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41.
Protoplasts of Boergesenia forbesii (Harvey) were treated with inhibitors of protein synthesis in order to investigate their effects on cellulose synthesis. Cellulose synthesis was reversibly inhibited by 10 μM cycloheximide as assayed by fluorescence microscopy of Tinopal binding to cellulose. Freeze fracture and image analysis of cycloheximide- treated cells indicated a reduction in the number of intramembrane particles; however, the terminal synthesizing complexes remained at all times. Treatment with 10 μM actinomycin D, when applied during the first hour of protoplast formation, irreversibly inhibits cellulose synthesis and terminal complex formation. De novo protein synthesis is required for cell wall regeneration by protoplasts. The data suggest that the structural subunits visualized in the terminal complex do not undergo significant turnover, but that there may exist an essential proteinaceous component of cellulose synthesis which must be continually renewed. 相似文献
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Brincks EL Gurung P Langlois RA Hemann EA Legge KL Griffith TS 《Journal of immunology (Baltimore, Md. : 1950)》2011,187(9):4581-4588
An immune response of appropriate magnitude should be robust enough to control pathogen spread but not simultaneously lead to immunopathology. Primary infection with influenza A virus (IAV) results in a localized pulmonary infection and inflammation and elicits an IAV-specific CD8 T cell immune response necessary for viral clearance. Clearance of IAV-infected cells, and recovery from infection, is mediated by perforin/granzyme B- and Fas/FasL-mediated mechanisms. We recently reported that TRAIL is another means by which IAV-specific CD8 T cells can kill IAV-infected cells. The current study examined the role of TRAIL in the pulmonary CD8 T cell response to a clinically significant IAV [A/PR/8/34 (PR8; H1N1)] infection (i.e., leads to observable, but limited, morbidity and mortality in wild-type [WT] mice). Compared with WT mice, IAV-infected Trail(-/-) mice experienced increased morbidity and mortality despite similar rates of viral clearance from the lungs. The increased morbidity and mortality in Trail(-/-) mice correlated with increased pulmonary pathology and inflammatory chemokine production. Analysis of lung-infiltrating lymphocytes revealed increased numbers of IAV-specific CD8 T cells in infected Trail(-/-) mice, which correlated with increased pulmonary cytotoxic activity and increased pulmonary expression of MIG and MIP-1α. In addition, there was decreased apoptosis and increased proliferation of IAV-specific CD8 T cells in the lungs of Trail(-/-) mice compared with WT mice. Together, these data suggest that TRAIL regulates the magnitude of the IAV-specific CD8 T cell response during a clinically significant IAV infection to decrease the chance for infection-induced immunopathology. 相似文献
44.
VLJ Whitehall TD Dumenil DM McKeone CE Bond ML Bettington RL Buttenshaw L Bowdler GW Montgomery LF Wockner BA Leggett 《Epigenetics》2014,9(11):1454-1460
The CpG Island Methylator Phenotype (CIMP) is fundamental to an important subset of colorectal cancer; however, its cause is unknown. CIMP is associated with microsatellite instability but is also found in BRAF mutant microsatellite stable cancers that are associated with poor prognosis. The isocitrate dehydrogenase 1 (IDH1) gene causes CIMP in glioma due to an activating mutation that produces the 2-hydroxyglutarate oncometabolite. We therefore examined IDH1 alteration as a potential cause of CIMP in colorectal cancer. The IDH1 mutational hotspot was screened in 86 CIMP-positive and 80 CIMP-negative cancers. The entire coding sequence was examined in 81 CIMP-positive colorectal cancers. Forty-seven cancers varying by CIMP-status and IDH1 mutation status were examined using Illumina 450K DNA methylation microarrays. The R132C IDH1 mutation was detected in 4/166 cancers. All IDH1 mutations were in CIMP cancers that were BRAF mutant and microsatellite stable (4/45, 8.9%). Unsupervised hierarchical cluster analysis identified an IDH1 mutation-like methylation signature in approximately half of the CIMP-positive cancers. IDH1 mutation appears to cause CIMP in a small proportion of BRAF mutant, microsatellite stable colorectal cancers. This study provides a precedent that a single gene mutation may cause CIMP in colorectal cancer, and that this will be associated with a specific epigenetic signature and clinicopathological features. 相似文献
45.
Larry J Leamy Scott A Kelly Joseph Nietfeldt Ryan M Legge Fangrui Ma Kunjie Hua Rohita Sinha Daniel A Peterson Jens Walter Andrew K Benson Daniel Pomp 《Genome biology》2014,15(12)
Background
Individuality in the species composition of the vertebrate gut microbiota is driven by a combination of host and environmental factors that have largely been studied independently. We studied the convergence of these factors in a G10 mouse population generated from a cross between two strains to search for quantitative trait loci (QTLs) that affect gut microbiota composition or ileal Immunoglobulin A (IgA) expression in mice fed normal or high-fat diets.Results
We found 42 microbiota-specific QTLs in 27 different genomic regions that affect the relative abundances of 39 taxa, including four QTL that were shared between this G10 population and the population previously studied at G4. Several of the G10 QTLs show apparent pleiotropy. Eight of these QTLs, including four at the same site on chromosome 9, show significant interaction with diet, implying that diet can modify the effects of some host loci on gut microbiome composition. Utilization patterns of IghV variable regions among IgA-specific mRNAs from ileal tissue are affected by 54 significant QTLs, most of which map to a segment of chromosome 12 spanning the Igh locus. Despite the effect of genetic variation on IghV utilization, we are unable to detect overlapping microbiota and IgA QTLs and there is no significant correlation between IgA variable pattern utilization and the abundance of any of the taxa from the fecal microbiota.Conclusions
We conclude that host genetics and diet can converge to shape the gut microbiota, but host genetic effects are not manifested through differences in IgA production.Electronic supplementary material
The online version of this article (doi:10.1186/s13059-014-0552-6) contains supplementary material, which is available to authorized users. 相似文献46.
L. A. Marquez-Cedillo P. M. Hayes B. L. Jones A. Kleinhofs W. G. Legge B. G. Rossnagel K. Sato S. E. Ullrich D. M. Wesenberg North American Barley Genome Mapping Project 《TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik》2000,101(1-2):173-184
Characterization of the determinants of economically important phenotypes showing complex inheritance should lead to the more
effective use of genetic resources. This study was conducted to determine the number, genome location and effects of QTLs
determining malting quality in the two North American barley quality standards. Using a doubled-haploid population of 140
lines from the cross of Harrington×Morex, malting quality phenotype data sets from eight environments, and a 107-marker linkage
map, QTL analyses were performed using simple interval mapping and simplified composite interval mapping procedures. Seventeen
QTLs were associated with seven grain and malting quality traits (percentage of plump kernels, test weight, grain protein
percentage, soluble/total protein ratio, α-amylase activity, diastatic power and malt-extract percentage). QTLs for multiple
traits were coincident. The loci controlling inflorescence type [vrs1 on chromosome 2(2H) and int-c on chromosome 4(4H)] were coincident with QTLs affecting all traits except malt-extract percentage. The largest effect QTLs,
for the percentage of plump kernels, test weight protein percentage, S/T ratio and diastatic power, were coincident with the
vrs1 locus. QTL analyses were conducted separately for each sub-population (six-rowed and two-rowed). Eleven new QTLs were detected
in the subpopulations. There were significant interactions between the vrs1 and int-c loci for grain-protein percentage and S/T protein ratio. Results suggest that this mating of two different germplasm groups
caused a disruption of the balance of traits. Information on the number, position and effects of QTLs determining components
of malting quality may be useful for maintaining specific allele configurations that determine target quality profiles.
Received: 28 May 1999 / Accepted: 9 November 1999 相似文献
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Summary A solid state fermentation (SSF) process for the production of lignin peroxidase was optimized to enhance enzyme production
by Phanerochaete chrysosporium. Optimization of the corncob SSF medium caused a significant reduction in fermentation time to give maximum lignin peroxidase
yield. Supplementation of the SSF medium by low concentrations of peptone, yeast extract and Tween-80 enhanced lignin peroxidase
production. Maximum yield of lignin peroxidase was 13.7 U/gds (units per gram dry substrate) noted after 5 days of SSF with
70% moisture and 20% (v/w) inoculum. 相似文献
50.