全文获取类型
收费全文 | 7162篇 |
免费 | 29篇 |
国内免费 | 68篇 |
专业分类
系统科学 | 82篇 |
丛书文集 | 73篇 |
教育与普及 | 7篇 |
理论与方法论 | 64篇 |
现状及发展 | 3427篇 |
研究方法 | 416篇 |
综合类 | 3078篇 |
自然研究 | 112篇 |
出版年
2017年 | 55篇 |
2016年 | 52篇 |
2013年 | 58篇 |
2012年 | 137篇 |
2011年 | 235篇 |
2010年 | 53篇 |
2008年 | 153篇 |
2007年 | 178篇 |
2006年 | 175篇 |
2005年 | 152篇 |
2004年 | 162篇 |
2003年 | 180篇 |
2002年 | 237篇 |
2001年 | 290篇 |
2000年 | 264篇 |
1999年 | 166篇 |
1992年 | 115篇 |
1991年 | 76篇 |
1990年 | 88篇 |
1989年 | 76篇 |
1988年 | 71篇 |
1987年 | 94篇 |
1986年 | 90篇 |
1985年 | 148篇 |
1984年 | 97篇 |
1983年 | 84篇 |
1982年 | 72篇 |
1981年 | 75篇 |
1980年 | 92篇 |
1979年 | 165篇 |
1978年 | 157篇 |
1977年 | 166篇 |
1976年 | 150篇 |
1975年 | 170篇 |
1974年 | 171篇 |
1973年 | 140篇 |
1972年 | 144篇 |
1971年 | 191篇 |
1970年 | 257篇 |
1969年 | 181篇 |
1968年 | 160篇 |
1967年 | 191篇 |
1966年 | 154篇 |
1965年 | 102篇 |
1964年 | 52篇 |
1959年 | 69篇 |
1958年 | 91篇 |
1957年 | 87篇 |
1956年 | 55篇 |
1954年 | 61篇 |
排序方式: 共有7259条查询结果,搜索用时 0 毫秒
31.
D. V. Amin R. B. Doctor A. O. Girdhar U. H. Shah 《Cellular and molecular life sciences : CMLS》1980,36(12):1410-1411
Summary Prostaglandin (PG) release was measured from the isolated perfused rabbit heart. The effects of -adrenergic stimulation and blockade suggest that PG synthesis is regulated in part by adrenergic mechanisms. 相似文献
32.
Incorporation of 32P into adrenal mitochondrial phospholipids (PL) incrased in ACTH-treated rats, but it decreased in diabetics, inspite of the fact that these animals showed adrenal overacity. Since diabetics did not show increased 11 beta-hydroxylation. as opposed to ACTH-treated rats, it is suggested that the stimulation of this enzyme activity by exogenous ACTH is related to an increased turnover of PL at the mitochondrial membrane. The process is impaired in diabetics and prevents the stimulation of 11 beta-hydroxylation. 相似文献
33.
R. K. Raina D. Njoroge J. N. Ng'ang'a B. V. Telang 《Cellular and molecular life sciences : CMLS》1977,33(11):1499-1500
Summary
Naja mossambica pallida venom administered i.v. (300 /kg) produces an initial brief fall in blood pressure, due to a direct myocardial depressant effect, and a sustained fall due to central depressant effect.This study was supported by University of Nairobi research grants (670–376). We also thank Mr E. Njogu for photographic assistance. 相似文献
34.
J. J. Cazzulo Berta M. Franke de Cazzulo 《Cellular and molecular life sciences : CMLS》1982,38(11):1335-1337
Summary Cell-free extracts ofTrypanosoma cruzi contain proteolytic activity able to degrade endogenous substrates. The activity was maximal at pH 3 to 4, had an optimal temperature of 65°C, and was strongly inhibited by N--p-tosyl-L-lysine chloromethyl ketone.This investigation received financial support from the UNDP/World Bank/WHO Special Programme for Research and Training in Tropical Diseases, the Fundación Julio Cherny, and the Ministerio de Salud Pública y Medio Ambiente de la República Argentina. The authors gratefully acknowledge the technical assistance of Mr Esteban Bontempi. 相似文献
35.
Summary The biochemical changes in the hemolymph and tissues were followed during regeneration of the optic tentacles of the snailCryptozona ligulata (Pulmonata-Stylommatophora). There is a remarkable increase in total carbohydrates in hemolymph and tissues and glycogen in tissues at the expense of free amino acids and fatty acids. It is clear that ablation of the optic tentacles stimulates carbohydrate synthesis through glyconeogenic routes. The optic tentacles regenerate completely in 18–21 days. 相似文献
36.
K. Mašek M. Zaoral J. Ježek V. Krchňák 《Cellular and molecular life sciences : CMLS》1979,35(10):1397-1398
Summary The immunoadjuvant activity of muramyl dipeptide seems to be critically dependent on the type of substitution of the -carboxyl group of the D-isoglutamine residue. Moreover the nonapeptide L-Ala-D-isoGlu-L-Lys-D-Ala-(Gly)5-OME also shows a definite effect. 相似文献
37.
38.
Minimum information about a microarray experiment (MIAME)-toward standards for microarray data. 总被引:36,自引:0,他引:36
A Brazma P Hingamp J Quackenbush G Sherlock P Spellman C Stoeckert J Aach W Ansorge C A Ball H C Causton T Gaasterland P Glenisson F C Holstege I F Kim V Markowitz J C Matese H Parkinson A Robinson U Sarkans S Schulze-Kremer J Stewart R Taylor J Vilo M Vingron 《Nature genetics》2001,29(4):365-371
Microarray analysis has become a widely used tool for the generation of gene expression data on a genomic scale. Although many significant results have been derived from microarray studies, one limitation has been the lack of standards for presenting and exchanging such data. Here we present a proposal, the Minimum Information About a Microarray Experiment (MIAME), that describes the minimum information required to ensure that microarray data can be easily interpreted and that results derived from its analysis can be independently verified. The ultimate goal of this work is to establish a standard for recording and reporting microarray-based gene expression data, which will in turn facilitate the establishment of databases and public repositories and enable the development of data analysis tools. With respect to MIAME, we concentrate on defining the content and structure of the necessary information rather than the technical format for capturing it. 相似文献
39.
40.
Mutations in the gene encoding the basal body protein RPGRIP1L, a nephrocystin-4 interactor, cause Joubert syndrome 总被引:7,自引:0,他引:7
Arts HH Doherty D van Beersum SE Parisi MA Letteboer SJ Gorden NT Peters TA Märker T Voesenek K Kartono A Ozyurek H Farin FM Kroes HY Wolfrum U Brunner HG Cremers FP Glass IA Knoers NV Roepman R 《Nature genetics》2007,39(7):882-888
Protein-protein interaction analyses have uncovered a ciliary and basal body protein network that, when disrupted, can result in nephronophthisis (NPHP), Leber congenital amaurosis, Senior-L?ken syndrome (SLSN) or Joubert syndrome (JBTS). However, details of the molecular mechanisms underlying these disorders remain poorly understood. RPGRIP1-like protein (RPGRIP1L) is a homolog of RPGRIP1 (RPGR-interacting protein 1), a ciliary protein defective in Leber congenital amaurosis. We show that RPGRIP1L interacts with nephrocystin-4 and that mutations in the gene encoding nephrocystin-4 (NPHP4) that are known to cause SLSN disrupt this interaction. RPGRIP1L is ubiquitously expressed, and its protein product localizes to basal bodies. Therefore, we analyzed RPGRIP1L as a candidate gene for JBTS and identified loss-of-function mutations in three families with typical JBTS, including the characteristic mid-hindbrain malformation. This work identifies RPGRIP1L as a gene responsible for JBTS and establishes a central role for cilia and basal bodies in the pathophysiology of this disorder. 相似文献