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系统地论述了氧气底吹熔炼氧枪的结构、工作原理、设计计算方法、材质及蚀损机理.指出了延长氧枪使用寿命的措施。 相似文献
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基于CVSD编码的无线语音系统方案的设计 总被引:2,自引:0,他引:2
简要介绍了连续可变斜率增量(CVSD)调制的原理。与目前应用较为广泛的其它语音编码方式相比较,CVSD拥有更优的数字特性。着重介绍了由CML公司研制开发的基于CVSD的语音编码芯片———CMX649的特点及相关的应用方式。CMX649能够成功地应用在广泛的语音编码系统中,尤其适合无线语音系统应用。在此基础上,给出了一种实用性很强的低成本、低功耗无线语音系统的设计与应用方案。该方案可提供清晰可靠的语音传输,可广泛应用于农村地区,具有广阔的市场空间。 相似文献
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D Averill D Blockus B Brabson J Brom C Jung H Ogren DR Rust M Derrick P Kooijman JS Loos B Musgrave LE Price J Repond K Sugano B Cork C Akerlof J Chapman D Errede MT Ken DI Meyer H Neal D Nitz R Thun R Tschirhart S Abachi P Baringer BG Bylsma R DeBonte D Koltick EH Low RL McIlwain DH Miller CR Ng EI Shibata 《Canadian Metallurgical Quarterly》1989,39(1):123-137
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LA Knapp E Lehmann L Hennes ME Eberle DI Watkins 《Canadian Metallurgical Quarterly》1997,50(2):170-177
Skeletal development of transgenic mice with a type II collagen mutation was analyzed and compared with wild-type littermates. The single base substitution in Col2a1 resulted in a glycine to serine mutation within the helical domain and corresponded to one previously identified in a patient with the lethal human chondrodysplasia, hypochondrogenesis (Horton et al. [1992] Proc. Natl. Acad. Sci. U.S.A. 89:4583-4587). Skeletal staining of embryos from 14.5 through 18.5 days of gestation demonstrated a dwarf phenotype in the transgenic embryos, most notably short limb bones and vertebral column that was first detected at 15.5 days post-coitus. In addition to the reduced length, the extent of ossification was less in the transgenic mice. The architecture of the long bone growth plate was abnormal in the transgenic tissue, in particular there was no discernible proliferative zone. There were few stacks of characteristically flattened cells and the overall length of the growth plate in the mutant embryos was reduced. At the ultrastructural level, there were fewer collagen fibrils present in the transgenic mouse cartilage compared to that of wild-type littermates. Ultrastructural localization of collagen types II, IX and XI revealed a similar pattern between the transgenic and wild-type pups, suggesting that the collagen fibrils present in the matrix of littermates with both phenotypes had a similar composition. Skeletal analysis and cartilage histochemistry indicated that effect of the type II collagen mutation was to reduce the density of the collagen fibrils within the cartilage matrix which was associated with delayed bone formation and resulted in a short-limbed phenotype. 相似文献
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DI Rodenhiser JD Andrews DN Mancini JH Jung SM Singh 《Canadian Metallurgical Quarterly》1997,373(2):185-195
Glutamatergic synaptic potentials induced by micromolar concentrations of the potassium conductance blocker 4-aminopyridine (4-AP) were recorded intracellularly from rat neostriatal neurons in the presence of 10 microM bicuculline (BIC). These synaptic potentials originate from neostriatal cortical and thalamic afferents and were completely blocked by 10 microM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) plus 100 microM D-2-amino-5-phosphonovaleric acid (2-APV). Their inter-event time intervals could be fitted to exponential distributions, suggesting that they are induced randomly. Their amplitude distributions had most counts around 1 mV and fewer counts with values up to 5 mV. Since input resistance of the recorded neurons is about 40 M omega, the amplitudes agree to quantal size measurements in mammalian central neurons. The action of a D2 agonist, quinpirole, was studied on the frequency of these events. Mean amplitude of synaptic potentials was preserved in the presence of 2-10 microM quinpirole, but the frequency of 4-AP-induced glutamatergic synaptic potentials was reduced in 35% of cases. The effect was blocked by the D2 antagonist sulpiride (10 microM). Input resistance, membrane potential, or firing threshold did not change during quinpirole effect, suggesting a presynaptic site of action for quinpirole in some but not all glutamatergic afferents that make contact on a single cell. The present experiments show that dopaminergic presynaptic modulation of glutamatergic transmission in the neostriatum does not affect all stimulated afferents, suggesting that it is selective towards some of them. This may control the quality and quantity of afferent flow upon neostriatal neurons. 相似文献
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According to FDA regulations, a combination drug is not efficacious unless each component contributes to the claimed effects. For a univariate endpoint, this implies that the combination at specific doses must be superior to each of its components at the same doses. More demanding is the property of synergy, in which the effect of the combination must be superior to the effect expected based on those of its components. If it is equal to those effects, it is additive, and if it is inferior, it is antagonistic. We give regions in the combination dose plane where these concepts are well defined. If the effect of the combination is greater than the greatest effect achievable by any of its components it is therapeutically synergistic. A combination can be antagonistic, yet its components can still contribute to the claimed effects. If it is additive, synergistic or therapeutically synergistic, its components must contribute to the claimed effects. We relate these concepts and provide designs and sequential procedures for determining whether a combination is therapeutically synergistic, synergistic, additive, antagonistic and contributing or antagonistic and non-contributing. 相似文献