全文获取类型
收费全文 | 55426篇 |
免费 | 249篇 |
国内免费 | 563篇 |
专业分类
系统科学 | 1252篇 |
丛书文集 | 251篇 |
教育与普及 | 291篇 |
理论与方法论 | 536篇 |
现状及发展 | 31536篇 |
研究方法 | 906篇 |
综合类 | 19273篇 |
自然研究 | 2193篇 |
出版年
2013年 | 827篇 |
2012年 | 682篇 |
2011年 | 2730篇 |
2009年 | 622篇 |
2008年 | 899篇 |
2007年 | 967篇 |
2006年 | 1067篇 |
2005年 | 1267篇 |
2004年 | 2379篇 |
2003年 | 1959篇 |
2002年 | 1591篇 |
2001年 | 1316篇 |
2000年 | 837篇 |
1999年 | 945篇 |
1998年 | 651篇 |
1997年 | 780篇 |
1996年 | 517篇 |
1994年 | 684篇 |
1993年 | 701篇 |
1992年 | 874篇 |
1991年 | 742篇 |
1990年 | 819篇 |
1989年 | 645篇 |
1988年 | 623篇 |
1987年 | 613篇 |
1986年 | 679篇 |
1985年 | 853篇 |
1984年 | 754篇 |
1983年 | 634篇 |
1982年 | 783篇 |
1981年 | 813篇 |
1980年 | 893篇 |
1979年 | 1327篇 |
1978年 | 1203篇 |
1977年 | 1202篇 |
1976年 | 1086篇 |
1975年 | 1073篇 |
1974年 | 917篇 |
1973年 | 1173篇 |
1972年 | 1251篇 |
1971年 | 1258篇 |
1970年 | 1348篇 |
1969年 | 1248篇 |
1968年 | 1203篇 |
1967年 | 1063篇 |
1966年 | 890篇 |
1965年 | 722篇 |
1964年 | 482篇 |
1958年 | 562篇 |
1957年 | 473篇 |
排序方式: 共有10000条查询结果,搜索用时 312 毫秒
91.
Studies of intracellular traffic in yeast and mammalian systems have implicated members of the Rab family of small GTP-binding proteins as regulators of membrane fusion. We have used the patch clamp technique to measure exocytotic fusion events directly and investigate the role of GTP-binding proteins in regulating exocytosis in mast cells. Intracellular perfusion of mast cells with GTP-gamma S is sufficient to trigger complete exocytotic degranulation in the absence of other intracellular messengers. Here we show that GTP is a potent inhibitor of GTP-gamma S-induced degranulation, indicating that sustained activation of a GTP-binding protein is sufficient for membrane fusion. We have found that synthetic oligopeptides, corresponding to part of the effector domain of Rab3a, stimulate complete exocytotic degranulation, similar to that induced by GTP-gamma S. The response is selective for Rab3a sequence and is strictly dependent on Mg2+ and ATP. This suggests that sustained activation of a Rab3 protein causes exocytotic fusion. The peptide response can be accelerated by GDP-beta S, suggesting that Rab3a peptides compete with endogenous Rab3 proteins for a binding site on a target effector protein, which causes fusion on activation. 相似文献
92.
93.
通过对“洋务运动博物馆”东立面形象的反思 ,讨论了建筑形态设计中隐喻手法的运用 ;就此引申 ,探讨传统问题 ,指出正确理解传统与创新的四个方面。 相似文献
94.
R. Poggioli A. V. Vergoni A. Bertolini 《Cellular and molecular life sciences : CMLS》1985,41(2):265-266
Summary Hydrochlorothiazide, acutely injected in rats, has a weak analgesic activity per se and potentiates and prolongs the antinociceptive effect of morphine.This work was supported in part by grants from Consiglio Nazionale delle Ricerche, and by Ministero della Pubblica Istruzione, Roma. 相似文献
95.
Crnković-Mertens I Wagener N Semzow J Gröne EF Haferkamp A Hohenfellner M Butz K Hoppe-Seyler F 《Cellular and molecular life sciences : CMLS》2007,64(9):1137-1144
Cancer cells are typically characterized by apoptosis deficiency. In order to investigate a possible role for the anti-apoptotic
livin gene in renal cell cancer (RCC), we analyzed its expression in tumor tissue samples and in RCC-derived cell lines. In addition,
we studied the contribution of livin to the apoptotic resistance of RCC cells by RNA interference (RNAi). Livin gene expression was detected in a significant portion of RCC tumor tissue specimens (13/14, 92.9%) and tumor-derived cell
lines (12/15, 80.0%). Moreover, targeted inhibition of livin by RNAi markedly sensitized RCC cells towards proapoptotic stimuli, such as UV irradiation or the chemotherapeutic drugs
etoposide, 5-fluorouracil, and vinblastine. These effects were specific for livin expressing tumor cells. We conclude that livin can contribute significantly to the apoptosis resistance of RCC cells. Targeted inhibition of livin could represent a novel therapeutic strategy to increase the sensitivity of renal cancers towards pro-apoptotic agents.
Received 30 November 2006; received after revision 22 February 2007; accepted 20 March 2007 相似文献
96.
97.
98.
Summary Traces of nor-adrenaline restore the vascular action of adrenaline altered in epinephrectomized dogs to the reaction of the normal animal. Therefore it is claimed that the adrenals discharge one or several substances into the blood stream, which are necessary for the usual peripheral vascular action of adrenaline. Further investigations are in progress. 相似文献
99.
David H. Hubel 《自然科学进展(英文版)》2007,17(13):1-3
The visual field is topographically mapped onto the primary visual cortex (V1), forming a retinotopic map which is far more detailed for the foveal regions than for the periphery. We found that receptive field (RF) size in monkey V1 increases with eccentricity, and that a 1—2 m2 V1 region contains roughly a complete set of machinery necessary to analyze a visual-field area whose size is about that of the RFs of the cells. This allows V1 to be anatomically uniform, and is in sharp contrast with the retina. 相似文献
100.
Rogaeva E Meng Y Lee JH Gu Y Kawarai T Zou F Katayama T Baldwin CT Cheng R Hasegawa H Chen F Shibata N Lunetta KL Pardossi-Piquard R Bohm C Wakutani Y Cupples LA Cuenco KT Green RC Pinessi L Rainero I Sorbi S Bruni A Duara R Friedland RP Inzelberg R Hampe W Bujo H Song YQ Andersen OM Willnow TE Graff-Radford N Petersen RC Dickson D Der SD Fraser PE Schmitt-Ulms G Younkin S Mayeux R Farrer LA St George-Hyslop P 《Nature genetics》2007,39(2):168-177
The recycling of the amyloid precursor protein (APP) from the cell surface via the endocytic pathways plays a key role in the generation of amyloid beta peptide (Abeta) in Alzheimer disease. We report here that inherited variants in the SORL1 neuronal sorting receptor are associated with late-onset Alzheimer disease. These variants, which occur in at least two different clusters of intronic sequences within the SORL1 gene (also known as LR11 or SORLA) may regulate tissue-specific expression of SORL1. We also show that SORL1 directs trafficking of APP into recycling pathways and that when SORL1 is underexpressed, APP is sorted into Abeta-generating compartments. These data suggest that inherited or acquired changes in SORL1 expression or function are mechanistically involved in causing Alzheimer disease. 相似文献