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961.
962.
DNA discrepancy     
May A 《Nature》2003,421(6920):210
  相似文献   
963.
Despite a long history of research on the Early Cambrian in China most available data on small skeletal fossils concern fossil associations of the shallow carbonate platform. Information on skeletal fossils from marginal shelf environments of the Yangtze Platform is scanty, which may reflect the rarity of fossils in deeper sedimentary environments but is also due to limitation of carbonate distribution and outcrops, difficulties in fossil extraction, and a general research focus on the Precambrian-Cambrian boundary beds on the carbonate platform. Here we present a documentation of Meishucunian to Qiongzhusian small skeletal fossils from the lower Hetang Formation and the chert unit at its base from the Jiangshan region, Zhejiang Province, representing a relatively deep shelf environment compared to the inner shelf region. The earliest association (Meishucunian) from the chert unit underlying the Hetang Formation is mainly characterized by the occurrence of Protohertzina anabarica, P. unguliformis, Fengzuella zhejiangensis, and Kaiyangites novilis, which differs somewhat in composition from SSF-associations of typical inner shelf deposits. The enigmatic skeletal fossil Fengzuella zhejiangensis, which exhibits an unusual secretional growth mode previously unrecognized from the Early Cambrian, is described in detail. A younger (Qiongzhusian) fossil association contains numerous arthropod remains, such as disarticulated spines of arthropods (Jiangshanodus- and Kijacus-type), which have previously been considered as conodont-like fossils, and bradoriid valves.  相似文献   
964.
0 IntroductionAblockcipherwithoutdataextensionorexpressionisaper mutation .Thesecurityofablockcipherschemeiscorrela tivewiththe permutations.Quicktrickle permutation[1 ] canmakethedatadisorderedwhenactingatthedataandmakeallprobabledistancebetweentwoelementsappear,soithasgoodcryptographicpropertiesandcanbeusedintheblockcipherwhichrequireshighsecurity.Aprivatekeyblockcipherisapermutationinn dimensionvectorspaceoverF2 atthecontrolofakey[2 ,3] .Moreover,manyblockciphersusepermutationstoexecuteso…  相似文献   
965.
Research on data combination for Phased-array Ground Penetrating Radar   总被引:1,自引:0,他引:1  
0 IntroductionGroundPenetratingRadar (GPR)isanewandefficientex ploringmeanstodetecttheobjectinshallowsubsurface.Comparedwithotherdetectingmethods,GPRhasmanyadvan tages,suchasquickness,highresolution ,convenientoperationetc.SoGPRisappliedtonationaldefenseandnationaleconomy .IndevelopmentofGPRtechnology ,therecomeforthcontinuous waveradar,FMcontinuous waveradar,andshockpulseradar.Amongoftheseradars,shockpulseradarsendsgreatamplitudeimpulsewithperiodinns,receivingequivalentsamplingtoreali…  相似文献   
966.
During agonist-dependent long-term stimulation of cells, histamine receptor subtypes are frequently down-regulated. However, the mechanisms underlying the modulation of receptor expression during long-term histamine stimulation have yet to be resolved. Based on our recently reported results showing an H1-mediated down-regulation of histamine H2 receptor mRNA in endothelial cells, our aim was to characterize the mechanism controlling rapid and long-term histamine-mediated modulation of H2 receptor expression in more detail. We were able to show that the histamine-induced down-regulation of H2 receptor mRNA and cell surface expression lasting for 24 h was accompanied by augmentation of the receptor protein level in the cytoplasmatic fraction of endothelial cells for this time period. Furthermore, changes in receptor protein levels in whole-cell lysate were negligible, indicating that the rapid and prolonged modulation of cell surface H2 receptor levels by histamine was regulated solely via internalization. The role of nitric oxide (NO) as a key mediator in histamine-stimulated cell responses was underlined by subsequent studies showing the attenuation of histamine-induced H2 receptor mRNA down-regulation and protein trafficking following NO synthase isozyme inhibition.Received 11 March 2003; received after revision 11 June 2003; accepted 17 June 2003  相似文献   
967.
In vertebrates, different isoforms of fibroblast growth factor 2 (FGF2) exist, which differ by their N-terminal extension. They show different localization and expression levels and exert distinct biological effects. Nevertheless, genetic inactivation of all FGF2 isoforms in the mouse results in only mild phenotypes. Here, we analyzed mouse FGF2, and show that, as in the human, mouse FGF2 contains CTG-initiated high molecular-weight (HMW) isoforms, which contain a nuclear localization signal, and which mediate localization of this isoform to the nucleus. Using green fluorescent protein-FGF2 fusions, we furthermore observed, that C-terminal deletions disable nuclear localization of the short low-molecular-weight (LMW) 18-kDa isoform. This loss of specific localization is accompanied by a loss in heparin binding. We therefore suggest that, first, localization of mouse FGF2 is comparable to that in other vertebrates and, second, FGF2 contains at least two sequences important for nuclear localization, a nuclear localization sequence at the N terminus which is only contained in the HMW isoform, and another sequence at the C terminus, which is only required for localization of the LMW 18-kDa isoform. Received 1 July 2003; accepted 14 August 2003  相似文献   
968.
Targeting of the Akt/PKB kinase to the actin skeleton   总被引:2,自引:0,他引:2  
Serine/threonine kinase Akt/PKB intracellular distribution undergoes rapid changes in response to agonists such as Platelet-derived growth factor (PDGF) or Insulin-like growth factor (IGF). The concept has recently emerged that Akt subcellular movements are facilitated by interaction with nonsubstrate ligands. Here we show that Akt is bound to the actin skeleton in in situ cytoskeletal matrix preparations from PDGF-treated Saos2 cells, suggesting an interaction between the two proteins. Indeed, by immunoprecipitation and subcellular fractioning, we demonstrate that endogenous Akt and actin physically interact. Using recombinant proteins in in vitro binding and overlay assays, we further demonstrate that Akt interacts with actin directly. Expression of Akt mutants strongly indicates that the N-terminal PH domain of Akt mediates this interaction. More important, we show that the partition between actin bound and unbound Akt is not constant, but is modulated by growth factor stimulation. In fact, PDGF treatment of serum-starved cells triggers an increase in the amount of Akt associated with the actin skeleton, concomitant with an increase in Akt phosphorylation. Conversely, expression of an Akt mutant in which both Ser473 and Thr308 have been mutated to alanine completely abrogates PDGF-induced binding. The small GTPases Rac1 and Cdc42 seem to facilitate actin binding, possibly increasing Akt phosphorylation.Received 10 September 2003; accepted 25 September 2003  相似文献   
969.
Cannabinoid CB1 receptors and vanilloid VR1 receptors are co-localized to some extent in sensory neurons of the spinal cord and dorsal root ganglia. In this study, we over-expressed both receptor types in human embryonic kidney (HEK)-293 cells and investigated the effect of the CB1 agonist HU-210 on the VR1-mediated increase in intracellular Ca2+ ([Ca2+]i), a well-known response of the prototypical VR1 agonist capsaicin. After a 5-min pre-treatment, HU-210 (0.1 microM) significantly enhanced the effect of several concentrations of capsaicin on [Ca2+]i in HEK-293 cells over-expressing both rat CB1 and human VR1 (CB1-VR1-HEK cells), but not in cells over-expressing only human VR1 (VR1-HEK cells). This effect was blocked by the CB1 receptor antagonist SR141716A (0.5 microM), and by phosphoinositide-3-kinase and phospholipase C inhibitors. The endogenous agonist of CB1 and VR1 receptors, anandamide, was more efficacious in inducing a VR1-mediated stimulation of [Ca2+]i in CB1-VR1-HEK cells than in VR1-HEK cells, and part of its effect on the former cells was blocked by SR141716A (0.5 microM). Pre-treatment of CB1-VR1-HEK cells with forskolin, an adenylate cyclase activator, enhanced the capsaicin effect on [Ca2+]i. HU-210, which in the same cells inhibits forskolin-induced enhancement of cAMP levels, blocked the stimulatory effect of forskolin on capsaicin. Our data suggest that in cells co-expressing both CB1 and VR1 receptors, pre-treatment with CB1 agonists inhibits or stimulates VR1 gating by capsaicin depending on whether or not cAMP-mediated signalling has been concomitantly activated.  相似文献   
970.
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