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   40030篇
  免费   78篇
  国内免费   97篇
系统科学   237篇
丛书文集   862篇
教育与普及   107篇
理论与方法论   285篇
现状及发展   18089篇
研究方法   1652篇
综合类   18431篇
自然研究   542篇
  2013年   285篇
  2012年   580篇
  2011年   1137篇
  2010年   273篇
  2008年   713篇
  2007年   725篇
  2006年   766篇
  2005年   775篇
  2004年   692篇
  2003年   720篇
  2002年   744篇
  2001年   1128篇
  2000年   1040篇
  1999年   702篇
  1992年   667篇
  1991年   556篇
  1990年   582篇
  1989年   586篇
  1988年   590篇
  1987年   601篇
  1986年   600篇
  1985年   755篇
  1984年   580篇
  1983年   494篇
  1982年   425篇
  1981年   415篇
  1980年   555篇
  1979年   1243篇
  1978年   1063篇
  1977年   1062篇
  1976年   731篇
  1975年   791篇
  1974年   1188篇
  1973年   1011篇
  1972年   1057篇
  1971年   1255篇
  1970年   1650篇
  1969年   1273篇
  1968年   1247篇
  1967年   1286篇
  1966年   1064篇
  1965年   780篇
  1964年   221篇
  1959年   449篇
  1958年   692篇
  1957年   580篇
  1956年   488篇
  1955年   419篇
  1954年   464篇
  1948年   287篇
排序方式: 共有10000条查询结果,搜索用时 31 毫秒
1.
2.
Archive for History of Exact Sciences - We show that Dedekind, in his proof of the principle of definition by mathematical recursion, used implicitly both the concept of an inductive cone from an...  相似文献   
3.
4.
G protein-coupled receptor (GPCR) signalling is mediated through transactivation-independent signalling pathways or the transactivation of protein tyrosine kinase receptors and the recently reported activation of the serine/threonine kinase receptors, most notably the transforming growth factor-β receptor family. Since the original observation of GPCR transactivation of protein tyrosine kinase receptors, there has been considerable work on the mechanism of transactivation and several pathways are prominent. These pathways include the “triple membrane bypass” pathway and the generation of reactive oxygen species. The recent recognition of GPCR transactivation of serine/threonine kinase receptors enormously broadens the GPCR signalling paradigm. It may be predicted that the transactivation of serine/threonine kinase receptors would have mechanistic similarities with transactivation of tyrosine kinase pathways; however, initial studies suggest that these two transactivation pathways are mechanistically distinct. Important questions are the relative importance of tyrosine and serine/threonine transactivation pathways, the contribution of transactivation to overall GPCR signalling, mechanisms of transactivation and the range of cell types in which this phenomenon occurs. The ultimate significance of transactivation-dependent signalling remains to be defined but it appears to be prominent and if so will represent a new cell signalling frontier.  相似文献   
5.
6.
Summary A study was undertaken on the variations of the redox potential level produced by streptomycinin vitro andin vivo. We have been able to show that, owing to an oxidative effect, streptomycin produces an increase of the redox potential level. This oxidative effect varies in degree according to the condition of the patient.We also found that in the blood and in the spinal fluid of patients suffering from tubercular meningitis factors are present which inhibit the action of streptomycin.The results of our findings lead to the conclusion that the dose of streptomycin must be varied according to the condition of the patient if the constant level required for an efficient therapy is to be maintained in the blood and in the spinal fluid.  相似文献   
7.
8.
9.
Summary By condensing 2:4:5-triamino-6-hydroxy-pyrimidine with dihydroxyacetone (diacetate), diaminoacetone or acetone-1,3-di (p-formylaminobenzoic acid) not the expected 8- or 9-oxymethyl resp. -aminomethyl-pteridines but 8-or 9-methyl-pteridines were obtained. With p-tolyl-d-isoglucosamine not a tetrahydroxybutyl-pteridine but a trihydroxybutyl-pteridine was formed. For an explanation of these results it is supposed that from the dihydro-pteridines formed at first by intramolecular splitting off of H2O or R·NH2 aromatization takes place.  相似文献   
10.
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