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21.
全球气候变暖、空气污染、水污染和能源危机等问题引起了世人的关注,世界各国都在加紧开发储量巨大、无污染、可再生的风电资源,节能减排,保护我们赖以生存的地球。我国可开发利用的风能储量达10亿千瓦,2007年装机容量仅600万千瓦,2010年将达2000万千瓦。风电开发速度迅猛、潜力巨大,特别是对我国沿海岛屿,交通不便的边远山区,地广人稀的草原牧场,以及远离电网的农村、边疆,作为解决生产和生活能源的一种可靠途径,具有十分重要的意义。本文以国电龙源江苏如东风电特许权二期项目工程GE1.5MW—sle风机安装为例,介绍风机安装机械化施工技术,并在此基础上总结经验,其它型号风机安装可参照。 相似文献
22.
23.
HCl中咪唑衍生物复配对碳钢的缓蚀作用研究 总被引:4,自引:0,他引:4
研制了一种咪唑衍生物(BBIM),利用失重法、动电位扫描极化法及SEM研究了BBIM与碘化钾和甲醛在质量分数5% HCl中按一定比例复配对碳钢的缓蚀效果,讨论了浓度、温度对缓蚀性能的影响,同时对缓蚀机理进行了探讨。结果表明两种复配缓蚀剂在5%HCl腐蚀环境中对碳钢均具有良好的缓蚀作用,是一种混合型缓蚀剂,缓蚀作用机理为协同机理。 相似文献
24.
不同方法测定黄土和古土壤样品粒度的比较 总被引:6,自引:0,他引:6
用激光粒度仪和沉降法分别测量了黄土和古土壤的粒度分布,通过对比两种方法测量结果,认为激光法测量的重复性和测量精度较高,小于5μm颗粒含量低于沉降法,平均粒径较沉降法偏粗;造成这种差异的原因主要是不同方法的原理不同和样品中颗粒形状不规则所致.黄土风化成壤过程中形成的次生碳酸盐矿物可能主要存在于小于5μm的颗粒内. 相似文献
25.
对我国恩施土家族15种特色民族药用植物的资源分布、化学成分、药理作用以及国内外研究进展进行了概述,并分析了研究中存在的问题,得到了一些结果结论,对土家族民族药用植物资源的综合开发利用具有一定指导意义或参考价值. 相似文献
26.
Pancreatitis is usually inflammation of the pancreas without infection. Our understanding of pancreatitis has been built on autopsy studies, surgical biopsies and surrogate markers of inflammation and fibroses, including abdominal imaging techniques and pancreatic functional studies. However, the discovery that a number of different environmental factors and various genetic abnormalities are seen in patients with similar appearing pancreatitis phenotypes teaches us that end-stage pathology is not the disorder. Understanding complex associations and interactions requires that the components and their interactions be organized, stratified and functionally defined. Systems biology, in the broad sense, provides the approach and tools to define the complex mechanisms driving pathology. As the mathematics behind these pathways and mechanisms are defined and calibrated, the potential pathology of patients with early signs of disease can be predicted, and a number of patient-specific targets for intervention can be defined. 相似文献
27.
Kitamura T Kometani K Hashida H Matsunaga A Miyoshi H Hosogi H Aoki M Oshima M Hattori M Takabayashi A Minato N Taketo MM 《Nature genetics》2007,39(4):467-475
Inactivation of TGF-beta family signaling is implicated in colorectal tumor progression. Using cis-Apc(+/Delta716) Smad4(+/-) mutant mice (referred to as cis-Apc/Smad4), a model of invasive colorectal cancer in which TGF-beta family signaling is blocked, we show here that a new type of immature myeloid cell (iMC) is recruited from the bone marrow to the tumor invasion front. These CD34(+) iMCs express the matrix metalloproteinases MMP9 and MMP2 and the CC-chemokine receptor 1 (CCR1) and migrate toward the CCR1 ligand CCL9. In adenocarcinomas, expression of CCL9 is increased in the tumor epithelium. By deleting Ccr1 in the background of the cis-Apc/Smad4 mutant, we further show that lack of CCR1 prevents accumulation of CD34(+) iMCs at the invasion front and suppresses tumor invasion. These results indicate that loss of transforming growth factor-beta family signaling in tumor epithelium causes accumulation of iMCs that promote tumor invasion. 相似文献
28.
Sobacchi C Frattini A Guerrini MM Abinun M Pangrazio A Susani L Bredius R Mancini G Cant A Bishop N Grabowski P Del Fattore A Messina C Errigo G Coxon FP Scott DI Teti A Rogers MJ Vezzoni P Villa A Helfrich MH 《Nature genetics》2007,39(8):960-962
Autosomal recessive osteopetrosis is usually associated with normal or elevated numbers of nonfunctional osteoclasts. Here we report mutations in the gene encoding RANKL (receptor activator of nuclear factor-KB ligand) in six individuals with autosomal recessive osteopetrosis whose bone biopsy specimens lacked osteoclasts. These individuals did not show any obvious defects in immunological parameters and could not be cured by hematopoietic stem cell transplantation; however, exogenous RANKL induced formation of functional osteoclasts from their monocytes, suggesting that they could, theoretically, benefit from exogenous RANKL administration. 相似文献
29.
Liu F Thirumangalathu S Gallant NM Yang SH Stoick-Cooper CL Reddy ST Andl T Taketo MM Dlugosz AA Moon RT Barlow LA Millar SE 《Nature genetics》2007,39(1):106-112
Fungiform taste papillae form a regular array on the dorsal tongue. Taste buds arise from papilla epithelium and, unusually for epithelial derivatives, synapse with neurons, release neurotransmitters and generate receptor and action potentials. Despite the importance of taste as one of our five senses, genetic analyses of taste papilla and bud development are lacking. We demonstrate that Wnt-beta-catenin signaling is activated in developing fungiform placodes and taste bud cells. A dominant stabilizing mutation of epithelial beta-catenin causes massive overproduction of enlarged fungiform papillae and taste buds. Likewise, genetic deletion of epithelial beta-catenin or inhibition of Wnt-beta-catenin signaling by ectopic dickkopf1 (Dkk1) blocks initiation of fungiform papilla morphogenesis. Ectopic papillae are innervated in the stabilizing beta-catenin mutant, whereas ectopic Dkk1 causes absence of lingual epithelial innervation. Thus, Wnt-beta-catenin signaling is critical for fungiform papilla and taste bud development. Altered regulation of this pathway may underlie evolutionary changes in taste papilla patterning. 相似文献
30.
Site- and state-specific lysine methylation of histones is catalyzed by a family of proteins that contain the evolutionarily
conserved SET domain and plays a fundamental role in epigenetic regulation of gene activation and silencing in all eukaryotes.
The recently determined three-dimensional structures of the SET domains from chromosomal proteins reveal that the core SET
domain structure contains a two-domain architecture, consisting of a conserved anti-parallel β-barrel and a structurally variable
insert that surround a unusual knot-like structure that comprises the enzyme active site. These structures of the SET domains,
either in the free state or when bound to cofactor S-adenosyl-L-homocysteine and/or histone peptide, mimicking an enzyme/cofactor/substrate complex, further yield the structural insights
into the molecular basis of the substrate specificity, methylation multiplicity and the catalytic mechanism of histone lysine
methylation.
Received 10 June 2006; accepted 22 August 2006 相似文献