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21.
Essential oil from wood and from needles of Pinus balfouriana, growing in six geographically well-separated locations in California, was analysed by GLC. Several monoterpenoid components, in particular -pinene from needles, were found to be usable for distinguishing between trees from the northern and southern parts of the geographic range. Similarity coefficients were calculated and dendrograms constructed. These demonstrated the distinct separation of the northern from the southern populations, and thus substantiated the proposal by Mastrogiuseppe to regard the southern populations as a subspecies. While the northern populations exhibited a tendency to produce larger seeds with longer wings, the difference was of only moderate diagnostic value.  相似文献   
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A randomisation test is described for assessing relative abundance predictions from the maximum entropy approach to biodiversity. The null model underlying the test randomly allocates observed abundances to species, but retains key aspects of the structure of the observed communities; site richness, species composition, and trait covariance. Three test statistics are used to explore different characteristics of the predictions. Two are based on pairwise comparisons between observed and predicted species abundances (RMSE, RMSESqrt). The third statistic is novel and is based on community‐level abundance patterns, using an index calculated from the observed and predicted community entropies (EDiff). Validation of the test to quantify type I and type II error rates showed no evidence of bias or circularity, confirming the dependencies quantified by Roxburgh and Mokany (2007) and Shipley (2007) have been fully accounted for within the null model. Application of the test to the vineyard data of Shipley et al. (2006) and to an Australian grassland dataset indicated significant departures from the null model, suggesting the integration of species trait information within the maximum entropy framework can successfully predict species abundance patterns. The paper concludes with some general comments on the use of maximum entropy in ecology, including a discussion of the mathematics underlying the Maxent optimisation algorithm and its implementation, the role of absent species in generating biased predictions, and some comments on determining the most appropriate level of data aggregation for Maxent analysis.  相似文献   
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The role of the zebra mussel Dreissena polymorpha in redistribution of total particulate material (TPM) between the water column and bottom sediment was estimated using the TPM budget for a mussel bed in the Curonian lagoon, the Baltic Sea. Seasonal clearance rates were derived from the TPM budget assuming two resuspension scenarios: no resuspension and full resuspension of biodeposits. Estimated clearance rates for both scenarios were compared with the rates calculated from the population clearance rate model. Seasonal clearance rates estimated using the population model (1.1 and 11.8 l g−1 SFDW day−1) fitted well into the interval of seasonal clearance rates calculated from TPM budgets assuming no resuspension of biodeposits (3.2 and 21.4 l g SFDW−1 day−1). In the scenario with biodeposits resuspension clearance rates were much higher (57.4 and 148.9 g SFDW−1 day−1). The ratio of clearance to residence time was highly dependent on the fate of biodeposits. Therefore its use in interpretation of the species impact on TPM was limited. An alternative measure based on the ratio of the amount of TPM biodeposited to TPM transported into the bed was used. It was found that zebra mussels are able to deposit between 10 and 30% of the incoming TPM, and the amount of biodeposited material was correlated with water residence time. Results indicate that the impact of zebra mussels on TPM in the lagoon is small relative to the high transport rates of TPM over the bed. However, annual biosedimentation rate (~590 g m−2) in the mussel bed was higher than physical deposition rate (~380 g m−2) in accumulation areas devoid of large suspension feeders. We suggest that a local impact due to enhanced availability of organic material to other trophic groups of associated benthic organisms may be more significant than effects on TPM pathways at an ecosystem scale.  相似文献   
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A series of new monophosphates of 1-[2-(phosphonomethoxy)alkyl]thymines, such as PMPTp, 3-MeO-PMPTp, HPMPTp, and FPMPTp, were synthesized and tested for their ability to inhibit human thymidine phosphorylase. Kinetic measurements of enzyme activity were performed using thymidine and inorganic phosphate as the substrates. The data show that some monophosphates provide a considerable increase of the multisubstrate inhibitory effect. The highest inhibitory potency was found with (R)-FPMPTp 4c (K i dT = 4.09 ± 0.47 μM, K i(Pi) = 2.13 ± 0.29 μM) and (R) 3-MeO-PMPTp 4d (K i dT = 5.78 ± 0.71 μM, K i(Pi) = 2.71 ± 0.37 μM).  相似文献   
27.
The acquisition of massive but localized chromosome translocations, a phenomenon termed chromothripsis, has received widespread attention since its discovery over a year ago. Until recently, chromothripsis was believed to originate from a single catastrophic event, but the molecular mechanisms leading to this event are yet to be uncovered. Because a thorough interpretation of the data are missing, the phenomenon itself has wrongly acquired the status of a mechanism used to justify many kinds of complex rearrangements. Although the assumption that all translocations in chromothripsis originate from a single event has met with criticism, satisfactory explanations for the intense but localized nature of this phenomenon are still missing. Here, we show why the data used to describe massive catastrophic rearrangements are incompatible with a model comprising a single event only and propose a molecular mechanism in which a combination of known cellular pathways accounts for chromothripsis. Instead of a single traumatic event, the protection of undamaged chromosomes by telomeres can limit repetitive breakage-fusion-bridge events to a single chromosome arm. Ultimately, common properties of chromosomal instability, such as aneuploidy and centromere fission, might establish the complex genetic pattern observed in this genomic state.  相似文献   
28.
Chromosome duplication and transmission into daughter cells requires the precisely orchestrated binding and release of cohesin. We found that the Drosophila histone chaperone NAP1 is required for cohesin release and sister chromatid resolution during mitosis. Genome-wide surveys revealed that NAP1 and cohesin co-localize at multiple genomic loci. Proteomic and biochemical analysis established that NAP1 associates with the full cohesin complex, but it also forms a separate complex with the cohesin subunit stromalin (SA). NAP1 binding to cohesin is cell-cycle regulated and increases during G2/M phase. This causes the dissociation of protein phosphatase 2A (PP2A) from cohesin, increased phosphorylation of SA and cohesin removal in early mitosis. PP2A depletion led to a loss of centromeric cohesion. The distinct mitotic phenotypes caused by the loss of either PP2A or NAP1, were both rescued by their concomitant depletion. We conclude that the balanced antagonism between NAP1 and PP2A controls cohesin dissociation during mitosis.  相似文献   
29.

The nucleus-encoded 17β-hydroxysteroid dehydrogenase type 10 (17β-HSD10) regulates cyclophilin D (cypD) in the mitochondrial matrix. CypD regulates opening of mitochondrial permeability transition pores. Both mechanisms may be affected by amyloid β peptides accumulated in mitochondria in Alzheimer's disease (AD). In order to clarify changes occurring in brain mitochondria, we evaluated interactions of both mitochondrial proteins in vitro (by surface plasmon resonance biosensor) and detected levels of various complexes of 17β-HSD10 formed in vivo (by sandwich ELISA) in brain mitochondria isolated from the transgenic animal model of AD (homozygous McGill-R-Thy1-APP rats) and in cerebrospinal fluid samples of AD patients. By surface plasmon resonance biosensor, we observed the interaction of 17β-HSD10 and cypD in a direct real-time manner and determined, for the first time, the kinetic parameters of the interaction (ka 2.0?×?105 M1s?1, kd 5.8?×?104 s?1, and KD 3.5?×?10–10 M). In McGill-R-Thy1-APP rats compared to controls, levels of 17β-HSD10–cypD complexes were decreased and those of total amyloid β increased. Moreover, the levels of 17β-HSD10–cypD complexes were decreased in cerebrospinal fluid of individuals with AD (in mild cognitive impairment as well as dementia stages) or with Frontotemporal lobar degeneration (FTLD) compared to cognitively normal controls (the sensitivity of the complexes to AD dementia was 92.9%, that to FTLD 73.8%, the specificity to AD dementia equaled 91.7% in a comparison with the controls but only 26.2% with FTLD). Our results demonstrate the weakened ability of 17β-HSD10 to regulate cypD in the mitochondrial matrix probably via direct effects of amyloid β. Levels of 17β-HSD10–cypD complexes in cerebrospinal fluid seem to be the very sensitive indicator of mitochondrial dysfunction observed in neurodegeneration but unfortunately not specific to AD pathology. We do not recommend it as the new biomarker of AD.

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