首页 | 本学科首页   官方微博 | 高级检索  
文章检索
  按 检索   检索词:      
出版年份:   被引次数:   他引次数: 提示:输入*表示无穷大
  收费全文   11643篇
  免费   49篇
  国内免费   80篇
系统科学   61篇
丛书文集   29篇
教育与普及   21篇
理论与方法论   32篇
现状及发展   5437篇
研究方法   588篇
综合类   5476篇
自然研究   128篇
  2012年   206篇
  2011年   301篇
  2010年   77篇
  2009年   74篇
  2008年   203篇
  2007年   242篇
  2006年   247篇
  2005年   236篇
  2004年   203篇
  2003年   195篇
  2002年   247篇
  2001年   436篇
  2000年   427篇
  1999年   288篇
  1992年   236篇
  1991年   194篇
  1990年   215篇
  1989年   191篇
  1988年   202篇
  1987年   219篇
  1986年   190篇
  1985年   252篇
  1984年   226篇
  1983年   171篇
  1982年   176篇
  1981年   180篇
  1980年   170篇
  1979年   403篇
  1978年   340篇
  1977年   250篇
  1976年   290篇
  1975年   260篇
  1974年   272篇
  1973年   226篇
  1972年   244篇
  1971年   308篇
  1970年   374篇
  1969年   254篇
  1968年   307篇
  1967年   292篇
  1966年   249篇
  1965年   178篇
  1964年   99篇
  1959年   88篇
  1958年   162篇
  1957年   100篇
  1956年   91篇
  1955年   85篇
  1954年   77篇
  1948年   64篇
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
861.
Zusammenfassung Supernatanten aus Kulturen überempfindlicher Lymphozyten und dem spezifischen Antigen mit MIF-Aktivität können die Entstehung der Pseudopodien normaler Makrophagen verhindern und zeigen nach längerem Kultivieren zuweilen toxische Eigenschaften.  相似文献   
862.
Introduction Liquid-liquid dispersions in agitated vessels are fre-quently used in the chemical industry for conducting operations such as solvent extraction and heterogene-ous reactions. In liquid-liquid two-phase flow systems, usually consisting of an a…  相似文献   
863.
Mutations in PRKCSH, encoding the beta-subunit of glucosidase II, an N-linked glycan-processing enzyme in the endoplasmic reticulum (ER), cause autosomal dominant polycystic liver disease. We found that mutations in SEC63, encoding a component of the protein translocation machinery in the ER, also cause this disease. These findings are suggestive of a role for cotranslational protein-processing pathways in maintaining epithelial luminal structure and implicate noncilial ER proteins in human polycystic disease.  相似文献   
864.
865.
Bobrov K  Mayne AJ  Dujardin G 《Nature》2001,413(6856):616-619
The electronic properties of insulators such as diamond are of interest not only for their passive dielectric capabilities for use in electronic devices, but also for their strong electron confinement on atomic scales. However, the inherent lack of electrical conductivity in insulators usually prevents the investigation of their surfaces by atomic-scale characterization techniques such as scanning tunnelling microscopy (STM). And although atomic force microscopy could in principle be used, imaging diamond surfaces has not yet been possible. Here, we demonstrate that STM can be used in an unconventional resonant electron injection mode to image insulating diamond surfaces and to probe their electronic properties at the atomic scale. Our results reveal striking electronic features in high-purity diamond single crystals, such as the existence of one-dimensional fully delocalized electronic states and a very long diffusion length for conduction-band electrons. We expect that our method can be applied to investigate the electronic properties of other insulating materials and so help in the design of atomic-scale electronic devices.  相似文献   
866.
Summary SWR/J mice posses high arylsulfatase C, estrone sulfatase, and dehydroepiandrosterone sulfatase activities in liver, spleen and kidney compared to A/J mice. This internstrain activity variation appears to be determined by at least 1 autosomal gene. Murine arylsulfatase C activity occurs in both hydrophobic and hydrophilic forms which differ with respect to certain biochemical properties and exhibit different subcellular distributions. The hydrophilic isozyme is a major component in kidney and brain extracts and a minor isozyme in liver and spleen extracts. The hydrophobic arylsulfatase C isozyme appears to be identical to steroid sulfatase. The hydrophilic arylsulfatase C isozyme does not possess steroid sulfatase activity; however, hydrophilic and hydrophobic arylsulfatase C share certain properties, suggesting that they may be structurally related. The autosomal gene(s) affects both arylsulfatase isozymes.This research was supported in part by National Institutes of Health grant GM 27707.  相似文献   
867.
Summary Superoxide dismutase activity was slow throughout the cell cycle of surface cultures ofPhysarum polycephalum. This activity increased markedly when the organism was induced to spherulate. Glutathione (GSH) and hydrogen peroxide (H2O2) concentrations changed very little during the cell cycle. During spherulation GSH decreased; H2O2 and the cyanide-resistant respiration of plasmodial homogenates increased.  相似文献   
868.
869.
Y Shimizu  G A Van Seventer  K J Horgan  S Shaw 《Nature》1990,345(6272):250-253
Regulated adhesion of T cells to extracellular matrix (ECM) proteins is likely to be essential in T cell migration. Constitutive binding of various other cell types to ECM components is mediated by members of the VLA (very late antigen) subfamily of integrins. We describe here the regulated binding of resting CD4+ human T cells to ECM through three VLA integrins: VLA-4 and VLA-5 binding to fibronectin (FN), and a novel pathway of VLA-6 binding to laminin (LN). Binding to ECM is regulated in two ways. First, unlike other VLA-mediated interactions, VLA binding activity of the T cells is rapidly and dramatically augmented with cell activation without change in level of expression of the VLA molecules. Second, binding is regulated with T-cell differentiation; memory T cells express three- to four-fold more VLA-4, VLA-5, and VLA-6 than do naive cells, and bind more efficiently through them to FN and LN.  相似文献   
870.
The amyloid β-peptide (Aβ) is a 4-kDa species derived from the amyloid precursor protein, which accumulates in the brains of patients with Alzheimer’s disease. Although we lack full understanding of the etiology and pathogenesis of selective neuron death, considerable data do imply roles for both the toxic Aβ and increased oxidative stress. Another significant observation is the accumulation of abnormal, ubiquitin-conjugated proteins in affected neurons, suggesting dysfunction of the proteasome proteolytic system in these cells. Recent reports have indicated that Aβ can bind and inhibit the proteasome, the major cytoslic protease for degrading damaged and ubiquitin-conjugated proteins. Earlier results from our laboratory showed that moderately oxidized proteins are preferentially recognized and degraded by the proteasome; however, severely oxidized proteins cannot be easily degraded and, instead, inhibit the proteasome. We hypothesized that oxidatively modified Aβ might have a stronger (or weaker) inhibitory effect on the proteasome than does native Aβ. We therefore also investigated the proteasome inhibitory action of Aβ 1–40 (a peptide comprising the first 40 residues of Aβ) modified by the intracellular oxidant hydrogen peroxide, and by the lipid peroxidation product 4-hydroxynonenal (HNE). H2O2 modification of Aβ 1–40 generates a progressively poorer inhibitor of the purified human 20S proteasome. In contrast, HNE modification of Aβ 1–40 generates a progressively more selective and efficient inhibitor of the degradation of fluorogenic peptides and oxidized protein substrates by human 20S proteasome. This interaction may contribute to certain pathological manifestations of Alzheimer’s disease Received 26 September 2000; accepted 26 September 2000  相似文献   
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号