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991.
992.
Overexpression of oncogenic STK15/BTAK/Aurora A kinase in human pancreatic cancer. 总被引:27,自引:0,他引:27
Donghui Li Jijiang Zhu Pervez F Firozi James L Abbruzzese Douglas B Evans Karen Cleary Helmut Friess Subrata Sen 《Clinical cancer research》2003,9(3):991-997
PURPOSE: Multiple chromosome abnormalities, including gain of chromosome20q, have been detected frequently in human pancreatic cancers. Overexpression of the STK15/BTAK/Aurora A gene located on chromosome 20q13, which encodes a centrosome-associated serine/threonine kinase, has been shown to induce chromosomal instability, leading to aneuploidy and cell transformation in multiple in vitro experimental systems. The purpose of this study was to investigate the expression and copy number alteration of STK15 in pancreatic cancer. EXPERIMENTAL DESIGN: STK15 expression at both the mRNA and protein levels together with the copy number of STK15 gene was measured in nine pancreatic carcinoma cell lines: (a) HPAF-II; (b) Aspc-1; (c) Panc-1; (d) Panc-3; (e) Panc-28; (f) Panc-48; (g) HS766T; (h) MIAPaCa-2; and (i) BxPc3. STK15 protein expression was also examined in normal pancreatic tissues and tumors by Western blotting and immunohistochemistry. RESULTS: STK15 was overexpressed in all of the nine cell lines examined, but gene amplification was infrequent. Western Blot analysis of primary tumor tissues revealed 2-10 times overexpression of STK15 protein compared with normal adjacent tissues from pancreatic cancer patients. Concurrent overexpression of cdc20, an STK15-associated protein, and reduced expression of cdc25, a mitosis-activating protein phosphatase, were detected in the same tumor samples. Elevated STK15 protein expression was detected in 22 of 38 tumor sections (58%) from pancreatic cancer patients. The extent of STK15 expression was not significantly correlated with the size, degree of differentiation, and metastasis status of the tumors. CONCLUSIONS: These results show that STK15 is overexpressed in pancreatic tumors and carcinoma cell lines and suggest that overexpression of STK15 may play a role in pancreatic carcinogenesis. 相似文献
993.
目的 为了特异封闭白血病细胞survivin的表达,抑制其功能,本实验构建了survivin反义核酸载体并导入白血病细胞系中。方法 应用RT—PCR获得survivin的cDNA片段,反向插入pcDNA3质粒载体中;经限制性酶切和测序鉴定所构建的反义核酸是否正确;采用电转染方法将重组体导入HL—60细胞中;RT—PCR技术检测转染细胞survivin表达的变化。结果 经限制性酶切和测序鉴定证明survivin反义核酸已成功构建;RT—PCR产物电泳结果显示,与转染前细胞、空质粒转染细胞相比,转染survivin反义核酸的细胞survivin mRNA水平明显降低。结论 本实验已成功建立了survivin反义核酸真核表达载体,而且在白血病细胞系中发挥了特异封闭作用,为进一步研究survivin反义核酸在白血病治疗中的作用提供了实验基础。 相似文献
994.
Z Zhu K Hattori H Zhang X Jimenez D L Ludwig S Dias P Kussie H Koo H J Kim D Lu M Liu R Tejada M Friedrich P Bohlen L Witte S Rafii 《Leukemia》2003,17(3):604-611
Vascular endothelial growth factor (VEGF) and its receptors (VEGFR) have been implicated in promoting solid tumor growth and metastasis via stimulating tumor-associated angiogenesis. We recently showed that certain 'liquid' tumors such as leukemia not only produce VEGF, but also express functional VEGFR, resulting in an autocrine loop for tumor growth and propagation. A chimeric anti-VEGFR2 (or kinase insert domain-containing receptor, KDR) antibody, IMC-1C11, was shown to be able to inhibit VEGF-induced proliferation of human leukemia cells in vitro, and to prolong survival of nonobese diabetic-severe combined immune deficient (NOD-SCID) mice inoculated with human leukemia cells. Here we produced two fully human anti-KDR antibodies (IgG1), IMC-2C6 and IMC-1121, from Fab fragments originally isolated from a large antibody phage display library. These antibodies bind specifically to KDR with high affinities: 50 and 200 pM for IMC-1121 and IMC-2C6, respectively, as compared to 270 pM for IMC-1C11. Like IMC-1C11, both human antibodies block VEGF/KDR interaction with an IC(50) of approximately 1 nM, but IMC-1121 is a more potent inhibitor to VEGF-stimulated proliferation of human endothelial cells. These anti-KDR antibodies strongly inhibited VEGF-induced migration of human leukemia cells in vitro, and when administered in vivo, significantly prolonged survival of NOD-SCID mice inoculated with human leukemia cells. It is noteworthy that the mice treated with antibody of the highest affinity, IMC-1121, survived the longest period of time, followed by mice treated with IMC-2C6 and IMC-1C11. Taken together, our data suggest that anti-KDR antibodies may have broad applications in the treatment of both solid tumors and leukemia. It further underscores the efforts to identify antibodies of high affinity for enhanced antiangiogenic and antitumor activities. 相似文献
995.
996.
中国健康志愿者单剂口服甲磺酸加替沙星片的药代动力学研究 总被引:2,自引:1,他引:2
目的研究中国健康成年志愿者单剂口服甲磺酸加替沙星片的药代动力学。方法按GCP指导原则设计试验方案,选择9名健康受试者分别依次单剂口服200、400、600mg三个剂量的甲磺酸加替沙星片后,应用HPLC测定血药浓度,采用3P97软件进行数据处理,求出药代动力学参数。结果受试者分别给药后,药-时曲线符合二房室模型,主要药代动力学参数Cmax分别为(2.028±0.362)mg/L、(3.749±0.446)mg/L、(4.876±0.569)mg/L;t1/2β分别为(7.489±0.806)h、(7.063±0.890)h、(7.735±0.8701)h;AUC0-t分别为(12.24±1.51)mg·h/L、(26.02±3.38)mg·h/L、(39.22±6.57)mg·h/L;原型药主要经肾排泄,48h尿药累积排泄率分别为(61.90±7.70)%、(60.90±5.70)%和(58.74±13.49)%。结论9名健康受试者分别口服给药后,药-时曲线符合二房室模型,甲磺酸加替沙星在200~600mg剂量范围内药物体内过程呈线性动力学特征而无饱和性,主要排泄途径为肾脏。 相似文献
997.
998.
目的:建立西沙必利胶囊的溶出度测定方法。方法:依照《中国药典》,以盐酸溶液(0.05→1000)500ml为溶出介质,转速为50r/min,分光光度法检测,检测波长为308nm。结果:在5.057~12.136μg/ml范围内(r=0.9998),浓度与其吸收度呈良好线性关系,平均回收率为99.89%,RSD-0.29%。结论:该方法操作简便,准确可靠。 相似文献
999.
1000.
基底外侧杏仁核注射戊巴比妥钠对睡眠和行为的影响 总被引:3,自引:0,他引:3
目的 观察基底外侧杏仁核(BLA)内注射戊巴比妥钠对睡眠和行为的影响。方法 多导睡眠描记术和杏仁核微量注射。结果 戊巴比妥钠引起觉醒减少,慢波睡眠和总睡眠时间增多,开野实验中踩格数和修饰行为减少,而强迫游泳实验的不动时间延长。结论 戊巴比妥钠作用于BLA可产生明显的促睡眠效应和镇静作用,BLA参与了睡眠和行为的调节。 相似文献