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   416447篇
  免费   53184篇
  国内免费   198篇
  469829篇
  2018年   3556篇
  2016年   4626篇
  2015年   6599篇
  2014年   7617篇
  2013年   11022篇
  2012年   12244篇
  2011年   12586篇
  2010年   8454篇
  2009年   7878篇
  2008年   11109篇
  2007年   11471篇
  2006年   10665篇
  2005年   10286篇
  2004年   9936篇
  2003年   9914篇
  2002年   9535篇
  2001年   19728篇
  2000年   19935篇
  1999年   15734篇
  1998年   5477篇
  1997年   6038篇
  1996年   5741篇
  1995年   5362篇
  1994年   5255篇
  1993年   5383篇
  1992年   13353篇
  1991年   13181篇
  1990年   12564篇
  1989年   12366篇
  1988年   11279篇
  1987年   10925篇
  1986年   10209篇
  1985年   10159篇
  1984年   8502篇
  1983年   7339篇
  1982年   5642篇
  1981年   5023篇
  1980年   4845篇
  1979年   7997篇
  1978年   6397篇
  1977年   5822篇
  1976年   5488篇
  1975年   6028篇
  1974年   6220篇
  1973年   6150篇
  1972年   5551篇
  1971年   5106篇
  1970年   4258篇
  1969年   4101篇
  1968年   3674篇
排序方式: 共有10000条查询结果,搜索用时 0 毫秒
991.
26 male F2 hybrids between spontaneously hypertensive (SHR) and normotensive control (WKY) rats (SHRxWKY)F2 were segregated according to their c-src genotype into SS and WW homozygous groups, corresponding to SHR or WKY and WS heterozygous group. Na, K cotransport in erythrocytes in the WW group was equal to that of WKY and differs significantly from that of WS and SS groups (the rate of Na, K cotransport in latter groups was close to that of SHR). Ca content of RBC in WW group was equal to that of WKY, lower than that of WS and SS groups which in turn was significantly lower than in SHR, indicating polygenic control of the trait. Authors conclude that the c-src locus itself or some other loci inherited in conjunction with c-src determines both the increase of Na, K cotransport and calcium content in erythrocytes of SHR.  相似文献   
992.
This work presents the data on the complex evaluation of the population of group A streptococci, studied at each of four phases (reservation, epidemic transformation, epidemic spread, reservational transformation) of the course of the epidemic process of streptococcal infection of the respiratory tracts (tonsillitis) in an organized group of adults. The characterization of the phases of the infective agent in accordance with the level of the carrier state, the size of streptococcal foci and the virulence of streptococci is given. Thus, the study shows that the heterogeneity of group A streptococci with respect to their virulence reaches its maximum level at the phases of reservation and epidemic spread and its minimum level at the phases of epidemic and reservational transformation. The size of streptococcal foci in carriers and the virulence of streptococci isolated from them are the inter-related unidirectional signs of the population of the infective agent and, at the same time, the main factors responsible for the phase character of the epidemic process and the morbidity level in tonsillitis.  相似文献   
993.
994.
The use of a mixture model in the analysis of count data   总被引:1,自引:0,他引:1  
V T Farewell  D A Sprott 《Biometrics》1988,44(4):1191-1194
A mixture model is presented for the analysis of data on premature ventricular contractions. The analysis is shown to be straightforward and the conclusions relatively simple.  相似文献   
995.
996.
Structural analysis of human profilin has revealed two tryptophan residues, W3 and W31, which interact with polyproline. The codons for these residues were mutated to encode phenylalanine and the mutant proteins overexpressed in Eschericia coli. The isolated proteins were diminished in their ability to bind polyproline, whereas phosphatidylinositol 4,5-bisphosphate (PIP2) binding remained unchanged. In many strains of Saccharomyces cerevisiae, disruption of the gene encoding profilin, PFY1, is lethal. It was found that expression of the gene for human profilin is capable of suppressing this lethality. The polyproline-binding mutant alleles of the human gene were cloned into various yeast expression vectors. Each of the mutant genes resulted in suppression of the lethality of pfy1Delta. It was observed that the mutant protein expression levels paralleled the growth rates of the strains. The severity of various morphological abnormalities of the strains was also attenuated with increased protein levels, suggesting that profilin polyproline-binding mutations are deleterious to cell growth unless overexpressed. Both tryptophan mutations were combined to give a third mutant allele that was found both unable to bind polyproline and to suppress the lethality of a pfy1 deletion. Immunoprecipitation experiments suggested that the mutants were unaltered in their affinity for actin and PIP2. These data strongly suggest that polyproline binding is an essential function of profilin.  相似文献   
997.
998.
999.
A tracer method is described that uses the stable isotope 30Si to measure rates of silicic acid uptake by diatom cultures and natural populations of marine phytoplankton. The method involves (i) incubation of organisms requiring silicic acid for growth in the presence of 30Si-labeled silicic acid, (ii) collection of the resulting particulate silicon, (iii) conversion of the particulate silicon to BaSiF6, (iv) determination of the 30Si content of BaSiF6 by solid sample mass spectrometry, and (v) calculation of the uptake rate from the 30Si enrichment of the particulate matter during the incubation. The maximum overall error in the uptake rate measurement is ±10%.  相似文献   
1000.
The uptake of L-glutamate into BHK21-C13 cells in culture has been studied. This amino acid appears to be transported via a relatively high affinity, low capacity, Na+-dependent transport system capable of the rapid accumulation of substrate amino acids. Kinetic studies of the inhibition of L-glutamate uptake has provided information as to the substrate and the molecular configuration required for transport via the glutamate transport system. This system exhibited marked substrate specificity and was only capable of transporting L-glutamate and aspartate and certain closely related acidic amino acid analogues.  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