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51.
小鼠基因组研究进展李善如1,2王冬平1陈永福2(1.军事医学科学院实验动物中心,北京100071)(2.中国农业大学生物学院,北京100094)TheDevelopmentofMouseGenomeResearchLIShanru1,2WANGDon... 相似文献
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WANG Da Zhong CHEN Yi Yu 《动物分类学报》1998,(1)
本文根据系统学原理,提出了建立新类元的依据;并据此从分类和系统发育上论证了近金线属AnchicyclocheilusLietLan独立成属的可能性,认为应将近金线属归于金线属;修订了金线属SinocyclocheilusFang的鉴别特征。 相似文献
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腐马素是由串珠镰刀菌产生的真菌毒素,其中腐马素B1可引发马脑白质软化症等疾病。本文用高效液相色谱法从串珠镰刀菌玉米培养物中分离出了腐马素B1并通过紫外光谱和快原子轰击质谱进行了鉴定。 相似文献
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Park SH Kim JH Bae SS Hong KW Lee DS Leem JY Choi BT Shin HK 《Biochemical and biophysical research communications》2011,(4):602-608
Alzheimer’s disease (AD), which is characterized by progressive cognitive impairment, is the most common neurodegenerative disease. Here, we investigated the preventive effect of a phosphodiesterase III inhibitor, cilostazol against cognitive decline in AD mouse model. In vitro studies using N2a cells stably expressing human amyloid precursor protein Swedish mutation (N2aSwe) showed that cilostazol decreased the amyloid β (Aβ) levels in the conditioned medium and cell lysates. Cilostazol attenuated the expression of ApoE, which is responsible for Aβ aggregation, in N2aSwe. Intracerebroventricular injection of Aβ25–35 in C57BL/6J mice resulted in increased immunoreactivity of Aβ and p-Tau, and microglia activation in the brain. Oral administration of cilostazol for 2 weeks before Aβ administration and once a day for 4 weeks post-surgery almost completely prevented the Aβ-induced increases of Aβ and p-Tau immunoreactivity, as well as CD11b immunoreactivity. However, post-treatment with cilostazol 4 weeks after Aβ administration, when Aβ was already accumulated, did not prevent the Aβ-induced neuropathological responses. Furthermore, cilostazol did not affect the neprilysin and insulin degrading enzymes involved in the degradation of the Aβ peptide, but decreased ApoE levels in Aβ-injected brain. In addition, cilostazol significantly improved spatial learning and memory in Aβ-injected mice. The findings suggest that a phosphodiesterase III inhibitor, cilostazol significantly decreased Aβ accumulation and improved memory impairment induced by Aβ25–35. The beneficial effects of cilostazol might be explained by the reduction of Aβ accumulation and tau phosphorylation, not through an increase in Aβ degradation but via a significant decrease in ApoE-mediated Aβ aggregation. Cilostazol may be the basis of a novel strategy for the therapy of AD. 相似文献
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Lee H Kim Y Choi Y Choi S Hong E Oh ES 《Biochemical and biophysical research communications》2011,(1):1133-153
The cell surface heparan sulfate proteoglycan, syndecan-2, is crucial for the tumorigenic activity of colon cancer cells. However, the role played by the cytoplasmic domain of the protein remains unclear. Using colon cancer cells transfected with various syndecan-2-encoding genes with deletions in the cytoplasmic domain, it was shown that syndecan-2-induced migration activity requires the EFYA sequence of the C-terminal region; deletion of these residues abolished the rise in cell migration seen when the wild-type gene was transfected and syndecan-2 interaction with syntenin-1, suggesting that syntenin-1 functioned as a cytosolic signal effector downstream from syndecan-2. Colon cancer cells transfected with the syntenin-1 gene showed increased migratory activity, whereas migration was decreased in cells in which syntenin-1 was knock-down using small inhibitory RNA. In addition, syntenin-1 expression potentiated colon cancer cell migration induced by syndecan-2, and syndecan-2-mediated cell migration was reduced when syntenin-1 expression diminished. However, syntenin-1-mediated migration enhancement was not noted in colon cancer cells transfected with a gene encoding a syndecan-2 mutant lacking the cytoplasmic domain. Furthermore, in line with the increase in cell migration, syntenin-1 mediated Rac activation stimulated by syndecan-2. Together, the data suggest that the cytoplasmic domain of syndecan-2 regulates colon cancer cell migration via interaction with syntenin-1. 相似文献