全文获取类型
收费全文 | 14586篇 |
免费 | 39篇 |
国内免费 | 59篇 |
专业分类
系统科学 | 60篇 |
丛书文集 | 96篇 |
教育与普及 | 31篇 |
理论与方法论 | 53篇 |
现状及发展 | 6488篇 |
研究方法 | 703篇 |
综合类 | 7088篇 |
自然研究 | 165篇 |
出版年
2013年 | 117篇 |
2012年 | 251篇 |
2011年 | 404篇 |
2010年 | 122篇 |
2008年 | 280篇 |
2007年 | 311篇 |
2006年 | 290篇 |
2005年 | 323篇 |
2004年 | 316篇 |
2003年 | 273篇 |
2002年 | 261篇 |
2001年 | 449篇 |
2000年 | 436篇 |
1999年 | 319篇 |
1994年 | 306篇 |
1992年 | 267篇 |
1991年 | 199篇 |
1990年 | 238篇 |
1989年 | 223篇 |
1988年 | 236篇 |
1987年 | 231篇 |
1986年 | 185篇 |
1985年 | 292篇 |
1984年 | 204篇 |
1983年 | 171篇 |
1982年 | 193篇 |
1981年 | 163篇 |
1980年 | 212篇 |
1979年 | 446篇 |
1978年 | 321篇 |
1977年 | 331篇 |
1976年 | 289篇 |
1975年 | 325篇 |
1974年 | 342篇 |
1973年 | 364篇 |
1972年 | 402篇 |
1971年 | 415篇 |
1970年 | 483篇 |
1969年 | 412篇 |
1968年 | 436篇 |
1967年 | 409篇 |
1966年 | 362篇 |
1965年 | 240篇 |
1959年 | 118篇 |
1958年 | 220篇 |
1957年 | 159篇 |
1956年 | 140篇 |
1955年 | 124篇 |
1954年 | 92篇 |
1948年 | 97篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
21.
22.
The development and maturation of an oligodendroglial cell is comprised of three intimately related processes that include proliferation, differentiation, and myelination. Here we review how proliferation and differentiation are controlled by distinct molecular mechanisms and discuss whether differentiation is merely a default of inhibited proliferation. We then address whether differentiation and myelination can be uncoupled in a similar manner. This task is particularly challenging because an oligodendrocyte cannot myelinate without first differentiating, and these processes are therefore not mutually exclusive. Is it solely the presence of the axon that distinguishes a differentiated oligodendrocyte from a myelinating one? Uncoupling these two processes requires identifying specific signals that regulate myelination without affecting the differentiation process. We will review current understanding of the relationship between differentiation and myelination and discuss whether these two processes can truly be uncoupled. 相似文献
23.
24.
Although theoretical studies show that overcompensatory density-dependent mechanisms can potentially generate regular or chaotic fluctuations in animal numbers, the majority of realistic single-species models of invertebrate populations are not overcompensatory enough to cause sustained population cycles. The possibility that overcompensation may generate cycles or chaos in vertebrate populations has seldom been considered. Here we show that highly overcompensatng density-dependent mortality can generate recurrent population crashes consistent with those observed in a naturally limited population of Soay sheep. The observed interval of three or more years between crashes points to sharp 'focusing' of mortality over a narrow range of population density. 相似文献
25.
Shiga toxin and some other protein toxins that act on targets in the cytosol have previously been shown to enter the trans-Golgi network. Transport by this route may be necessary for translocation of the toxin to the cytosol and for intoxication, but it is not known whether the enzymatically active part of the toxins actually enters the cytosol from the trans-Golgi network. It has been suggested that such toxins are transported in a retrograde manner to the endoplasmic reticulum and that translocation occurs in this organelle, but retrograde transport of endocytosed material beyond the trans-Golgi network has never been demonstrated. Here we show that in butyric acid-treated A431 cells endocytosed Shiga toxin is not only transported to the trans-Golgi network, but also to all Golgi stacks, to the endoplasmic reticulum and to the nuclear envelope. Furthermore, butyric acid sensitizes the cells to Shiga toxin, which is consistent with the possibility that retrograde transport is required for translocation of the toxin to the cytosol. 相似文献
26.
27.
Edouard T Montagner A Dance M Conte F Yart A Parfait B Tauber M Salles JP Raynal P 《Cellular and molecular life sciences : CMLS》2007,64(13):1585-1590
Activating and inactivating mutations of SHP-2 are responsible, respectively, for the Noonan (NS) and the LEOPARD (LS) syndromes.
Clinically, these developmental disorders overlap greatly, resulting in the apparent paradox of similar diseases caused by
mutations that oppositely influence SHP-2 phosphatase activity. While the mechanisms remain unclear, recent functional analysis
of SHP-2, along with the identification of other genes involved in NS and in other related syndromes (neurofibromatosis-1,
Costello and cardio-facio-cutaneous syndromes), strongly suggest that Ras/MAPK represents the major signaling pathway deregulated
by SHP-2 mutants. We discuss the idea that, with the exception of LS mutations that have been shown to exert a dominant negative
effect, all disease-causing mutations involved in Ras/MAPK-mediated signaling, including SHP-2, might lead to enhanced MAPK
activation. This suggests that a narrow range of MAPK signaling is required for appropriate development. We also discuss the
possibility that LS mutations may not simply exhibit dominant negative activity.
Received 30 November 2006; received after revision 8 February 2007; accepted 13 March 2007 相似文献
28.
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
29.
Gösta Lindeberg 《Cellular and molecular life sciences : CMLS》1948,4(12):476-477
Zusammenfassung Es wurde die Zugkraft nasser Flachsfasern nach Behandlung mit verschiedenen Chemikalien geprüft. Es wurde gefunden, daß die Mittellamelle der Flachsfaser verschiedene miteinander verbundene Systeme enthält, nämlich Pektin, Lignin und eine im Oxalat unlös iche alkaliempfindliche Komponente. 相似文献
30.