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   849136篇
  免费   91869篇
  国内免费   688篇
  2018年   8331篇
  2017年   7873篇
  2016年   11434篇
  2015年   15898篇
  2014年   18402篇
  2013年   25927篇
  2012年   29197篇
  2011年   29485篇
  2010年   19872篇
  2009年   17894篇
  2008年   25929篇
  2007年   26506篇
  2006年   25029篇
  2005年   24174篇
  2004年   23956篇
  2003年   22892篇
  2002年   22133篇
  2001年   39121篇
  2000年   39409篇
  1999年   31322篇
  1998年   11065篇
  1997年   11489篇
  1996年   10783篇
  1995年   10086篇
  1994年   9833篇
  1993年   9584篇
  1992年   25261篇
  1991年   24519篇
  1990年   23849篇
  1989年   23204篇
  1988年   21574篇
  1987年   20112篇
  1986年   18668篇
  1985年   18488篇
  1984年   15356篇
  1983年   12845篇
  1982年   9803篇
  1981年   8766篇
  1980年   8157篇
  1979年   13827篇
  1978年   10751篇
  1977年   9655篇
  1976年   8749篇
  1975年   9769篇
  1974年   10405篇
  1973年   10278篇
  1972年   9228篇
  1971年   8397篇
  1970年   7162篇
  1969年   6950篇
排序方式: 共有10000条查询结果,搜索用时 234 毫秒
991.
992.
993.
994.
995.
Power spectra and coherence function of EEG of various cortical areas of both hemispheres were analyzed in 9 patients with extremely protracted loss of consciousness. Five patients were in the state of posttraumatic apallic syndrome lasting for more than 4 years in one patient, and 4-9 months with successive lethal outcome in 4 patients. One patient for more than 2 years was in a state of areactivity to external signals. In 3 patients the process of recovery of consciousness and speech began in 1-2 months. At the apallic syndrome, only low-frequency EEG components were present in spectrograms, and the values of coherence function were sharply decreased. With recovering consciousness and speech, a gradual appearance of alpha-activity was observed as well as an increase of coherence values at the frequency of the alpha-rhythm. The recovery of intercentral EEG relations in the motor-verbal cortical area was shown to play a special role in further normalization of connections in the cerebral cortex.  相似文献   
996.
997.
998.
Numerous clinical and epidemiological studies link enteroviruses such as the Coxsackie virus group with the autoimmune disease type 1 diabetes mellitus (DM). In addition, there are reports that patients with type 1 DM are characterized by skewing of TCR Vbeta chain selection among peripheral blood and intraislet T lymphocytes. To examine these issues, we analyzed TCR Vbeta chain-specific up-regulation of the early T cell activation marker, CD69, on CD4 T cells after incubation with Coxsackievirus B4 (CVB4) Ags. CD4 T cells bearing the Vbeta chains 2, 7, and 8 were the most frequently activated by CVB4. Up-regulation of CD69 by different TCR families was significantly more frequent in new onset type 1 DM patients (p = 0.04), 100% of whom (n = 8) showed activation of CD4 T cells bearing Vbeta8, compared with 50% of control subjects (n = 8; p = 0.04). T cell proliferation after incubation with CVB4 Ags required live, nonfixed APCs, suggesting that the selective expansion of CD4 T cells with particular Vbeta chains resulted from conventional antigen processing and presentation rather than superantigen activity. Heteroduplex analysis of TCR Vbeta chain usage after CVB4 stimulation indicated a relatively polyclonal, rather than oligo- or monoclonal response to viral Ags. These results provide evidence that new-onset patients with type 1 DM and healthy controls are primed against CVB4, and that CD4 T cell responses to the virus have a selective TCR Vbeta chain usage which is driven by viral Ags rather than a superantigen.  相似文献   
999.
Glucose serves as the major energy substrate and the main precursor for the synthesis of glycosaminoglycans in chondrocytes. Facilitated glucose transport represents the first rate-limiting step in glucose metabolism. This study examines molecular regulation of facilitated glucose transport in normal human articular chondrocytes by proinflammatory cytokines. IL-1beta and TNF-alpha, and to a lesser degree IL-6, accelerate facilitated glucose transport as measured by [(3)H]2-deoxyglucose uptake. IL-1beta induces an increased expression of glucose transporter (GLUT) 1 mRNA and protein, and GLUT9 mRNA. GLUT3 and GLUT8 mRNA are constitutively expressed in chondrocytes and are not regulated by IL-1beta. GLUT2 and GLUT4 mRNA are not detected in chondrocytes. IL-1beta stimulates GLUT1 protein glycosylation and plasma membrane incorporation. IL-1beta regulation of glucose transport in chondrocytes depends on protein kinase C and p38 signal transduction pathways, and does not require phosphoinositide 3-kinase, extracellular signal-related kinase, or c-Jun N-terminal kinase activation. IL-1beta-accelerated glucose transport in chondrocytes is not mediated by endogenous NO or eicosanoids. These results demonstrate that stimulation of glucose transport represents a component of the chondrocyte response to IL-1beta. Two classes of GLUTs are identified in chondrocytes, constitutively expressed GLUT3 and GLUT8, and the inducible GLUT1 and GLUT9.  相似文献   
1000.
 Patterns of abundance of large piscivorous fish (>200 mm TL) were documented at two spatial and four temporal scales within the main lagoon of One Tree Reef on Australia’s Great Barrier Reef. Grouper (Serranidae), snapper (Lutjanidae) and wrasses (Labridae) were the most abundant large piscivores. On a large scale (hundreds of metres), patterns of predator abundance were consistently greater on the inner edge than centre of the lagoon over a range of temporal scales: days, weeks, months and years. On a small spatial scale (tens of metres), the abundance of large predatory fish was patchy. At both spatial scales, fish were consistently aggregated in particular areas and associated with specific structural features of the reef habitat. Predator abundance was high where live corals were predominant and the topography was more complex. Hence, predation pressure and its potential effects on the distribution and abundance of prey populations, both in time and space, may vary greatly within lagoonal environments. Accepted: 25 May 1997  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