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991.
医院人力资源管理的探索 总被引:6,自引:1,他引:6
分析了当前医院人力资源管理的现状及背景,并结合桐城市人民医院的一些创新性探索,就如何做好医院人力资源管理工作进行探讨。 相似文献
992.
993.
994.
人肝癌细胞株VEGF/VEGFR的检测及意义探讨 总被引:2,自引:1,他引:2
王腾 殷咏梅 陆彬彬 王朝霞 德伟 束永前 WANG Teng YIN Yong-mei LU Bin-bin WANG Zhao-xi DE Wei SHU Yong-qian 《南京医科大学学报(自然科学版)》2006,26(5):334-336,F0003
目的:筛选血管内皮生长因子(vascular endothelial growth factor,VEGF)高表达肝癌细胞株,为进一步研究VEGF在肝癌治疗中的作用提供理论依据。并探讨VEGF受体在肝癌细胞株的表达及意义。方法:ELISA法及Western blot法分别检测人肝癌细胞株培养上清及细胞内VEGF蛋白的表达。免疫细胞化学方法检测VEGFR在人肝癌细胞中的表达。结果:5株肝癌细胞株均见VEGF蛋白表达,其中SMMC-7721的VEGF表达量最高,VEGF特异性受体Fit-1在HepG2、HHCC、SMMC-7721、Bcl-7402见阳性表达,KDR在HepG2、HHCC、Bel-7402、QGY-7701见阳性表达。结论:肝癌细胞株中VEGF表达量不尽一致,VEGF在肝癌发生发展中可能存在自分泌作用方式。 相似文献
995.
996.
Intranuclear filamentous and crystalline inclusion bodies have been described in the nuclei of a variety of cells in both normal and pathological states. The functional significance of these structures remains to be elucidated. Moreover, although the proteinaceous nature of these inclusions has been inferred in some histochemical studies, the identity of their constituent proteins remains to be determined. In the present study, immunohistochemistry was used to investigate the presence of intranuclear inclusions in neurones of the human brain which are intensely immunoreactive for the neuronal cytoskeletal protein class III beta tubulin. The ability to label these structures immunohistochemically was exploited to investigate the topographic pattern of distribution of these inclusions in the human brain. Intranuclear inclusions were rod-shaped, polygonal, or irregular in shape. They were present in neurones and ependymal cells. Intranuclear inclusion-bearing neurones were distributed in an anatomically heterogeneous pattern in the brain. Areas exhibiting relatively high densities of inclusions included the substantia inominata and anterior olfactory nucleus, dentate gyrus, substantia nigra, inferior olivary nucleus, and dentate nucleus of the cerebellum. In addition, intranuclear inclusions were prevalent in neurones in layers II, V, and VI of the cerebral cortex. They were particularly prevalent in the mesial basal temporal neocortex. The relationship of these structures to the intranuclear rods and sheets of the classical microscopists is uncertain. The demonstration that they are composed, at least in part, of tubulin, a major cytoskeletal protein, provides important clues regarding the mechanisms underlying their formation and provides a springboard for developing hypotheses regarding their functional significance. Furthermore, the ability to demonstrate these inclusions immunohistochemically provides an avenue for further studies directed at elucidating the potential involvement of these inclusions in various pathological settings. 相似文献
997.
In order to investigate the effects of TGF-β1 on the expression of MMP-2, -9 and TIMP1 in human retinal pigment epithelial (RPE) cells, the third-sixth passage cultured RPE cells were treated with TGF-β~ at different concentrations (0.01, 0. 1, 1.0, 10 ng/mL), the expression of MMP-2, -9 and TIMP-1 mRNA was detected by semi-quantitative RT-PCR assays. MMP-2, -9 and TIMP-1 mRNA were expressed in the cultured RPE cells. The values of MMP-2/β-actin in the cells treated with 0.1, 1.0, 10 ng/mL TGF-β1 were 1.04±0.04, 1.07±0.02 and 1.11±0.03, respectively, significantly higher than in the control group (0. 96±0.03, P<0. 05-0. 01). The expression of MMP-2 mRNA could be up-regulated by TGF-β1, in a dose-dependent manner. The expression of MMP-9 mRNA in the cultured RPE cells was slightly up-regulated by various TGF-β1 concentrations treatment. The values of TIMP-1/β-actin in the cells treated with 0.01 and 0. 1 ng/mL TGF-β1 were 0. 85±0.01 and 0.97 ± 0.02 respectively, significantly lower than in the control group (1.07±0.04, P<0.01), indicating that the expression of TIMP-1 mRNA was down-regulated by TGF-β1 at low concentrations. But along with the increase of TGF-β1 concentrations (1.0 and 10 ng/mL), the expression of TIMP-1 mRNA was slightly up-regulated, not significantly different from that in the control group (P>0.05). It was concluded that TGF-β1 might play an important role in the up-regulation of the expression of MMP-2 in RPE cells and result in a directional shift in the balance between MMP and TIMP. This may be facilitated for RPE cells to migrate in the pathogenesis of vitreoretinopathy. 相似文献
998.
目的对硬指叶苔L ep id oz ia v itrea的醇提物和水提物的化学成分进行研究,从中寻找生物活性成分。方法采用柱色谱方法进行化合物分离,通过波谱方法确定化合物结构。结果从其乙醇提取物中分离得到植物醇(Ⅰ)、7-羟基去氢白菖烯(Ⅱ)、瑞香内酯(Ⅲ)、胡萝卜苷(Ⅳ);从其水提取物中分离得到两个多元醇类化合物,分别是D-g lycero-d-ga lacto-heptito l(Ⅴ)、D-erythro-L-ga lacto-octito l(Ⅵ)。结论6个化合物均为首次从该植物中分离得到。 相似文献
999.
Beschorner R Schluesener HJ Nguyen TD Magdolen V Luther T Pedal I Mattern R Meyermann R Schwab JM 《Neuropathology and applied neurobiology》2000,26(6):522-527
Urokinase-type plasminogen activator receptor (uPAR/CD87) together with its ligand, urokinase-type plasminogen activator (uPA), constitutes a proteolytic system associated with tissue remodelling and leucocyte infiltration. uPAR is a member of the glycosyl phosphatidyl inositol (GPI) anchored protein family. The functional role of uPAR comprises fibrinolysis by conversion of plasminogen to plasmin. In addition, uPAR promotes cell adhesion, migration, proliferation, re-organization of the actin cytoskeleton, and angiogenesis. Furthermore, uPAR is involved in prevention of scar formation and is chemoattractant to macrophages and leucocytes. In order to investigate the pathophysiological role of uPAR following human CNS injury we examined necrotic brain lesions resulting from traumatic brain injury (TBI; n = 28) and focal cerebral infarctions (FCI; n = 17) by immunohistochemistry. Numbers of uPAR+ cells and uPAR+ blood vessels were counted. Following brain damage, uPAR+ cells increased significantly within 12 h, reached a maximum after 3-4 days and remained elevated until later stages. uPAR was expressed by infiltrating granulocytes, activated microglia/macrophages and endothelial cells. Numbers of uPAR+ vessels increased in parallel subsiding earlier following FCI than post TBI. The restricted, lesion-associated accumulation of uPAR+ cells in the brain parenchyma and upregulated expression by endothelial cells suggests a crucial role for the influx of inflammatory cells and blood-brain barrier (BBB) disturbance. Through a failure in BBB function, uPAR participates in formation of brain oedema and thus contributes to secondary brain damage. In conclusion, the study defines the localization, kinetic course and cellular source of uPAR as a potential pharmacological target following human TBI and FCI. 相似文献
1000.