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   187944篇
  免费   14827篇
  国内免费   52篇
  2018年   1897篇
  2017年   1843篇
  2016年   2379篇
  2015年   2356篇
  2014年   3195篇
  2013年   4509篇
  2012年   5207篇
  2011年   5703篇
  2010年   3974篇
  2009年   3600篇
  2008年   5168篇
  2007年   5487篇
  2006年   5117篇
  2005年   4822篇
  2004年   4938篇
  2003年   4870篇
  2002年   4829篇
  2001年   8432篇
  2000年   8615篇
  1999年   6379篇
  1998年   2071篇
  1997年   2092篇
  1996年   1847篇
  1995年   1739篇
  1992年   5252篇
  1991年   5420篇
  1990年   5185篇
  1989年   5162篇
  1988年   4794篇
  1987年   4536篇
  1986年   4111篇
  1985年   4293篇
  1984年   3456篇
  1983年   2964篇
  1982年   2001篇
  1981年   1790篇
  1980年   1782篇
  1979年   3261篇
  1978年   2605篇
  1977年   2320篇
  1976年   2136篇
  1975年   2585篇
  1974年   2924篇
  1973年   2821篇
  1972年   2674篇
  1971年   2432篇
  1970年   2138篇
  1969年   2052篇
  1968年   1939篇
  1967年   1764篇
排序方式: 共有10000条查询结果,搜索用时 187 毫秒
131.
Interferon gamma (IFNγ) is known to inhibit the proliferation of some transformed cell lines. Recently, we demonstrated the transactivation of the epidermal growth factor receptor (EGFR) in response to IFNγ (Burova et al., 2007) and provided direct evidence for the dependence of IFNγ-induced EGFR transactivation on the EGFR expression level in epithelial cells (Gonchar et al., 2008). This study examines an antiproliferative effect of IFNγ on human epithelial cell lines—A431 and HeLa that express high levels of EGFR, as well as HEK293 that expresses low levels of EGFR. To characterize the IFNγ-induced changes in these cells, we studied cell growth, the cell cycle, and induction of apoptosis. The response to IFNγ differed in the compared cell lines; cell growth was inhibited in both A431 and HeLa cells, but not in HEK293 cells, as was shown by the cell count and MTT. The cell-cycle phases analyzed by flow cytometry were disturbed in A431 and HeLa cells in response to IFNγ. On the contrary, in HEK293 cells, the IFNγ treatment did not alter distribution by cell cycle phases. Our results indicate that IFNγ produces an antiproliferative effect that depends on the increased expression of EGFR in A431 and HeLa cells. Furthermore, it was demonstrated that IFNγ induced the caspase 3 activation in A431 cells, which suggests the involvement of active caspase 3 in the IFNγ-induced apoptosis.  相似文献   
132.
133.
134.
The effect of gold nanoparticles on mouse epididymal sperm has been studied using the model system of nuclear chromatin decondensation in vitro. It is shown that the treatment of gametes, preliminary membrane-freed by sodium dodecyl sulfate, in the mediums containing gold nanoparticles (with diameter ∼2.5 nm) in concentrations 1.0 × 1015 or 0.5 × 1015 particles/ml and following incubation in dithiothreitol solution (DTT) resulted in failure of chromatin decondensation process and nucleus structure. We conclude that gold nanoparticles possess spermatotoxicity. The mechanism of cytotoxic effect of gold nanoparticles may be related with their interaction with molecules of double-helix DNA. The model system studied in this research is applicable for further investigations of cytotoxic effects of nanoparticles of different origin and made of different metals.  相似文献   
135.
136.
137.
138.
139.
140.
Mice were fed a diet containing 1.5% cholesterol, and the total cholesterol balance and the distribution of the consumed sterol among excreta, liver, and carcass were determined, using experimental periods of 9–14 days. It was observed that an average of approximately 12% of the cholesterol was either destroyed or chemically modified. When, however, 1% sulfasuxidine and 0.04% streptomycin were added to the diet, all the sterol “put in” was recovered, within the limits of error of the method. These results were tentatively interpreted to indicate that under the conditions of these experiments, microorganisms of the intestine were primarily responsible for the destruction or modification of the consumed sterol, as observed in the absence of antibacterial drugs.  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