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   531827篇
  免费   61484篇
  国内免费   433篇
  593744篇
  2016年   5539篇
  2015年   7978篇
  2014年   9181篇
  2013年   13541篇
  2012年   14898篇
  2011年   15065篇
  2010年   10164篇
  2009年   9451篇
  2008年   13659篇
  2007年   13932篇
  2006年   13272篇
  2005年   13034篇
  2004年   12737篇
  2003年   12616篇
  2002年   12161篇
  2001年   21151篇
  2000年   21294篇
  1999年   17281篇
  1998年   6557篇
  1997年   6879篇
  1996年   6793篇
  1995年   6182篇
  1994年   6171篇
  1993年   6149篇
  1992年   14882篇
  1991年   14655篇
  1990年   14162篇
  1989年   14107篇
  1988年   13058篇
  1987年   12809篇
  1986年   11800篇
  1985年   12089篇
  1984年   10098篇
  1983年   8839篇
  1982年   7010篇
  1981年   6637篇
  1980年   6124篇
  1979年   10148篇
  1978年   7922篇
  1977年   7658篇
  1976年   7180篇
  1975年   7864篇
  1974年   8611篇
  1973年   8457篇
  1972年   7776篇
  1971年   7153篇
  1970年   6347篇
  1969年   6275篇
  1968年   5708篇
  1967年   4885篇
排序方式: 共有10000条查询结果,搜索用时 0 毫秒
991.
Sporadic (less than regular weekly) coital activity is associated with a particular type of infertility—the short hyperthermic (luteal) phase. This preliminary report is the first suggestion that a reduced frequency of human sexual activity might, itself, be associated with subfertile reproductive function.  相似文献   
992.
993.
994.
995.
The interferon inducing effect of hyperthermia was studied in normal and tumor-bearing mice. Circulating interferon was temporarily detected one day after subcutaneous transplantation of 1.6 X 10(6) Ehrlich's ascites tumor cells. Hyperthermia of 43.5 degrees C for 5 min did not induce the interferon formation in mice with or without subcutaneous tumor of the cells. These findings showed that the induction of interferon formation was not main cause of the hyperthermia-induced tumor inhibition.  相似文献   
996.
The final steps in the synthesis of acetyl-CoA by CO dehydrogenase (CODH) have been studied by following the exchange reaction between CoA and the CoA moiety of acetyl-CoA. This reaction had been studied earlier (Pezacka, E., and Wood, H. G. (1986) J. Biol. Chem. 261, 1609-1615 and Ramer, W. E., Raybuck, S. A., Orme-Johnson, W. H., and Walsh, C. T. (1989) Biochemistry 28, 4675-4680). The CoA/acetyl-CoA exchange activity was determined at various controlled redox potentials and was found to be activated by a one-electron reduction with half-maximum activity occurring at -486 mV. There is approximately 2000-fold stimulation of the exchange by performing the reaction at -575 mV relative to the rate at -80 mV. Binding of CoA to CODH is not sensitive to the redox potential; therefore, the reductive activation affects some step other than association/dissociation of CoA. We propose that a metal center on CODH with a midpoint reduction potential of less than or equal to -486 mV is activated by a one-electron reduction to cleave the carbonyl-sulfur bond and/or bind the acetyl group of acetyl-CoA. Based on a comparison of the redox dependence of this reaction with that for methylation of CODH (Lu, W-P., Harder, S. R., and Ragsdale, S. W. (1990) J. Biol. Chem. 265, 3124-3133) and CO2 reduction and formation of the Ni-Fe-C EPR signal (Lindahl, P. A., Münck, E., and Ragsdale, S. W. (1990) J. Biol. Chem. 265, 3873-3879), we propose that the assembly of the acetyl group of acetyl-CoA, i.e. binding the methyl group of the methylated corrinoid/iron-sulfur protein, binding CO, and methyl migration to form the acetyl-CODH intermediate, occur at the novel Ni-Fe3-4-containing site in CODH. CO has two effects on the CoA/acetyl-CoA exchange: it activates the reaction due to its reductive capacity and its acts as a noncompetitive inhibitor. We also discovered that the CoA/acetyl-CoA exchange was inhibited by nitrous oxide via an oxidative mechanism. In the presence of a low-potential electron donor, CODH becomes a nitrous oxide reductase which catalytically converts N2O to N2. This study combined with earlier results (Lu, W-P., Harder, S. R., and Ragsdale, S. W. (1990) J. Biol. Chem. 265, 3124-3133) establishes that the two-subunit form of CODH is completely active in all reactions known to be catalyzed by CODH.  相似文献   
997.
The ventral sebaceous gland of the Djungarian hamster is a macroscopically visible organ situated in the midventral area of the abdominal wall. It consists of densely packed acini arranged in lobules with common excretory ducts. The rich vascular network of the gland is characterized by fenestrated capillaries. Fenestrated endothelium has not yet been reported as a characteristic and regular finding within sebaceous glands. Results are discussed with regard to proliferation rate of sebocytes and the demand of fluid and nutrient supply.  相似文献   
998.
F Osman  C Cotton  B Tomsett  P Strike 《Biochimie》1991,73(2-3):321-327
A mutant of Aspergillus nidulans, designated nuv11, has been isolated as hypersensitive to the monofunctional alkylating agent MNNG and the quasi-UV-mimetic mutagen 4-NQO. The mutation was recessive, resulting from mutation of a single gene which mapped to chromosome IV, and was non-allelic to the previously characterised repair-deficient mutations uvsB and uvsH which are also located on this linkage group. The nuv11 mutation results in slow growth, deficient intragenic and intergenic meiotic recombination, increased spontaneous chromosome instability, and increased intragenic and intergenic mitotic recombination in homozygous diploids. By screening a wild-type gene bank of A nidulans, a clone (pNUV11A40) has been isolated which complements the nuv11 mutation, restoring wild-type responses to both MNNG and 4-NQO.  相似文献   
999.
We report the first resolution of both the conformational distribution and end-to-end diffusion coefficient of a flexible molecule. This molecular information was recovered using only the donor intensity decay in a single solvent at a single viscosity, as observed by the technique of frequency-domain fluorometry. This technique can be extended to measurements of structural fluctuations of biological macromolecules.  相似文献   
1000.
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