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   2023篇
  免费   94篇
  2022年   5篇
  2021年   27篇
  2020年   10篇
  2019年   12篇
  2018年   13篇
  2017年   26篇
  2016年   42篇
  2015年   57篇
  2014年   58篇
  2013年   110篇
  2012年   109篇
  2011年   111篇
  2010年   71篇
  2009年   61篇
  2008年   123篇
  2007年   103篇
  2006年   120篇
  2005年   120篇
  2004年   122篇
  2003年   144篇
  2002年   132篇
  2001年   64篇
  2000年   50篇
  1999年   58篇
  1998年   27篇
  1997年   25篇
  1996年   15篇
  1995年   12篇
  1994年   12篇
  1993年   20篇
  1992年   25篇
  1991年   23篇
  1990年   18篇
  1989年   12篇
  1988年   16篇
  1987年   17篇
  1986年   17篇
  1985年   15篇
  1984年   15篇
  1983年   13篇
  1982年   9篇
  1981年   11篇
  1980年   8篇
  1979年   8篇
  1978年   6篇
  1977年   4篇
  1976年   9篇
  1975年   5篇
  1973年   8篇
  1970年   4篇
排序方式: 共有2117条查询结果,搜索用时 21 毫秒
51.
52.
53.
Journal of Computational Neuroscience - Feed-forward deep neural networks have better performance in object categorization tasks than other models of computer vision. To understand the relationship...  相似文献   
54.
Journal of Computational Neuroscience - When two-frame apparent motion stimuli are presented with an appropriate inter-stimulus interval (ISI), motion is perceived in the direction opposite to the...  相似文献   
55.
The Protein Journal - Difference circular dichroism (CD) spectroscopy was used here to characterize changes in structure of flexible peptides upon altering their environments. Environmental changes...  相似文献   
56.
The HMG-CoA reductase inhibitor simvastatin activates AMP-activated protein kinase (AMPK) and thereby induces histone acetylation. We postulated that combining simvastatin with the histone deacetylase (HDAC) inhibitor romidepsin would kill bladder cancer cells by inducing histone acetylation cooperatively. The combination of romidepsin and simvastatin induced robust apoptosis and killed bladder cancer cells synergistically. In murine subcutaneous tumor models using MBT-2 cells, a 15-day treatment with 0.5 mg/kg romidepsin and 15 mg/kg simvastatin was well tolerated and inhibited tumor growth significantly. Mechanistically, the combination induced histone acetylation by activating AMPK. The combination also decreased the expression of HDACs, thus further promoting histone acetylation. This AMPK activation was essential for the combination's action because compound C, an AMPK inhibitor, suppressed the combination-induced histone acetylation and the combination's ability to induce apoptosis. We also found that the combination increased the expression of peroxisome proliferator-activated receptor (PPAR) γ, leading to reactive oxygen species production. Furthermore, the combination induced endoplasmic reticulum (ER) stress and this ER stress was shown to be associated with increased AMPK expression and histone acetylation, thus playing an important role in the combination's action. Our study also suggests there is a positive feedback cycle between ER stress induction and PPARγ expression.  相似文献   
57.
Abstract

2′-Deoxy- and 2′-O-methyl-5′-O-terpyridyl derivatives of adenosine and cytidine were synthesized and used to construct 5′-end-modified oligonucleotides. These antisense agents complexed with Cu(II) exclusively cleaved a complementary RNA oligomer at the site opposite the terpyridine-nucleoside residue. We also found that the terpyridine·Cu(II) moiety stabilizes 2′-O-methyl RNA duplex. These suggest that after RNA hybridization, the terpyridine moiety is close to the RNA strand, presumably in an end capping manner.  相似文献   
58.
The detection of rare mutants using next generation sequencing has considerable potential for diagnostic applications. Detecting circulating tumor DNA is the foremost application of this approach. The major obstacle to its use is the high read error rate of next-generation sequencers. Rather than increasing the accuracy of final sequences, we detected rare mutations using a semiconductor sequencer and a set of anomaly detection criteria based on a statistical model of the read error rate at each error position. Statistical models were deduced from sequence data from normal samples. We detected epidermal growth factor receptor (EGFR) mutations in the plasma DNA of lung cancer patients. Single-pass deep sequencing (>100,000 reads) was able to detect one activating mutant allele in 10,000 normal alleles. We confirmed the method using 22 prospective and 155 retrospective samples, mostly consisting of DNA purified from plasma. A temporal analysis suggested potential applications for disease management and for therapeutic decision making to select epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI).  相似文献   
59.
60.
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