检索结果-内蒙古大学图书馆

DNA adduct formation and molecular analysis of in vivo lacI mutations in the mammary tissue of Big Blue® rats treated with 7,12-dimethylbenz[a]anthracene

引用

CARCINOGENESIS 2000年第2期21卷 265-273页

作者： Manjanatha, MG Shelton, SD Culp, SJ Blankenship, LR Casciano, DA US FDA Natl Ctr Toxicol Res Dept Hlth & Human Serv Div Genet Jefferson AR 72079 USA US FDA Natl Ctr Toxicol Res Dept Hlth & Human Serv Div Biochem Toxicol Jefferson AR 72079 USA

Recently we compared the lad and Hprt mutant frequencies (MFs) and types of mutations in lymphocytes of Big Blue(R) (BB) rats exposed to 7,12-dimethylbenz[a]anthracene (DMBA) under conditions that result in mammary gland tumors. In this study, we have examined the target mammary tissue for DMBA-induced DNA adducts, lad MF and types of lad mutations. seven-week-old female BE rats were given single doses of 0, 20 or 130 mg/kg DMBA by gavage and the DNA adducts and lad MFs in the mammary tissue were measured over a period of 14 days and 18 weeks, respectively, following treatment, The lacI MF in the mammary tissue increased for 10 weeks and then remained relatively constant;130 mg/kg DMBA produced a 14-fold increase in the MF (255 +/- 50 x 10(-6) p.f.u.) over control MF (18.3 +/- 4 x 10(-6) p.f.u.). P-32-post-labeling analysis of DNA from mammary tissue and splenic lymphocytes of treated rats revealed two major adducts, Comparison of these adducts with DMBA standards indicated that the adducts formed by DMBA involved both G:C and A:T base pairs. DNA sequencing revealed that the majority of DMBA-induced lad mutations were base pair sutbstitutions and that A:T-->T:A (44% of the independent mutations) and G:C-->T:A (24% of the independent mutations:) transversions were the predominant types. Furthermore, the mutational results revealed a 'hotspot' for a G-->T mutation in codon 95 (GTG-->TTG) of the lad gene in mammary tissue. These results suggest that DMBA is highly mutagenic to lad in mammary tissue and that adducts with bath G:C and A:T base pairs participate in forming mutations in DMBA-treated BB rats.

关键词： 9 10-二甲基-1 2-苯并蒽/毒性氨基酸取代动物基因修饰致癌物/毒性密码子/遗传学 DNA加合物 DNA损伤 DNA突变分析移码突变乳糖操纵子淋巴细胞/化学乳腺动物/化学乳腺动物/药物作用乳房肿瘤实验性/化学诱导乳房肿瘤实验性/遗传学诱变剂/毒性突变器官特异性点突变脾/细胞学动物女(雌)性大鼠

来源：评论

学校读者我要写书评

暂无评论

Aneuploidy precedes and segregates with chemical carcinogenesis

引用

CANCER GENETICS AND CYTOGENETICS 2000年第2期119卷 83-93页

作者： Duesberg, P Li, RH Rasnick, D Rausch, C Willer, A Kraemer, A Yerganian, G Hehlmann, R Univ Calif Berkeley Dept Mol & Cell Biol Berkeley CA 94720 USA Univ Heidelberg Med Klin Mannheim 3 D-6800 Mannheim Germany Cytogen Res & Dev Boston MA USA Brandeis Univ Foster Res Lab Waltham MA 02254 USA

A century ago, Boveri proposed that cancer is caused by aneuploidy, an abnormal balance of chromosomes, because aneuploidy correlates with cancer and because experimental aneuploidy generates "pathological" phenotypes. Half a century later, when cancers were found to be nonclonal for aneuploidy, but clonal for somatic gene mutations, this hypothesis was abandoned. As a result, aneuploidy is now generally viewed as a consequence, and mutated genes as a cause of cancer. However, we have recently proposed a two-stage mechanism of carcinogenesis that resolves the discrepancy between clonal mutation and nonclonal karyotypes. The proposal is as follows: in stage 1, a carcinogen "initiates" carcinogenesis by generating a preneoplastic aneuploidy;in stage 2, aneuploidy causes asymmetric mitosis because it biases balance-sensitive spindle and chromosomal proteins and alters centrosomes both numerically and structurally tin proportion to the degree of aneuploidy). Therefore, the karyotype of an initiated cell evolves autocatalytically, generating ever-new chromosome combinations, including neoplastic ones. Accordingly, the heterogeneous karyotypes of "clonal" cancers are an inevitable consequence of the karyotypic instability of aneuploid cells. The notorious long latent periods, of months to decades, from carcinogen to carcinogenesis, would reflect the low probability of evolving by chance karyotypes that compete favorably with normal cells, in principle analagous to natural evolution. Here, Mie have confirmed experimentally five predictions of the aneuploidy hypothesis: (1) the carcinogens dimethylbenzanthracene and cytosine arabinoside induced aneuploidy in a fraction of treated Chinese hamster embryo cells;(2) aneuploidy preceded malignant transformation;(3) transformation of carcinogen-treated cells occurred only months after carcinogen treatment, i.e., autocatalytically;(4) preneoplastic aneuploidy segregated with malignant transformation in vitro and with 14 of 14 tumo

关键词： 9 10-二甲基-1 2-苯并蒽/药理学 9 10-二甲基-1 2-苯并蒽/毒性非整倍性致癌物/药理学致癌物/毒性细胞系转化细胞转化肿瘤/化学诱导细胞转化肿瘤/遗传学细胞培养的/药物作用细胞培养的/超微结构仓鼠亚科仓鼠属阿糖胞苷/药理学阿糖胞苷/毒性 DNA突变分析核型分析甲基胆蒽/药理学甲基胆蒽/毒性模型生物学肿瘤实验性/化学诱导肿瘤实验性/遗传学癌前状态/化学诱导癌前状态/遗传学时间因素动物人类男(雄)性

来源：评论

学校读者我要写书评

暂无评论

COMPARATIVE METABOLISM AND DNA-BINDING OF 7,12-DIMETHYLBENZ[A]ANTHRACENE AND ITS WEAKLY CARCINOGENIC 5-FLUORO ANALOG

引用

CANCER LETTERS 1979年第4-5期6卷 263-272页

作者： DANIEL, FB CAZER, FD DAMBROSIO, SM HART, RW KIM, WH WITIAK, DT OHIO STATE UNIV COLL PHARM DEPT MED CHEM COLUMBUS OH 43210 USA OHIO STATE UNIV COLL MED DEPT RADIOL & PHARMACOL COLUMBUS OH 43210 USA OHIO STATE UNIV CTR COMPREHENS CANC COLUMBUS OH 43210 USA

Cultured Syrian hamster embryo cells readily convert both the carcinogenic polycyclic aromatic hydrocarbon, 7,12-dimethylbenz[a]anthracene (DMBA), and its weakly carcinogenic analogue, 5-fluoro-7,12-dimethylbenz[a]anthracene (5F-DMBA), to water soluble metabolites. DMBA binds to the hamster cell DNA at least 2.8-3.0 times more extensively than 5F-DMBA. Likewise, 5F-DMBA is converted to water soluble metabolites by [rat] liver microsomal preparations at a rate equal to DMBA, but the latter compound binds to DNA 2.6-3.2 times more effectively.

关键词： 9 10-二甲基-1 2-苯并蒽/类似物和衍生物 9 10-二甲基-1 2-苯并蒽/代谢 9 10-二甲基-1 2-苯并蒽/毒性苯并(a)蒽类/代谢生物转化细胞培养的仓鼠亚科 DNA/代谢胚胎哺乳动物金仓鼠微粒体肝/代谢肿瘤实验性/化学诱导构效关系动物女(雌)性男(雄)性大鼠

来源：评论

学校读者我要写书评

暂无评论

Absence of caveolin-1 sensitizes mouse skin to carcinogen-induced epidermal hyperplasia and tumor formation

引用

AMERICAN JOURNAL OF PATHOLOGY 2003年第6期162卷 2029-2039页

作者： Capozza, F Williams, TM Schubert, W McClain, S Bouzahzah, B Sotgia, F Lisanti, MP Albert Einstein Coll Med Dept Mol Pharmacol Bronx NY 10461 USA Albert Einstein Coll Med Albert Einstein Canc Ctr Bronx NY 10461 USA Albert Einstein Coll Med Dept Pathol Bronx NY 10461 USA Montefiore Med Ctr Bronx NY 10467 USA Albert Einstein Coll Med Div Cardiol Dept Med Bronx NY 10461 USA Albert Einstein Coll Med Div Infect Dis Dept Med Bronx NY 10461 USA

Caveolin-1 is the principal Protein component of caveolae membrane domains, which are located at the cell surface in most cell types. Evidence has accumulated suggesting that caveolin-1 may function as a suppressor of cell transformation in cultured cells. The human CAV-1 gene is located at a putative tumor suppressor locus (7q31.1/D7S522) and a known fragile site (FRA7G) that is deleted in a variety of epithelial-derived tumors. Mechanistically, caveolin-1 is known to function as a negative regulator of the Ras-p42/44 MAP kinase cascade and as a transcriptional repressor of cyclin D1, possibly explaining its transformation suppressor activity in cultured cells. However, it remains unknown whether caveolin-1 functions as a tumor suppressor gene in vivo. Here, we examine the tumor suppressor function of caveolin-1 using Cav-1 (-/-) null mice as a model system. Cav-1 null mice and their wild-type counterparts were subjected to carcinogen-induced skin tumorigenesis, using 7,12-dimethylbenzanthracene (DMBA). Mice were monitored weekly for the development of tumors. We demonstrate that Cav-1 null mice are dramatically more susceptible to carcinogen-induced tumorigenesis, as they develop skin tumors at an increased rate. After 16 weeks of DMBA-treatment, Cav-1 null mice showed a 10-fold increase in tumor incidence, a 15-fold increase in tumor number per mouse (multiplicity), and a 35-fold increase in tumor area per mouse, as compared with wild-type litter-mate mice. Moreover, before the development of tumors, DMBA-treatment induced severe epidermal hyperplasia in Cav-1 null mice. Both the basal cell layer and the suprabasal cell layers were expanded in treated Cav-1 null mice, as evidenced by immunostaining with cell-type specific differentiation markers (keratin-10 and keratin-14). In addition, cyclin D1 and phospho-ERK1/2 levels were up-regulated during epidermal hyperplasia, suggesting a possible mechanism for the increased susceptibility of Cav-1 null mice to tumorige

关键词： 9 10-二甲基-1 2-苯并蒽/毒性致癌物/毒性窖蛋白1 细胞质膜微囊蛋白/遗传学细胞质膜微囊蛋白/代谢细胞分裂/药物作用细胞周期蛋白D1/代谢表皮/药物作用表皮/病理学增生免疫组织化学角蛋白细胞/药物作用角蛋白细胞/代谢角蛋白细胞/超微结构小鼠近交C57BL 小鼠基因敲除显微镜检查电子丝裂原活化蛋白激酶1/代谢丝裂原活化蛋白激酶3 丝裂原激活蛋白激酶类/代谢肿瘤实验性/化学诱导肿瘤实验性/病理学磷酰化皮肤/药物作用皮肤/病理学皮肤/超微结构时间因素增量调节动物小鼠

来源：评论

学校读者我要写书评

暂无评论

A simple phenolic antioxidant protocatechuic acid enhances tumor promotion and oxidative stress in female ICR mouse skin: dose- and timing-dependent enhancement and involvement of bioactivation by tyrosinase

引用

CARCINOGENESIS 2000年第10期21卷 1899-1907页

作者： Nakamura, Y Torikai, K Ohto, Y Murakami, A Tanaka, T Ohigashi, H Kyoto Univ Grad Sch Agr Div Appl Life Sci Kyoto 6068502 Japan Kinki Univ Fac Biol Oriented Sci & Technol Dept Biotechnol Sci Wakayama 6496493 Japan Kanazawa Med Univ Dept Pathol 1 Uchinada Ishikawa 9200293 Japan

The modifying effects of topical application of the phenolic antioxidant protocatechuic acid (PA) on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced mouse skin tumor promotion were investigated. Dimethylbenz[a]anthracene-initiated female ICR mice were treated with TPA (1.6 nmol) twice weekly for 20 weeks to promote papilloma formation. Pre-treatment with 16 nmol PA 30 min prior to each TPA treatment significantly inhibited the number of papillomas per mouse by 52% (P < 0.05). On the other hand, PA pre-treatment at a high dose (1600 nmol) significantly enhanced tumor numbers by 38% (P < 0.05). Interestingly, in the group treated with a quite high dose (20000 nmol) of PA 5 min prior to each TPA application, the average number of tumors per mouse was reduced by 38%, whereas the same PA dose 3 h before TPA treatment significantly enhanced tumor numbers by 84% (P < 0.01). These results suggested that topically applied PA was converted to compound(s) lacking antioxidative properties and/or rather possessing the potential to enhance tumor development. A similar tendency was also observed in the short-term experiment of TPA-induced inflammation and oxidative stress;i.e. two groups pretreated with PA at 20 000 nmol, 30 min and 3 h before TPA treatment, did not show suppression or even significantly enhanced TPA-induced leukocyte infiltration, H2O2 generation, thiobarbituric acid-reacting substances level and proliferating cell nuclear antigen index, while PA treatment together with TPA significantly suppressed these parameters. Treatment with a high dose (20 000 nmol) of PA alone for 3 h enhanced oxidative stress by reducing glutathione levels in mouse skin, which was counteracted by the tyrosinase inhibitor arbutin, Oxidative stress responses such as leukocyte infiltration and H2O2 generation were also counteracted by arbutin, These results suggested that tyrosinase-dependent oxidative metabolism of PA was at least partially involved in the enhanced effects of PA on TPA-

关键词： 9 10-二甲基-1 2-苯并蒽/拮抗剂和抑制剂 9 10-二甲基-1 2-苯并蒽/毒性抗氧化剂/药代动力学抗氧化剂/药理学抗氧化剂/毒性生物转化致癌物/拮抗剂和抑制剂致癌物/药理学致癌物/毒性皮炎接触性/代谢剂量效应关系药物用药计划表药物协同作用谷胱甘肽/代谢谷胱甘肽过氧化酶/代谢谷胱甘肽转移酶/代谢过氧化氢/代谢小鼠近交ICR 一元酚单氧酶/代谢氧化性应激/药物作用乳头状瘤/化学诱导乳头状瘤/代谢乳头状瘤/预防和控制皮肤/药物作用皮肤/代谢皮肤/病理学皮肤肿瘤/化学诱导皮肤肿瘤/代谢皮肤肿瘤/预防和控制十四酰佛波乙酯/拮抗剂和抑制剂十四酰佛波乙酯/毒性动物女(雌)性小鼠

来源：评论

学校读者我要写书评

暂无评论

A probability-based multivariate statistical algorithm for autofluorescence spectroscopic identification of oral carcinogenesis

引用

PHOTOCHEMISTRY AND PHOTOBIOLOGY 1999年第4期69卷 471-477页

作者： Wang, CY Chen, CT Chiang, CP Young, ST Chow, SN Chiang, HK Natl Yang Ming Univ Inst Biomed Engn Taipei 112 Taiwan Natl Taiwan Univ Laser Med Res Ctr Taipei 10764 Taiwan Natl Taiwan Univ Sch Dent Taipei 10764 Taiwan

A probability-based multivariate statistical algorithm combining partial least-squares (PLS) and logistic regression was developed to identify the development stages of oral cancer through analysis of autofluorescence spectra of oral tissues. Tissues were taken from a 7,12-dimethylbenz[a]anthracene-induced hamster buccal pouch carcinogenesis model. Analyses were conducted at various excitation wavelengths, ranging from 280 nm to 400 nm in 20 mm increments, to assess classification performance at different excitations. For each excitation the PLS analysis and logistic regression were combined, on the basis of cross validation, to calculate the posterior probabilities of samples belonging to four stages of cancer development: normal tissues, hyperplasia, dysplasia and early cancers and frankly invasive cancers. Results showed that the 320 nm excitation wavelength optimally classified the cancer development stages: the accuracy rates for identifying samples at that excitation were 91.7%, 83.3%, 66.7% and 83.3% for the four respective stages. The average accuracy rate was 81.3%. These results suggest that the algorithm described in this study might be useful for the detection of human oral cancers.

关键词： 9 10-二甲基-1 2-苯并蒽/毒性算法致癌物/毒性仓鼠亚科金仓鼠口腔肿瘤/化学诱导口腔肿瘤/诊断多元分析光生物学光谱法荧光动物人类男(雄)性

来源：评论

学校读者我要写书评

暂无评论

CELL-MEDIATED MUTAGENESIS IN CULTURED CHINESE-HAMSTER CELLS BY POLYCYCLIC-HYDROCARBONS - MUTAGENICITY AND DNA REACTION RELATED TO CARCINOGENICITY IN A SERIES OF COMPOUNDS

引用

INTERNATIONAL JOURNAL OF CANCER 1979年第5期23卷 691-696页

作者： WIGLEY, CB NEWBOLD, RF AMOS, J BROOKES, P INST CANC RES DIV CHEM CARCINOGENESIS POLLARDS WOOD RES STN CHALFONT ST GILES HP8 4SP BUCKINGHAMSHIRE ENGLAND

Benz(a)anthracene, 3-methylcholanthrene and 7,12-dimethylbenz(a)anthracene, were studied in a cell-mediated mutagenesis system using BHK 21 cells to metabolize the hydrocarbons and V-79 cells as targets for detecting induced cytotoxicity and mutation. In large-scale experiments, the DNA of V-79 cells was analyzed by column chromatography to determine the nature and true extent of reaction of hydrocarbons with deoxyribonucleosides. Products with DNA formed by the 2 carcinogenic compounds were qualitatively very similar to those reported to occur in vivo and in primary cell cultures. Binding indices were calculated from the 3H content of DNA-hydrocarbon products, related to overall metabolism, for these 2 compounds together with benzo(a)pyrene and 7-methylbenz(a)anthracene using data from a previous study. These values reflected differences in carcinogenic potency between the compounds. Induced mutation frequencies were related to the extent of DNA reaction with each compound. At equivalent extents of DNA reaction with hydrocarbon products, levels of induced mutation were not significantly different.

关键词： 9 10-二甲基-1 2-苯并蒽/代谢 9 10-二甲基-1 2-苯并蒽/毒性苯并(a)蒽类/代谢苯并(a)蒽类/毒性致癌物细胞培养的色谱法仓鼠亚科仓鼠属 DNA/代谢甲基胆蒽/代谢甲基胆蒽/毒性诱变剂动物

来源：评论

学校读者我要写书评

暂无评论

Developmental Stage of the Rat Mammary Gland as Determinant of Its Susceptibility to 7, 12-Dimethylbenz[a]anthracene

引用

Journal of the National Cancer Institute 1978年第6期61卷 1439-1449页

作者： Russo, Irma H. Russo, Jose Experimental Pathology Laboratory Department of Biology Michigan Cancer Foundation Detroit MI 48201 110 East Warren Ave United States

Postnatal development of the mammary gland was studied In 80 noninbred Sprague-Dawley virgin rats ranging in age from 2 to 112 days, and the changes induced by 7, 12-dimethyl- benzlalanthracene (DMBA) were studied in 60 noninbred Sprague-Dawley virgin rats that, at the age of 55 days, were inoculated intragastrically with 10 mg DMBA/100 g body weight. To correlate the sequential structural changes In the two groups, animals of both groups were killed weekly and their mammary glands removed and processed for wholemount. Terminal end- buds (TEB), terminal ducts (TD), alveolar buds (AB), and lobules per square millimeter were counted in wholemount preparations under a stereomicroscope. During postnatal development, the mammary gland tree grew by sprouting numerous ducts ending in club-shaped TEB. The density of TEB reached a peak when the rats were 21 days old (25±2 TEB/mm2), decreased sharply until the animals were 63 days old, and then decreased slowly until they were 84 days of age. The number of TEB decreased because of their differentiation mainly into AB or their evolution to TD. AB later differentiated into lobules. AB increased in number steadily to a plateau when the animals were 70-84 days old. After DMBA was administered to the rats at 55 days of age, the number of TEB remained higher than that in the control animals and the TEB became larger and had higher mitotic activities. Such TEB were called Intraductal proliferations (IDP);they evolved to adenocarcinomas. DMBA increased the number of TD and decreased the number of AB and lobules in relation to the control animals. These findings led to the conclusion that DMBA administration to 55-day-old rats alters the differentiation of TEB-AB-lobules, inducing instead the sequence TEB-IDP- adenocarcinoma. © 1978, Oxford University Press. All rights reserved.

关键词： 9 10-二甲基-1 2-苯并蒽/毒性腺癌/病因学年龄因素苯并(a)蒽类/毒性乳腺动物/药物作用乳腺动物/生长和发育乳房肿瘤实验性/病因学乳房肿瘤实验性/病理学癌前状态/病因学癌前状态/病理学动物女(雌)性男(雄)性妊娠大鼠

来源：评论

学校读者我要写书评

暂无评论

Regulation of preB cell apoptosis by aryl hydrocarbon receptor/transcription factor-expressing stromal/adherent cells

引用

Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.) 1999年第3期221卷 242-52页

作者： R I Near R A Matulka K K Mann S U Gogate A F Trombino D H Sherr Department of Environmental Health Boston University Schools of Medicine and Public Health Boston Massachusetts 02118 USA. rocket1@bu.edu

Polycyclic aromatic hydrocarbons (PAH) are environmental chemicals that mediate immunosuppression. In long-term bone marrow B-cell lymphopoiesis models, PAH induce apoptosis in immature (preB) lymphocytes. Since the biologic function of PAH is often mediated by the aryl hydrocarbon receptor/transcription factor (AhR), the role of the AhR or AhR-regulated genes was assessed in preB cell apoptosis. Specifically, a bone marrow-derived preB cell line (BU-11) was cultured on monolayers of the AhR + bone marrow-derived stromal cell line BMS2, hepatoma sublines that express various levels of AhR activity (Hepa-1c1c7 and variants), AhR+ thymic epithelial cells, and primary bone marrow stromal cells from wildtype or AhR-/- mice. Cultures were treated with one of two prototypic PAH, 7,12-dimethylbenz[a] anthracene (DMBA) or benz[a]pyrene (B[a]P), and the percentage of cells undergoing apoptosis measured. The data demonstrated that: 1) bone marrow- and hepatic-derived stromal/adherent cells support preB cell growth and regulate apoptosis induced by DMBA or B[a]P; 2) B[a]P is more effective than DMBA when preB cells are maintained on Hepa-1c1c7 monolayers than when maintained on BMS2 monolayers; 3) DMBA is more effective than B[a]P when preB cells are cultured on BMS2 monolayers; 4) alpha-naphthoflavone, an AhR antagonist and cytochrome P-450 inhibitor, blocks preB cell apoptosis in both BU-11/Hepa-1c1c7 and BU-11/BMS2 cultures; 5) although preB cells grow well in Hepa-1c1c7 or BMS2 supernatants, addition of PAH in the absence of hepatic- or bone marrow-derived adherent cells does not result in preB cell apoptosis; 6) preB cell apoptosis is dependent on AhR activity in adherent hepatic- or bone marrow-derived stromal cells; and 7) apoptosis is induced by DMBA when preB cells are maintained on primary bone marrow stromal cell monolayers from wildtype but not from AhR-/- mice. Collectively, the data indicated that AhR-regulated activities in the hematopoietic microenvironment inf

关键词： 9 10-二甲基-1 2-苯并蒽/毒性细胞凋亡/药物作用 B淋巴细胞/代谢苯并芘/毒性苯黄酮类/药理学骨髓细胞细胞系 DNA碎片裂/遗传学流式细胞术基因表达调控/药物作用血细胞生成肝/药物作用小鼠基因敲除多环碳氢化合物芳香族/毒性 RNA 信使/遗传学受体芳基烃/遗传学间质细胞/代谢转录因子/遗传学动物小鼠

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：