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   185342篇
  免费   14742篇
  国内免费   53篇
  2018年   1994篇
  2017年   1943篇
  2016年   2485篇
  2015年   2340篇
  2014年   3164篇
  2013年   4637篇
  2012年   5104篇
  2011年   5583篇
  2010年   3998篇
  2009年   3525篇
  2008年   4968篇
  2007年   5184篇
  2006年   4923篇
  2005年   4576篇
  2004年   4732篇
  2003年   4637篇
  2002年   4607篇
  2001年   8444篇
  2000年   8634篇
  1999年   6366篇
  1998年   2049篇
  1997年   2064篇
  1996年   1848篇
  1993年   1730篇
  1992年   5229篇
  1991年   5399篇
  1990年   5157篇
  1989年   5142篇
  1988年   4756篇
  1987年   4509篇
  1986年   4091篇
  1985年   4253篇
  1984年   3440篇
  1983年   2936篇
  1982年   1957篇
  1981年   1756篇
  1980年   1751篇
  1979年   3232篇
  1978年   2570篇
  1977年   2298篇
  1976年   2102篇
  1975年   2569篇
  1974年   2916篇
  1973年   2837篇
  1972年   2680篇
  1971年   2442篇
  1970年   2129篇
  1969年   2045篇
  1968年   1932篇
  1967年   1763篇
排序方式: 共有10000条查询结果,搜索用时 453 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