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991.
992.
Phospholipid binding by a synaptic vesicle protein homologous to the regulatory region of protein kinase C 总被引:43,自引:0,他引:43
Neurotransmitters are released at synapses by the Ca2(+)-regulated exocytosis of synaptic vesicles, which are specialized secretory organelles that store high concentrations of neurotransmitters. The rapid Ca2(+)-triggered fusion of synaptic vesicles is presumably mediated by specific proteins that must interact with Ca2+ and the phospholipid bilayer. We now report that the cytoplasmic domain of p65, a synaptic vesicle-specific protein that binds calmodulin contains an internally repeated sequence that is homologous to the regulatory C2-region of protein kinase C (PKC). The cytoplasmic domain of recombinant p65 binds acidic phospholipids with a specificity indicating an interaction of p65 with the hydrophobic core as well as the headgroups of the phospholipids. The binding specificity resembles PKC, except that p65 also binds calmodulin, placing the C2-regions in a context of potential Ca2(+)-regulation that is different from PKC. This is a novel homology between a cellular protein and the regulatory domain of protein kinase C. The structure and properties of p65 suggest that it may have a role in mediating membrane interactions during synaptic vesicle exocytosis. 相似文献
993.
Movement of internalized ligand-receptor complexes along a continuous endosomal reticulum 总被引:63,自引:0,他引:63
Complexes of cell-surface receptors and their ligands are commonly internalized by endocytosis and enter a prelysosomal endosomal pathway for further processing. Fluorescence microscopy and video recording of living cells to trace the passage of ligand-receptor complexes has identified the endosomal compartment as an extensive network of tubular cisternae. Endocytosed material entering this reticulum enters discrete swellings, identified as multivesicular bodies by electron microscopy, which move along the reticulum towards the pericentriolar area. 相似文献
994.
研究了 CO-W-P电刷镀层加热时结构的转变。实验测定了镀层的等温和变温晶化综合动力学曲线及各种动力学参数。提出了瞬时晶化温度的概念。详细分析了晶化过程中硬度的变化,发现晶化伴随有一个硬化效果很强烈的沉淀过程。CO-W-P刷镀层能显著增进热模具的使用寿命,主要原因在于模具成形时,同时发生晶化和沉淀析出过程,产生二次硬化效应,提高了模具表层的红硬性以及热磨损抗力。 相似文献
995.
用熔滴实验装置研究了矿、焦层装及混装时矿石软熔层的透气性,发现混装时软熔层的透气性获得大幅度改善。获得改善的原因在于混装时软溶层的结构发生了质的变化。 相似文献
996.
在不同耐肥性的6个小麦品种幼苗中,硝酸还原酶(NR)活力差异显著,耐肥性弱的品种NR活力高,活力是负相关关系。过氧化物酶活力,耐肥性强的高于耐肥性弱的。根据聚丙烯酰胺凝胶电泳分离出的过氧化物酶的同工酶谱,耐肥性强的品种均有8条酶带,且着色深,耐肥性弱的品种则有7条,着色较浅。此外通过根系活力测定,耐肥性强的低于耐肥性弱的品种,而叶绿素含量则高于耐肥性弱的品种。 相似文献
997.
998.
对丁苯胶代替天然胶生产海绵中底进行了探索,简要地介绍了材料选用、配方设计及生产工艺,通过对试片进行硬度、密度测试,获得了较为满意的结果,产品性能能满足使用要求。 相似文献
999.
本文给出将现有湍流模型用于浮力流的若干修正方案;分别运用湍流粘性系数模型和雷诺应力模型及它们的浮力修正型、双流体模型对几种典型的浮力流进行计算机模拟;最后提出选用浮力流湍流模型的建议. 相似文献
1000.
Expression and characterization of the cystic fibrosis transmembrane conductance regulator. 总被引:36,自引:0,他引:36
R J Gregory S H Cheng D P Rich J Marshall S Paul K Hehir L Ostedgaard K W Klinger M J Welsh A E Smith 《Nature》1990,347(6291):382-386
Cystic fibrosis (CF) is a common lethal genetic disease that manifests itself in airway and other epithelial cells as defective chloride ion absorption and secretion, resulting at least in part from a defect in a cyclic AMP-regulated, outwardly-rectifying Cl- channel in the apical surface. The gene responsible for CF has been identified and predicted to encode a membrane protein termed the CF transmembrane conductance regulator (CFTR). Identification of a cryptic bacterial promoter within the CFTR coding sequence led us to construct a complementary DNA in a low-copy-number plasmid, thereby avoiding the deleterious effects of CFTR expression on Escherischia coli. We have used this cDNA to express CFTR in vitro and in vivo. Here we demonstrate that CFTR is a membrane-associated glycoprotein that can be phosporylated in vitro by cAMP-dependent protein kinase. Polyclonal and monoclonal antibodies directed against distinct domains of the protein immunoprecipitated recombinant CFTR as well as the endogenous CFTR in nonrecombinant T84 cells. Partial proteolysis fingerprinting showed that the recombinant and non-recombinant proteins are indistinguishable. These data, which establish several characteristics of the protein responsible for CF, will now enable CFTR function to be studied and will provide a basis for diagnosis and therapy. 相似文献