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721.
对公路工程中钢筋混凝土盖板涵现行施工图中跨径和钢筋用量进行了分析,对跨径不统一问题进行了探讨. 相似文献
722.
沈尤佳 《贵州师范大学学报(社会科学版)》2012,(1):39-44
国有资产流失是改革时期理论界关注的热点。国资流失主要表现在地方政府与收购方自由谈判的产权交易中,完全架空了全民所有的性质。现有文献多数从资产定价、内部人控制、关联交易、无形资产未作评估等角度解释国有资产流失,本文则试图从国有资产实际控制权地方化的视角提供新的解释。2002年以前,"有控制权无所有权"的"责权利不对称"成为国资流失的制度原因,因为地方政府无资产能力也无法律责任承担国资的保值增值;2002年赋予地方政府"出资人所有权"的政策设计,尽管在理论上可以减少甚至消除"代理成本",然而,地方政府获得出资人所有权地位的法理基础不足,在地方政府承担多重身份的背景下,反而加速了地方政府对国有资产的变卖。 相似文献
723.
724.
Roth L Koncina E Satkauskas S Crémel G Aunis D Bagnard D 《Cellular and molecular life sciences : CMLS》2009,66(4):649-666
The semaphorin family is a large group of proteins controlling cell migration and axonal growth cone guidance. These proteins
are bi-functional signals capable of growth promotion or growth inhibition. Initially described in the nervous system, the
majority of studies related to semaphorins and semaphorin signalling are nowadays performed in model systems outside the nervous
system. Here, we provide an exhaustive review of the many faces of semaphorins both during developmental, regulatory and pathological
processes. Indeed, because of their crucial fundamental roles, the semaphorins and their receptors represent important targets
for the development of drugs directed at a variety of diseases.
Received 22 August 2008; received after revision 22 September 2008; accepted 24 September 2008
L. Roth, E. Koncina, S. Satkauskas: These authors contributed equally to this work. 相似文献
725.
R. George H.-L. Chan Z. Ahmed K. M. Suen C. N. Stevens J. A. Levitt K. Suhling J. Timms J. E. Ladbury 《Cellular and molecular life sciences : CMLS》2009,66(4):711-720
The three isoforms of the adaptor protein Shc play diverse roles in cell signalling. For example, the observation of p46 Shc
in the nuclei of hepatocellular carcinoma cells suggests a function quite distinct from the better characterised cytoplasmic
role. Ligands responsible for the transport of various Shc isoforms into organelles such as the nucleus have yet to be reported.
To identify such ligands a far western approach was used to determine the p52 Shc interactome. The Ran-GTPase nuclear transport
protein was identified and found to bind to p52 Shc in vitro with low micromolar affinity. Co-immunoprecipitation, pull down and fluorescence lifetime imaging microscopy experiments
in stable cells confirmed cellular interaction and nuclear localisation. The nuclear transport factor protein NTF2, which
functions in cohort with Ran, was shown to form a complex with both RAN and Shc, suggesting a mechanism for Shc entry into
the nucleus as part of a tertiary complex.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users.
Received 20 October 2008; received after revision 04 December 2008; accepted 15 December 2008 相似文献
726.
D. Parolini M. Meregalli M. Belicchi P. Razini R. Lopa B. Del Carlo A. Farini S. Maciotta N. Bresolin L. Porretti M. Pellegrino Y. Torrente 《Cellular and molecular life sciences : CMLS》2009,66(4):697-710
Among the heterogeneous population of circulating hematopoietic and endothelial progenitors, we identified a subpopulation
of CD133+ cells displaying myogenic properties. Unexpectedly, we observed the expression of the B-cell marker CD20 in blood-derived
CD133+ stem cells. The CD20 antigen plays a role in the modulation of intracellular calcium homeostasis through signaling pathways
activation. Several observations suggest that an increase in intracellular calcium concentration ([Ca2+]i) could be involved in the etiology of the Duchenne muscular dystrophy (DMD). Here, we show that a CD20-related signaling
pathway able to induce an increase in [Ca2+]i is differently activated after brain derived neurotrophic factor (BDNF) stimulation of normal and dystrophic blood-derived
CD133+ stem cells, supporting the assumption of a “CD20-related calcium impairment-affecting dystrophic cells. Presented findings
represent the starting point toward the expansion of knowledge on pathways involved in the pathology of DMD and in the behavior
of dystrophic blood-derived CD133+ stem cells.
Received 15 October 2008; received after revision 27 November 2008; accepted 05 December 2008 相似文献
727.
It has now been more than ten years since the discovery of the major apoptotic nuclease, DNA fragmentation factor (DFF), also
known as caspaseactivated DNase (CAD). Here we review the recent literature that has uncovered new insight into DFF’s regulation,
and both its positive and negative roles in human disease. Cells from mice deficient in DFF still undergo apoptotic death
without significant cellautonomous DNA degradation. Their corpses’ genomes are subsequently degraded by lysosomal DNase II
after phagocytosis. However,DFF-deficient mice are more susceptible to cancer. Indeed, several different cancers in humans
are associated with defects in DFF expression and it has been proposed that DFF is a p53-independent tumor suppressor. Negative
aspects of DFF expression include contributing to susceptibility to acquire systemic lupus erythematosus, to chromosomal translocations
that result in mixed lineage leukemias, and in the possible spreading of oncogenes and HIV due to horizontal gene transfer.
Received 06 August 2008; received after revision 03 September 2008; accepted 09 September 2008 相似文献
728.
Grou CP Carvalho AF Pinto MP Alencastre IS Rodrigues TA Freitas MO Francisco T Sá-Miranda C Azevedo JE 《Cellular and molecular life sciences : CMLS》2009,66(2):254-262
The peroxisomal protein import machinery displays remarkable properties. Be it its capacity to accept already folded proteins
as substrates, its complex architecture or its energetics, almost every aspect of this machinery seems unique. The list of
unusual properties is still growing as shown by the recent finding that one of its central components, Pex5p, is transiently
monoubiquitinated at a cysteine residue. However, the data gathered in recent years also suggest that the peroxisomal import
machinery is not that exclusive and similarities with p97/Cdc48-mediated processes and with multisubunit RING-E3 ligases are
starting to emerge. Here, we discuss these data trying to distill the principles by which this complex machinery operates.
Received 16 July 2008; received after revision 25 August 2008; accepted 29 August 2008 相似文献
729.
A. Hamadi T. B. Deramaudt K. Takeda P. Rondé 《Cellular and molecular life sciences : CMLS》2009,66(2):324-338
Cell migration requires the coordinated turnover of focal adhesions, a process that involves FAK phosphorylation. Since Src
is the major kinase implicated in FAK phosphorylation, we focus here on the role of Src activation on adhesion remodelling.
In astrocytoma cells, constitutively activated Src induces both FAK phosphorylation and adhesion rearrangement. To evaluate
how Src controls these processes, we used a recently described Src reporter to monitor the dynamics of Src phosphorylation.
Upon Src activation, focal adhesions started to disassemble while Src appeared highly expressed at newly formed membrane ruffles.
Kinetic analysis of time-lapse movies showed that loss of phospho-Src at focal adhesions was time-correlated with the appearance
of membrane ruffles containing phospho-Src. Moreover, FLIP analysis revealed a dynamic equilibrium of Src between focal adhesions
and membrane ruffles. We conclude that upon phosphorylation, Src is directly translocated from focal adhesions to membrane
ruffles, thereby promoting formation of new adhesion complexes.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users.
Received 21 July 2008; received after revision 10 October 2008; accepted 03 November 2008 相似文献
730.
A. Deshmukh F. Salehzadeh S. Metayer-Coustard R. Fahlman K. S. Nair L. Al-Khalili 《Cellular and molecular life sciences : CMLS》2009,66(8):1457-1466
Excessive nutrients, especially amino acids, impair insulin action on glucose metabolism in skeletal muscle. We tested the
hypothesis that the branched-chain amino acid leucine reduces acute insulin action in primary myotubes via a negative feedback mechanism involving ribosomal protein S6 kinase 1 (S6K1). The effect of S6K1 on glucose metabolism was
determined by applying RNA interference (siRNA). Leucine (5 mM) reduced glucose uptake and incorporation to glycogen by 13%
and 22%, respectively, compared to the scramble siRNA-transfected control at the basal level. Leucine also reduced insulin-stimulated
Akt phosphorylation, glucose uptake and glucose incorporation to glycogen (39%, 39% and 37%, respectively), and this reduction
was restored after S6K1 silencing. Depletion of S6K1 enhanced basal glucose utilization and protected against the development
of impaired insulin action, in response to excessive leucine. In conclusion, S6K1 plays an important role in the regulation
of insulin action on glucose metabolism in skeletal muscle.
Received 22 December 2008; received after revision 19 February 2009; accepted 23 February 2009 相似文献