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91.
92.
Coutrot Frédéric Marraud Michel Maigret Bernard Grison Claude Coutrot Philippe 《International journal of peptide research and therapeutics》2001,8(2):107-116
Summary The synthesis of three N-alkyl-6,7-dideoxy-1,2:3,4-di-O-isopropylidene-7-[(alkyl-carbonyl)amino]-L-glycero-α-D-galacto-octopyranuronamides6a-c, analogous model dipeptides containing two amide groups connected to the α-carbon bearing the fully protected galactose as
a side chain, has been realized with the aim of determining the conformational influence of the galactosyl moiety on the peptide
backbone. Molecular modeing of6a, X-ray crystallography of6c and IR and NMR experiments on6a-c in organic solvents show that the carbohydrate ring assumes a twist boat conformation. In non-polar organic solvents, the
NH of the left amide group interacts with one ketal oxygen of the galactosyl group. 相似文献
93.
Presynaptic kainate receptors that enhance the release of GABA on CA1 hippocampal interneurons 总被引:9,自引:0,他引:9
We report that kainate receptors are present on presynaptic GABAergic terminals contacting interneurons and that their activation increases GABA release. Application of kainate increased the frequency of miniature inhibitory postsynaptic currents recorded in CA1 interneurons. Local applications of glutamate but not of AMPA or NMDA also increased GABA quantal release. Application of kainate as well as synaptically released glutamate reduced the number of failures of GABAergic neurotransmission between interneurons. Thus, activation of presynaptic kainate receptors increases the probability of GABA release at interneuron-interneuron synapses. Glutamate may selectively control the communication between interneurons by increasing their mutual inhibition. 相似文献
94.
Oxygen-dependent gene expression in fishes 总被引:2,自引:0,他引:2
95.
96.
Cartesio Favalli Peter Leport Bernard M. Jaffe M.Gabriella Santoro Thomas Simmet Vera Del Gobbo Enrico Garaci 《Cellular immunology》1982,72(2):351-359
The effect of 16,16-dimethyl-PGE2-methyl ester (di-M-PGE2) on humoral and cellular immunoresponsiveness has been compared in normal mice and in mice immunosuppressed by splenectomy and thymectomy plus antithymocyte serum (ATS). Splenectomy resulted in immunosuppression manifested by augmentation of B-16 melanoma growth; this stimulatory effect was reversed by di-M-PGE2. In animals immunosuppressed by thymectomy plus ATS, di-M-PGE2 augmented the humoral and cellular immune responses; this was manifested by slowing of the growth of B-16 melanoma and by stimulating the number of plaque-forming cells, hemagglutinin titers, and delayed-hypersensitivity reactions to sheep erythrocytes. In contrast, in normal (nonthymectomized) mice, di-M-PGE2 was mildly immunosuppressive. Finally, adriamycin-immunosuppressed normal mice and this suppression were reversed by the addition of di-M-PGE2 to the treatment regimen. 相似文献
97.
Abu-Baker A Laganiere S Fan X Laganiere J Brais B Rouleau GA 《Traffic (Copenhagen, Denmark)》2005,6(9):766-779
Oculopharyngeal muscular dystrophy (OPMD) is an adult-onset disorder characterized by progressive eyelid drooping, swallowing difficulties and proximal limb weakness. The autosomal dominant form of this disease is caused by a polyalanine expansion from 10 to 12-17 residues, located at the N-terminus of the poly(A)-binding protein nuclear 1 (PABPN1). A distinct pathological hallmark of OPMD is the presence of filamentous intranuclear aggregates in patients' skeletal muscle cells. Wildtype PABPN1 protein is expressed ubiquitously and was shown to be mostly concentrated in discrete nuclear domains called 'speckles'. Using an established cell- culture model, we show that most mutant PABPN1- positive (alanine expanded form) intranuclear aggregates are structures distinct from intranuclear speckles. In contrast, the promyelocytic leukaemia protein, a major component of nuclear bodies, strongly colocalized to intranuclear aggregates of mutant PABPN1. Wildtype PABPN1 can freely shuttle between the nucleus and cytoplasm. We determined whether the nuclear environment is necessary for mutant PABPN1 inclusion formation and cellular toxicity. This was achieved by inactivating the mutant PABPN1 nuclear localization signal and by generating full-length mutant PABPN1 fused to a strong nuclear export sequence. A green fluorescence protein tag inserted at the N-terminus of both wildtype PABPN1 (ala10) and mutant PABPN1 (ala17) proteins allowed us to visualize their subcellular localization. Targeting mutant PABPN1 to the cytoplasm resulted in a significant suppression of both intranuclear aggregates formation and cellular toxicity, two histological consequences of OPMD. Our results indicate that the nuclear localization of mutant PABPN1 is crucial to OPMD pathogenesis. 相似文献
98.
Human TK? 143 cells were converted to TK+ phenotype with a plasmid containing the native herpes simplex virus 1 (HSV-1), thymidine kinase, a β gene, and a chimeric ovalbumin gene consisting of the coding sequences of the ovalbumin gene linked to the promoter-regulatory region of the HSV-1 α 4 gene. Comparison of the synthesis of ovalbumin and the α 4 gene product in the converted cells infected with ts mutants in α 4 gene and incubated at the permissive (33°C) and nonpermissive (39°C) temperatures revealed the following. (i) The synthesis of both ovalbumin and α 4 gene product was transiently induced at the permissive temperature but continued at elevated levels for many hours at the nonpermissive temperature. (ii) The synthesis of both ovalbumin and α 4 gene products resumed when the infected cells were shifted from permissive to nonpermissive temperature after the shut-off of α protein synthesis. (iii) Although both the β-TK and α 4-ovalbumin chimeric genes were covalently linked on the same plasmid, each was regulated independently. We conclude that α gene regulation is determined solely by (a) the inducer and (b) the induction sequence contained in the promoter-regulatory region and not by the location or the higher order structure of the immediate environment of the gene. 相似文献
99.
Bernard C. Patten 《Oecologia》1993,93(4):597-602
Conclusion For the abovementioned reasons, and with all due respect to the scholarship of Mansson and McGlade, who display a deep knowledge of thermodynamics and ecology, I cannot agree that Odum's use of energy concepts is wholly discredited. Refinements from microscopic thermodynamics may not have been faithfully carried along in his work, but does ecology really need these? Remember — the meal test.Having tussled with ecological complexity myself, I stand in awe of this man who has faced up to what most ecologists today are trying to deny — intractable, crushing, defeating complexity. If Odum has provided some of the first shaky stepping stones across this gulf, that's enough.I can finish by quoting from ny Festschrift paper again:It is often said of scientists who make unusual contributions against the grain of their disciplines that they are ahead of their time. In H.T. Odum's case, with maximum power, energy-circuit diagrams, emergy, transformity, and energy value the linchpins of a whole new theory of ecology, and paradigm within systems ecology, this can certainly be stated without hesitation. But in this instance, it is also possible to turn the observation around and suggest that ecology-as-science is behind its time, lagging the curve of need foreseen decades ago by a more pragmatic ecology-as-ethic and-concern. The growing man-and-environment tension, fostered by so-far unabatable growth of populations, technologies and economies, demands a science that incises complexity, finds the essence of systemness, and produces quantitative methods capable of moulding this essence to meet the imperatives of the new environmentalism. H.T. Odum has not, perhaps, provided a definitive theory to do this; no one could right now. But, he has given us an intriguing mix of science, art and religion that stands as one of the singular legacies of 20th-century ecology, pointing the way toward a new ecology of complexity that must, I think from need, fully arise in the 21st century. His time has been behind him. 相似文献
100.
Sujata S. Chaudhari Yasuyuki Arakane Charles A. Specht Bernard Moussian Karl J. Kramer Subbaratnam Muthukrishnan Richard W. Beeman 《PLoS genetics》2013,9(1)
Molting, or the replacement of the old exoskeleton with a new cuticle, is a complex developmental process that all insects must undergo to allow unhindered growth and development. Prior to each molt, the developing new cuticle must resist the actions of potent chitinolytic enzymes that degrade the overlying old cuticle. We recently disproved the classical dogma that a physical barrier prevents chitinases from accessing the new cuticle and showed that the chitin-binding protein Knickkopf (Knk) protects the new cuticle from degradation. Here we demonstrate that, in Tribolium castaneum, the protein Retroactive (TcRtv) is an essential mediator of this protective effect of Knk. TcRtv localizes within epidermal cells and specifically confers protection to the new cuticle against chitinases by facilitating the trafficking of TcKnk into the procuticle. Down-regulation of TcRtv resulted in entrapment of TcKnk within the epidermal cells and caused molting defects and lethality in all stages of insect growth, consistent with the loss of TcKnk function. Given the ubiquity of Rtv and Knk orthologs in arthropods, we propose that this mechanism of new cuticle protection is conserved throughout the phylum. 相似文献