosp Heart Sci Ctr Imperial Coll Sci Technol & Med Natl Heart & Lung InstDiv Cardiothorac Surg Harefield UB9 6JH Middx England

The purpose of this study was to assess the suitability of using endothelial cell (EC) lines for studies of endothelial/immune interactions. The immortal human EC lines HMEC-1, ECV304 and EaHy926 were compared to human umbilical vein endothelial cells (HUVEC) for constitutive and induced expression of surface antigens known to be involved in interactions with T cells. These cell lines were also compared to HUVEC in transendothelial migration assays. Flow cytometry was used to measure cell surface expression of platelet/endothelial cell adhesion molecule-1 (PECAM-1), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, major histocompatibility complex (MHC) class I and MHC class II, CD40, CD95 (fas) and lymphocyte function associated antigen-3 (LFA-3) before and after treatment with the cytokines tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma). Polymerase chain reaction (PCR) was used to detect expression of the MHC class II transactivator. Significant differences were found in the ability to respond to cytokines between HUVEC and the cell lines, the greatest differences being induction of VCAM-1 and E-selectin in response to TNF-or and induction of MHC class II antigens in response to IFN-gamma. Thus unlike HUVEC, induction of VCAM-1 and E-selectin was not detectable on EaHy926 and ECV304 and barely detectable on HMEC-1. MHC class II antigens were not induced on ECV304 in response to IFN-gamma and nor was the class II transactivator (CIITA). Unlike HUVEC and the other cell lines, ECV304 were constitutively negative for PECAM-1. Constitutive and induced expression of MHC class I, ICAM-1, LFA/3, CD40 and fas were most conserved between the cell lines and showed little difference to HUVEC. The migration of peripheral blood mononuclear cells (PBMC) through all cell lines was significantly reduced compared to through HUVEC, suggesting that there is a functional difference between the cell lines with

关键词：抗原表面/生物合成细胞黏附分子/生物合成细胞系细胞运动/药物作用内皮血管/细胞学内皮血管/药物作用内皮血管/免疫学内皮血管/代谢干扰素Ⅱ型/药理学白细胞单核/细胞学白细胞单核/免疫学核蛋白质类反式激活因子类/生物合成肿瘤坏死因子α/药理学人类

来源：评论

学校读者我要写书评

暂无评论

Mass spectrometric analysis of platelet-activating factor after isolation by solid-phase extraction and direct derivatization with pentafluorobenzoic anhydride

引用

JOURNAL OF THE AMERICAN SOCIETY FOR MASS SPECTROMETRY 2000年第2期11卷 176-181页

作者： Weintraub, ST Satsangi, RK Sprague, EA Prihoda, TJ Pinckard, RN Univ Texas Hlth Sci Ctr Dept Biochem San Antonio TX 78229 USA Univ Texas Hlth Sci Ctr Dept Radiol San Antonio TX 78229 USA Univ Texas Hlth Sci Ctr Dept Pathol San Antonio TX 78229 USA

Platelet-activating factor is the term used to denote a class of extremely patent lipid mediators that consist predominantly of 1-O-alkyl- and 1-O-acyl-2-acetyl-sn-glycero-3-phosphocholines. A method has been devised for rapid isolation of these acetylated phospholipids by solid-phase extraction prior to direct derivatization with pentafluorobenzoic anhydride and analysis by gas chromatography (GC)/electron-capture mass spectrometry. Recovery through the entire method (lipid isolation, derivatization, and purification) typically ranged from 70% to 85%. Using the direct derivatization procedure described here, the practical limit of detection for each of the standard alkyl- and acyl-platelet-activating factor homologs was 1 fmol injected into the GC. Results from the application of the method to the analysis of alkyl and acyl homologs of platelet-activating factor isolated from stimulated human umbilical vein endothelial cells are presented, exhibiting excellent accuracy and precision for a wide range of tissue levels of this class of potent autacoids. (C) 2000 American Society for Mass Spectrometry.

关键词：酐类/化学苯甲酸盐类/化学细胞培养的内皮血管/细胞学内皮血管/药物作用内皮血管/代谢气相色谱-质谱法指示剂和试剂质谱分析法血小板活化因子/化学人类

来源：评论

学校读者我要写书评

暂无评论

The effect of length on the sensitivity to phenylephrine and calcium in intact and skinned vascular smooth muscle

引用

JOURNAL OF MUSCLE RESEARCH AND CELL MOTILITY 1999年第1期20卷 11-18页

作者： Van Heijst, BGV De Wit, E Van der Heide, UA Blangé, T Jongsma, HJ De Beer, EL Univ Utrecht Fac Med Dept Med Physiol & Sports Med NL-3508 TA Utrecht Netherlands Univ Amsterdam Acad Med Ctr Dept Physiol NL-1100 DE Amsterdam Netherlands

The length dependency of the sensitivity to activators of the smooth muscle of different blood vessels is not yet fully understood. Muscle preparations of the aorta, the femoral artery and the portal vein of the rabbit were investigated for the length dependency of the sensitivity to phenylephrine and calcium in both intact and triton X-100 skinned preparations. For intact smooth muscles we found that at increased preparation length, the sensitivity of contraction was increased. The femoral artery showed the largest effect and the portal vein the smallest. In the skinned preparations of the three preparations the calcium sensitivity was not dependent on the preparation length. We conclude that the changes of the sensitivity in intact preparations are not caused by changes of the calcium sensitivity of the contractile proteins.

关键词：主动脉/药物作用主动脉/生理学钙/药理学剂量效应关系药物股动脉/药物作用股动脉/生理学肌收缩/药物作用肌收缩/生理学肌平滑血管/解剖学和组织学肌平滑血管/药物作用肌平滑血管/生理学苯福林/药理学门静脉/药物作用门静脉/生理学血管收缩药/药理学动物兔

来源：评论

学校读者我要写书评

暂无评论

Overexpression of VEGF 121 in immortalized endothelial cells causes conversion to slowly growing angiosarcoma and high level expression of the VEGF receptors VEGFR-1 and VEGFR-2 in vivo

引用

AMERICAN JOURNAL OF PATHOLOGY 2000年第4期156卷 1469-1476页

作者： Arbiser, JL Larsson, H Claesson-Welsh, L Bai, XH LaMontagne, K Weiss, SW Soker, S Flynn, E Brown, LF Emory Univ Sch Med Dept Dermatol Atlanta GA 30322 USA Emory Univ Sch Med Dept Pathol Atlanta GA 30322 USA Harvard Univ Sch Med Childrens Hosp Dept Surg Boston MA USA Harvard Univ Sch Med Beth Israel Deaconess Med Ctr Boston MA USA Uppsala Univ Rudbeck Lab Dept Genet & Pathol Uppsala Sweden

Vascular endothelial growth factor (VEGF or vascular permeability factor) is an important angiogenic factor that is up-regulated in numerous benign and malignant disorders, including angiosarcoma, hemangiomas, and solid tumors. To determine the functional role of VEGF in the development of endothelial tumors, we expressed primate VEGF 121 in an endothelial cell line, MS1, derived from primary murine cells by immortalization with a temperature-sensitive SV40 large T antigen. This cell line expresses the VEGFR-2 (Flk-1/Kdr) receptor for VEGF. Expression of VEGF 121 led to the development of slowly growing endothelial tumors, which were histologically well-differentiated angiosarcomas. The angiosarcomas generated from MS1 VEGF cells demonstrated up-regulation of the VEGF receptors VEGFR-2 and VEGFR-1 (Flt-1) in vivo compared with benign hemangiomas generated from MS1 cells. Treatment of these cells with the VEGFR-2 tyrosine kinase inhibitor SU 1498 led to decreased expression of ets-1, a transcription factor which has been shown to be stimulated by VEGF. These results suggest that high level expression of VEGF in endothelial cells may result in malignant transformation. This transformation process likely involves both autocrine and paracrine pathways.

关键词：细胞系转化细胞转化肿瘤内皮生长因子/代谢内皮血管/细胞学内皮血管/药物作用内皮血管/代谢内皮血管/生理学酶抑制剂/药理学血管肉瘤/病因学血管肉瘤/病理学淋巴因子/代谢小鼠裸磷酰化/药物作用灵长目原癌基因蛋白质类/代谢受体蛋白质酪氨酸激酶类/拮抗剂和抑制剂受体蛋白质酪氨酸激酶类/代谢受体生长因子/拮抗剂和抑制剂受体生长因子/代谢受体血管内皮生长因子血管内皮生长因子A 血管内皮生长因子受体1 血管内皮生长因子类动物男(雄)性小鼠

来源：评论

学校读者我要写书评

暂无评论

Linkage between α₁ adrenergic receptor and the Jak/STAT signaling pathway in vascular smooth muscle cells

引用

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2000年第1期268卷 25-30页

作者： Sasaguri, T Teruya, H Ishida, A Abumiya, T Ogata, J Natl Cardiovasc Ctr Dept Biosci Osaka 5658565 Japan Natl Cardiovasc Ctr Dept Epidemiol Osaka 5658565 Japan Natl Cardiovasc Ctr Dept Prevent Cardiol Osaka 5658565 Japan

The Jak/STAT pathway is activated following stimulation of the type I angiotensin II receptor. To examine whether this pathway is shared among other G-protein-coupled receptors, we studied the linkage between the alpha(1) adrenergic receptor and this pathway. The alpha(1) agonist phenylephrine induced tyrosine phosphorylation of Jak2, Tyk2, and STAT1 in vascular smooth muscle cells. The phosphorylation of Jak2 was prevented by the alpha(1) receptor antagonists prazosin and chloroethylclonidine, but not by WB4101, and that of STAT1 was inhibited by prazosin and the Jak2 inhibitor AG490. After stimulation with phenylephrine, Jak2 and STAT1 were found to associate with alpha(1B) receptor. Phenylephrine stimulated the DNA binding activity of STAT1. Protein synthesis promoted by phenylephrine was inhibited by prazosin, AG490, and the introduction of a decoy oligonucleotide for STAT1. These results suggested that alpha(1) receptor is linked to the Jak/STAT pathway and that this pathway mediates alpha(1) agonist-induced smooth muscle hypertrophy. (C) 2000 Academic Press.

关键词：肾上腺素能α激动剂/药理学氨基酸序列碱基序列细胞分裂/生理学细胞培养的 DNA结合蛋白质类/化学 DNA结合蛋白质类/遗传学 DNA结合蛋白质类/代谢 Janus激酶2 肌平滑血管/细胞学肌平滑血管/药物作用肌平滑血管/代谢寡脱氧核糖核苷酸类/遗传学苯福林/药理学磷酰化蛋白酪氨酸激酶类/化学蛋白酪氨酸激酶类/代谢蛋白质类/化学蛋白质类/代谢原癌基因蛋白质类受体肾上腺素能α1/代谢 STAT1转录因子信号传导 TYK2激酶反式激活因子类/化学反式激活因子类/遗传学反式激活因子类/代谢转染酪氨酸/代谢人类

来源：评论

学校读者我要写书评

暂无评论

Atorvastatin but not L-arginine improves endothelial function in type I diabetes mellitus: A double-blind study

引用

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 2000年第2期36卷 410-+页

作者： Mullen, MJ Wright, D Donald, AE Thorne, S Thomson, H Deanfield, JE Great Ormond St Hosp Sick Children Vasc Physiol Unit London WC1N 3JH England UCL Dept Stat Sci London England

OBJECTIVES We sought to determine the effects of oral L-arginine and the hexamethyglutaryl coenzyme A reductase inhibitor atorvastatin on endothelial function in young patients with type I diabetes mellitus (DM). BACKGROUND Endothelial dysfunction, a key early event in atherosclerosis, occurs in young patients with type I DM, and its reversal may benefit the progression of vascular disease. Cholesterol reduction in L-arginine improve endothelial function in nondiabetic subjects, but their effect in patients with type I DM is unknown. METHODS In a double-blind, 2 X 2 factorial study, we investigated the effect of L-arginine (7 g twice daily) and atorvastatin (40 mg/day) on conduit artery vascular function in 84 normocholesterolemic young adults (mean +/- SD: age 34 rears [range 18 to 46], low density lipoprotein [LDL] cholesterol 2.96 +/- 0.89 mmol/liter) with type I DM. Brachial artery dilation to flow (flow-mediated dilation [FMD]) and to the direct smooth muscle dilator glyceryl trinitrate (GTN) were assessed noninvasively using high resolution ultrasound at baseline and after six weeks of treatment. RESULTS Atorvastatin resulted in a 48 +/- 10% decrease in serum LDL cholesterol levels, whereas L-arginine levels increased by 247 +/- 141% after L-arginine therapy. By analysis of covariance, treatment with atorvastatin resulted in a significant increase in FMD (p = 0.018. L-Arginine therapy had no significant effect on endothelial function, and there was no significant change in dilation to GTN after either intervention. CONCLUSIONS In young patients with type I DM, improvement in endothelial dysfunction can be demonstrated after just six weeks of treatment with atorvastatin. In contrast to studies of hypercholesterolemia, however, L-arginine had no benefit. Treatment with atorvastatin at an early stage may have an impact on the progression of atherosclerosis in these high risk patients. (C) 2000 by the American College of Cardiology.

关键词：精氨酸/药理学糖尿病 1型/病理生理学双盲法内皮血管/药物作用庚酸类/药理学羟甲基戊二酰基CoA还原酶抑制剂/药理学吡咯类/药理学血管舒张/药物作用青少年成年人女(雌)性人类男(雄)性中年人

来源：评论

学校读者我要写书评

暂无评论

Ras/mitogen-activated protein kinase mediates norepinephrine-induced phospholipase D activation in rabbit aortic smooth muscle cells by a phosphorylation-dependent mechanism

引用

JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第1期293卷 268-274页

作者： Muthalif, MM Parmentier, JH Benter, IF Karzoun, N Ahmed, A Khandekar, Z Adl, MZ Bourgoin, S Malik, KU Univ Tennessee Coll Med Dept Pharmacol Memphis TN 38163 USA So Coll Optometry Memphis TN USA CHUL Ctr Rech St Foy PQ Canada

Phospholipase D (PLD) activity is regulated by phosphatidylinositol 4,5-biphosphate, protein kinase C (PKC), ADP-ribosylation factor, and Rho. The present study was designed to investigate the mechanism of norepinephrine (NE)-mediated PLD activation in rabbit aortic vascular smooth muscle cells (VSMC). NE (10 mu M) caused activation of PLD, as measured by the production of phosphatidylethanol in [H-3]oleic acid-labeled cells. NE also increased PKC activity in VSMC. However, treatment of cells with bisindolylmaleimide, a PKC inhibitor, or longterm treatment with phorbol-12-myristate-13-acetate that depletes PKC did not decrease NE-induced activation of PLD. NE-stimulated PLD activity was attenuated by farnesyl transferase inhibitors (FPT III and SCH-56582), which reduce activation of both Pas and mitogen-activated protein (MAP) kinase. Moreover, transfection of VSMC with a dominant negative Pas resulted in inhibition of NE-stimulated MAP kinase and PLD activities. Treatment of cells with PD-98059, a MAP kinase kinase inhibitor, also reduced NE-stimulated PLD activity. These data suggest that NE-stimulated PLD activity is mediated via activation of Pas and MAP kinase in rabbit VSMC. To study the mechanism of activation of PLD by Ras/MAP kinase, NE-induced phosphorylation of PLD was examined. In VSMC, PLD of molecular mass 120 kDa was identified with polyclonal PLD antibody. Phosphorylation of PLD by NE, measured as P-32 incorporation into PLD, was inhibited by PD-98059. Moreover, PLD immunoprecipitated from VSMC lysates was phosphorylated in vitro by MAP kinase. Collectively, these results show a novel pathway for activation of PLD that appears to be mediated through Ras/MAP kinase pathway by a mechanism involving phosphorylation.

关键词：肾上腺素能α激动剂/药理学印迹法蛋白质钙/代谢酶激活/药物作用基因 ras/遗传学丝裂原激活蛋白激酶类/生理学肌平滑血管/药物作用肌平滑血管/酶学去甲肾上腺素/药理学磷脂酶D/代谢磷酰化沉淀素试验 β半乳糖苷酶类/代谢动物男(雄)性兔

来源：评论

学校读者我要写书评

暂无评论

Interferon-γ augments CD95(APO-1/Fas) and pro-caspase-8 expression and sensitizes human vascular endothelial cells to CD95-mediated apoptosis

引用

AMERICAN JOURNAL OF PATHOLOGY 2002年第4期161卷 1485-1495页

作者： Li, JH Kluger, MS Madge, LA Zheng, L Bothwell, ALM Pober, JS Yale Univ Sch Med Boyer Ctr Mol Med Interdept Program Vasc Biol & Transplantat New Haven CT 06510 USA

We have examined the effects of interferon (IFN)-gamma on expression and function of CD95 (APO-1/Fas) and associated proteins in cultured human umbilical vein and dermal microvascular endothelial cells (HUVEC and HDMEC, respectively). Unstimulated cells express only low levels of CD95;IFN-gamma produces a time- and concentration-dependent increase of CD95 in both cell types at the mRNA and cell surface protein levels. IFN-gamma also produces an increase in expression of pro-caspase-8 (FLICE/MACH) but does not significantly change expression of either Fas-associated death domain (FADD) protein or cellular FLICE inhibitory protein (cFLIP), other proteins associated with the CD95 death-inducing signaling complex (DISC). Neither resting nor IFN-gamma-treated EC express detectable CD95L mRNA or protein. Untreated HUVEC and HDMEC show minimal apoptosis when transduced to express CD95L. Treatment of CD95L-transduced cells with IFN-gamma causes apoptosis within 24 to 36 hours that can be blocked by antagonistic anti-CD95 antibody or by the caspase-inhibitory peptide zVAD-FMK. The extent of apoptosis is increased by co-treatment with either the protein synthesis inhibitor cycloheximide or the phosphatidylinositol 3-kinase inhibitor LY294002. Untransduced HUVEC treated with IFN-gamma also undergo CD95-iniated apoptosis when mixed with CD95L-transduced HUVEC or when incubated with pharmacologically activated cytolytic T lymphocytes. overexpression of CD95 in HUVEC confers sensitivity to CD95L in the absence of IFN-gamma-treatment. We conclude that IFN-gamma induces sensitivity of endothelium to CD95L-mediated apoptosis, and that this response may result from increased expression of CD95 and/or pro-caspase-8.

关键词：氨基酸氯甲基酮类/药理学抗原 CD/遗传学细胞凋亡/药物作用半胱氨酸天冬氨酸蛋白酶8 半胱氨酸天冬氨酸蛋白酶9 半胱氨酸天冬氨酸蛋白酶/遗传学细胞死亡/药物作用细胞培养的内皮血管/细胞学内皮血管/药物作用内皮血管/生理学酶抑制剂/药理学酶前体/遗传学 Fas配体蛋白质基因表达调控/药物作用遗传载体干扰素γ/药理学膜糖蛋白类/遗传学微循环逆转录病毒科/遗传学逆转录聚合酶链反应皮肤/血液供给转染脐静脉人类

来源：评论

学校读者我要写书评

暂无评论

Modulation of the decay of Ca²⁺-activated Cl^- currents in rabbit portal vein smooth muscle cells by external anions

引用

JOURNAL OF PHYSIOLOGY-LONDON 1999年第2期516卷 365-376页

作者： Greenwood, IA Large, WA St Georges Hosp Sch Med Dept Pharmacol & Clin Pharmacol Cardiovasc Res Grp London SW17 0RE England

1. The effects of external anions on the decay kinetics of Ca2+-activated Cl- currents (I-Cl(ca)) were studied in smooth muscle cells isolated from rabbit portal vein using the perforated patch whole-cell voltage clamp technique. 2. In normal NaCl-containing external solution the decay of spontaneous Ca2+-activated Cl- currents (STICs) and Ca2+-activated Cl- 'tail' currents (I-tail) was described by a single exponential with a time constant (tau) that was prolonged by external anions which are more permeable than Cl- (Br-, I- and SCN-) and accelerated by less permeant anions. However, intracellular I- did not affect the tau of STICs and I-tail. 3. There was a positive correlation between the ability of an external anion to affect the decay tau of I-Cl(Ca) and its permeability relative to Cl-. 4. The voltage dependence of STIC and I-tail decay was not affected by external or internal anions. 5. External permeating anions were not obligatory for activation of I-Cl(Ca) and STIC tau was not altered in Cl--free external solution. 6. Modulation of tau by mole fractions of SCN- and Cl- ions was fitted by a logistic curve, suggesting competition between SCN- and Cl- ions for a binding site. 7. In conclusion, external anions affect the decay of I-Cl(Ca) by a mechanism compatible with an interaction with a binding site which modulates Cl- channel kinetics.

关键词：算法阴离子/药理学钙/生理学氯化物通道/药物作用氯化物通道/代谢电刺激电生理学动力学膜电位/生理学肌平滑血管/细胞学肌平滑血管/药物作用肌平滑血管/代谢膜片钳术门静脉/细胞学门静脉/药物作用门静脉/代谢氯化钠/药理学动物女(雌)性兔

来源：评论

学校读者我要写书评

暂无评论

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

请选择保存的检索档案：

请选择收藏分类：

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

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

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：