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991.
992.
Structure of Cdc42 in complex with the GTPase-binding domain of the 'Wiskott-Aldrich syndrome' protein. 总被引:16,自引:0,他引:16
N Abdul-Manan B Aghazadeh G A Liu A Majumdar O Ouerfelli K A Siminovitch M K Rosen 《Nature》1999,399(6734):379-383
The Rho-family GTP-hydrolysing proteins (GTPases), Cdc42, Rac and Rho, act as molecular switches in signalling pathways that regulate cytoskeletal architecture, gene expression and progression of the cell cycle. Cdc42 and Rac transmit many signals through GTP-dependent binding to effector proteins containing a Cdc42/Rac-interactive-binding (CRIB) motif. One such effector, the Wiskott-Aldrich syndrome protein (WASP), is postulated to link activation of Cdc42 directly to the rearrangement of actin. Human mutations in WASP cause severe defects in haematopoletic cell function, leading to clinical symptoms of thrombocytopenia, immunodeficiency and eczema. Here we report the solution structure of a complex between activated Cdc42 and a minimal GTPase-binding domain (GBD) from WASP. An extended amino-terminal GBD peptide that includes the CRIB motif contacts the switch I, beta2 and alpha5 regions of Cdc42. A carboxy-terminal beta-hairpin and alpha-helix pack against switch II. The Phe-X-His-X2-His portion of the CRIB motif and the alpha-helix appear to mediate sensitivity to the nucleotide switch through contacts to residues 36-40 of Cdc42. Discrimination between the Rho-family members is likely to be governed by GBD contacts to the switch I and alpha5 regions of the GTPases. Structural and biochemical data suggest that GBD-sequence divergence outside the CRIB motif may reflect additional regulatory interactions with functional domains that are specific to individual effectors. 相似文献
993.
994.
Metamorphic core complexes are domal uplifts of metamorphic and plutonic rocks bounded by shear zones that separate them from unmetamorphosed cover rocks. Interpretations of how these features form are varied and controversial, and include models involving extension on low-angle normal faults, plutonic intrusions and flexural rotation of initially high-angle normal faults. The D'Entrecasteaux islands of Papua New Guinea are actively forming metamorphic core complexes located within a continental rift that laterally evolves to sea-floor spreading. The continental rifting is recent (since approximately 6 Myr ago), seismogenic and occurring at a rapid rate ( approximately 25 mm yr-1). Here we present evidence-based on isostatic modelling, geological data and heat-flow measurements-that the D'Entrecasteaux core complexes accommodate extension through the vertical extrusion of ductile lower-crust material, driven by a crustal density inversion. Although buoyant extrusion is accentuated in this region by the geological structure present-which consists of dense ophiolite overlaying less-dense continental crust-this mechanism may be generally applicable to regions where thermal expansion lowers crustal density with depth. 相似文献
995.
996.
心跳间隔增量序列的多尺度分析及临床应用 总被引:1,自引:0,他引:1
通过对心跳间隔序列、心跳间隔增量序列的多尺度熵和多尺度标准差分析, 发现心跳间隔序列的多尺度熵主要反映年龄对心脏活动水平的影响, 不足以作为区分充盈性心衰的诊断依据. 然而, 心跳间隔增量序列的多尺度熵分析却显示充盈性心衰和房颤患者心率变异性的复杂性较健康人有显著降低, 揭示两种疾病的心率变异性有着共同的潜在动力学性质. 提出了以心跳间隔增量序列在尺度4下的样本熵作为充盈性心衰和房颤的诊断依据并给出了参考值. 通过分析不同心功能分级对结果的影响, 发现即使是轻度心衰也能显著区别于健康人, 意味着该参数可以用于心衰的早期诊断. 相似文献
997.
998.
Hemoglobin is widely used as an inhibitor of EDRF effects. Hemoglobin contracts pig coronary arteries in vitro. However, during this contraction, effects of substance P and bradykinin which act via the EDRF are not inhibited. This means that the hemoglobin contraction is not caused by inhibition of the EDRF. This contraction is caused by a substance released from the endothelium, and by eicosano?ds released from the smooth muscles. 相似文献
999.
Summary The elucidation of the pathophysiological mechanisms of cerebral ischemia/hypoxia dictates the use of experimental models which mimic this disabling brain condition. In vivo experimental models have been available for many decades and are responsible for the bulk of, though incomplete, knowledge we have about these mechanisms. Since study in isolation of each postulated mechanism is impossible in vivo, the need for an in vitro experimental model has intensified in recent years. Consequently, rat and guinea pig hippocampal slice preparations have emerged as the models of choice. This review attempts to highlight some of the results obtained using brain slices in the study of cerebral ischemia/hypoxia and compare them to those obtained in vivo. Both the biochemical and the physiological correlates of energy metabolism, ion homeostasis, neurotransmission and neuromodulation of this brain condition are reviewed. The agreements, and especially the disagreements, between the in vivo and in vitro findings are emphasized. Details are given of the possible roles of both lactic acid, Ca2+ and excitotoxins in the neuronal damage inflicted by cerebral ischemia/hypoxia. Recent attempts to protect brain slices against experimental cerebral ischemic/hypoxic damage are also reviewed here briefly. 相似文献
1000.
Plasmid-related anaerobic autotrophy of the novel archaebacterium Sulfolobus ambivalens 总被引:1,自引:0,他引:1
Three different species of the genus Sulfolobus, S. acidocaldarius, S. solfataricus (= Caldariella) and S. brierleyi, have been distinguished by the conditions required for optimal growth, by the component patterns of their DNA-dependent RNA polymerases and by DNA sequence data. Many isolates of these species are able to grow chemolithoautotrophically using CO2 as the sole carbon source and the oxidation of S(0) with O2 yielding sulphuric acid, as the energy source, though a few others grow only heterotrophically. We show here that a strain of a novel Sulfolobus species, S. ambivalens, is alternatively able to live by an anaerobic mode of chemolithoautotrophy, also using CO2 as the sole carbon source, but using reduction of S(0) with H2, yielding H2S as the energy source. This mode of growth is correlated with the amplification of a plasmid, pSL10. 相似文献