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利用美国伊利诺伊大学结构健康监测项目组研制的ISM400无线智能传感器,分别采用分布式和集中式数据采集方法,对一个简支层压板进行了振动测试试验.采用自然环境激励技术(NExT)和特征系统实现算法(ERA)相结合的一种时域联合算法,仅利用输出信号对结构模态参数进行识别,并将识别结果与有限元模型的计算结果进行了对比分析.根据分布式与集中式两种数据采集处理方法识别的振动频率和模态振型,与有限元数值模拟结果吻合较好,验证了基于分布式数据采集的无线智能传感器网络在结构模态识别中的可行性.在大型土木工程结构需要布置大量传感器时,分布式无线智能传感器网络因其高度集成化和节约电源等优点,比采用传统的集中式数据采集方法更加高效实用. 相似文献
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Organic chemists are now able to synthesize small quantities of almost any known natural product, given sufficient time, resources and effort. However, translation of the academic successes in total synthesis to the large-scale construction of complex natural products and the development of large collections of biologically relevant molecules present significant challenges to synthetic chemists. Here we show that the application of two nature-inspired techniques, namely organocascade catalysis and collective natural product synthesis, can facilitate the preparation of useful quantities of a range of structurally diverse natural products from a common molecular scaffold. The power of this concept has been demonstrated through the expedient, asymmetric total syntheses of six well-known alkaloid natural products: strychnine, aspidospermidine, vincadifformine, akuammicine, kopsanone and kopsinine. 相似文献
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Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis 总被引:1,自引:0,他引:1
International Multiple Sclerosis Genetics Consortium;Wellcome Trust Case Control Consortium Sawcer S Hellenthal G Pirinen M Spencer CC Patsopoulos NA Moutsianas L Dilthey A Su Z Freeman C Hunt SE Edkins S Gray E Booth DR Potter SC Goris A Band G Oturai AB Strange A Saarela J Bellenguez C Fontaine B Gillman M Hemmer B Gwilliam R Zipp F Jayakumar A Martin R Leslie S Hawkins S Giannoulatou E D'alfonso S Blackburn H Martinelli Boneschi F Liddle J Harbo HF Perez ML Spurkland A Waller MJ Mycko MP 《Nature》2011,476(7359):214-219
Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis. 相似文献
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Genetic analysis of autoimmune type 1 diabetes mellitus in mice. 总被引:57,自引:0,他引:57
J A Todd T J Aitman R J Cornall S Ghosh J R Hall C M Hearne A M Knight J M Love M A McAleer J B Prins 《Nature》1991,351(6327):542-547
Two genes, Idd-3 and Idd-4, that influence the onset of autoimmune type 1 diabetes in the nonobese diabetic mouse have been located on chromosomes 3 and 11, outside the chromosome 17 major histocompatibility complex. A genetic map of the mouse genome, analysed using the polymerase chain reaction, has been assembled specifically for the study. On the basis of comparative maps of the mouse and human genomes, the homologue of Idd-3 may reside on human chromosomes 1 or 4 and Idd-4 on chromosome 17. 相似文献
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