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Eichten SR Swanson-Wagner RA Schnable JC Waters AJ Hermanson PJ Liu S Yeh CT Jia Y Gendler K Freeling M Schnable PS Vaughn MW Springer NM 《PLoS genetics》2011,7(11):e1002372
Epigenetic variation describes heritable differences that are not attributable to changes in DNA sequence. There is the potential for pure epigenetic variation that occurs in the absence of any genetic change or for more complex situations that involve both genetic and epigenetic differences. Methylation of cytosine residues provides one mechanism for the inheritance of epigenetic information. A genome-wide profiling of DNA methylation in two different genotypes of Zea mays (ssp. mays), an organism with a complex genome of interspersed genes and repetitive elements, allowed the identification and characterization of examples of natural epigenetic variation. The distribution of DNA methylation was profiled using immunoprecipitation of methylated DNA followed by hybridization to a high-density tiling microarray. The comparison of the DNA methylation levels in the two genotypes, B73 and Mo17, allowed for the identification of approximately 700 differentially methylated regions (DMRs). Several of these DMRs occur in genomic regions that are apparently identical by descent in B73 and Mo17 suggesting that they may be examples of pure epigenetic variation. The methylation levels of the DMRs were further studied in a panel of near-isogenic lines to evaluate the stable inheritance of the methylation levels and to assess the contribution of cis- and trans- acting information to natural epigenetic variation. The majority of DMRs that occur in genomic regions without genetic variation are controlled by cis-acting differences and exhibit relatively stable inheritance. This study provides evidence for naturally occurring epigenetic variation in maize, including examples of pure epigenetic variation that is not conditioned by genetic differences. The epigenetic differences are variable within maize populations and exhibit relatively stable trans-generational inheritance. The detected examples of epigenetic variation, including some without tightly linked genetic variation, may contribute to complex trait variation. 相似文献
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Nelson MR Howard D Jensen OE King JR Rose FR Waters SL 《Biomechanics and modeling in mechanobiology》2011,10(6):883-900
We use a proof-of-concept experiment and two mathematical models to explore growth-induced tissue buckling, as may occur in
colorectal crypt formation. Our experiment reveals how growth of a cultured epithelial monolayer on a thin flexible substrate
can cause out-of-plane substrate deflections. We describe this system theoretically using a ‘bilayer’ model in which a growing
cell layer adheres to a thin compressible elastic beam. We compare this with the ‘supported-monolayer’ model due to Edwards
and Chapman (Bull Math Biol 69:1927–1942, 2007) for an incompressible expanding beam (representing crypt epithelium), which incorporates viscoelastic tethering to underlying
stroma. We show that the bilayer model can exhibit buckling via parametric growth (in which the system passes through a sequence
of equilibrium states, parameterised by the total beam length); in this case, non-uniformities in cell growth and variations
in cell–substrate adhesion are predicted to have minimal effect on the shape of resulting buckled states. The supported-monolayer
model reveals how competition between lateral supports and stromal adhesion influences the wavelength of buckled states (in
parametric growth), and how non-equilibrium relaxation of tethering forces influences post-buckled shapes. This model also
predicts that non-uniformities in growth patterns have a much weaker influence on buckled shapes than non-uniformities in
material properties. Together, the experiment and models support the concept of patterning by growth-induced buckling and
suggest that targeted softening of a growing cell layer provides greater control in shaping tissues than non-uniform growth. 相似文献
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The active vitamin D metabolite, 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)), has been shown to be an important regulator of innate and adaptive immune function. In addition, synthesis of 1,25(OH)(2)D(3) from 25-hydroxyvitamin D(3) (25(OH)D(3)) by the enzyme 1α-hydroxylase in monocytes upon activation by TLR signaling has been found to regulate innate immune responses of monocytes in an intracrine fashion. In this study we wanted to determine what cells expressed 1α-hydroxylase in stimulated peripheral blood mononuclear cell (PBMC) cultures and if conversion of 25(OH)D(3) to 1,25(OH)(2)D(3) in PBMC cultures regulated antigen-specific immune responses. Initially, we found that stimulation of PBMCs from animals vaccinated with Mycobacterium bovis (M. bovis) BCG with purified protein derivative of M. bovis (M. bovis PPD) induced 1α-hydroxylase gene expression and that treatment with a physiological concentration of 25(OH)D(3) down-regulated IFN-γ and IL-17F gene expression. Next, we stimulated PBMCs from M. bovis BCG-vaccinated and non-vaccinated cattle with M. bovis PPD and sorted them by FACS according to surface markers for monocytes/macrophages (CD14), B cells (IgM), and T cells (CD3). Sorting the PBMCs revealed that 1α-hydroxylase expression was induced in the monocytes and B cells, but not in the T cells. Furthermore, treatment of stimulated PBMCs with 25(OH)D(3) down-regulated antigen-specific IFN-γ and IL-17F responses in the T cells, even though 1α-hydroxylase expression was not induced in the T cells. Based on evidence of no T cell 1α-hydroxylase we hypothesize that activated monocytes and B cells synthesize 1,25(OH)(2)D(3) and that 1,25(OH)(2)D(3) down-regulates antigen-specific expression of IFN-γ and IL-17F in T cells in a paracrine fashion. 相似文献
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