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951.
Spatial heterogeneity in coral reef communities is well documented. This “species turnover” (beta diversity) on shallow warm-water
reefs strongly conforms to spatial gradients in the environment as well as spatially autocorrelated biotic processes such
as dispersal and competition. But the extent to which the environment and spatial autocorrelation create beta diversity on
deep cold-water coral reefs such as those formed by Lophelia pertusa (Scleractinia) is unknown. The effects of remotely sensed and ground-truthed data were tested on the community composition
of sessile suspension-feeding communities from the Mingulay Reef Complex, a landscape of inshore Lophelia reefs off the Scottish west coast. Canonical correspondence analysis determined that a statistically significant proportion
(68%) of the variance in community composition could be explained by remotely sensed environmental variables (northerly and
easterly aspect, seabed rugosity, depth), ground-truthed environmental variables (species richness and reef macrohabitat)
and geospatial location. This variation was further partitioned into fractions explained by pure effects of the environment
(51%), spatially structured environmental variables (12%) and spatial autocorrelation (5%). Beta diversity in these communities
reflected the effects of both measured and unmeasured and spatially dependent environmental variables that vary across the
reef complex, i.e., hydrography. Future work will quantify the significance and relative contributions of these variables
in creating beta diversity in these rich communities. 相似文献
952.
Henry F. Vischer Janneke W. Hulshof Saskia Hulscher Silvina A. Fratantoni Mark H.P. Verheij Jane Victorina Martine J. Smit Iwan J.P. de Esch Rob Leurs 《Bioorganic & medicinal chemistry》2010,18(2):675-688
Human cytomegalovirus (HCMV) is a widespread human pathogen, possessing onco-modulatory properties. Constitutive signaling of the HCMV-encoded chemokine receptor US28 and its ability to bind a broad spectrum of chemokines might facilitate HCMV-associated tumor progression. Novel nonpeptidergic chemotypes were identified as neutral antagonists or inverse agonists on US28, that allosterically inhibit chemokine binding to US28. 相似文献
953.
954.
Saskia Nijmeijer Rob Leurs Martine J. Smit Henry F. Vischer 《The Journal of biological chemistry》2010,285(38):29632-29641
Cells express distinct G protein-coupled receptor (GPCR) subtypes on their surface, allowing them to react to a corresponding variety of extracellular stimuli. Cross-regulation between different ligand-GPCR pairs is essential to generate appropriate physiological responses. GPCRs can physically affect each other''s functioning by forming heteromeric complexes, whereas cross-regulation between activated GPCRs also occurs through integration of shared intracellular signaling networks. Human herpesviruses utilize virally encoded GPCRs to hijack cellular signaling networks for their own benefit. Previously, we demonstrated that the Epstein-Barr virus-encoded GPCR BILF1 forms heterodimeric complexes with human chemokine receptors. Using a combination of bimolecular complementation and bioluminescence resonance energy transfer approaches, we now show the formation of hetero-oligomeric complexes between this viral GPCR and human CXCR4. BILF1 impaired CXCL12 binding to CXCR4 and, consequently, also CXCL12-induced signaling. In contrast, the G protein uncoupled mutant BILF1-K3.50A affected CXCL12-induced CXCR4 signaling to a much lesser extent, indicating that BILF1-mediated CXCR4 inhibition is a consequence of its constitutive activity. Co-expression of Gαi1 with BILF1 and CXCR4 restored CXCL12-induced signaling. Likewise, BILF1 formed heteromers with the human histamine H4 receptor (H4R). BILF1 inhibited histamine-induced Gαi-mediated signaling by H4R, however, without affecting histamine binding to this receptor. These data indicate that functional cross-regulation of Gαi-coupled GPCRs by BILF1 is at the level of G proteins, even though these GPCRs are assembled in hetero-oligomeric complexes. 相似文献
955.
Roselani I. Henry Simon A. Cobbold Richard J. W. Allen Asif Khan Rhys Hayward Adele M. Lehane Patrick G. Bray Susan M. Howitt Giancarlo A. Biagini Kevin J. Saliba Kiaran Kirk 《The Journal of biological chemistry》2010,285(24):18615-18626
The intraerythrocytic malaria parasite exerts tight control over its ionic composition. In this study, a combination of fluorescent ion indicators and 36Cl− flux measurements was used to investigate the transport of Cl− and the Cl−-dependent transport of “H+-equivalents” in mature (trophozoite stage) parasites, isolated from their host erythrocytes. Removal of extracellular Cl−, resulting in an outward [Cl−] gradient, gave rise to a cytosolic alkalinization (i.e. a net efflux of H+-equivalents). This was reversed on restoration of extracellular Cl−. The flux of H+-equivalents was inhibited by 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid and, when measured in ATP-depleted parasites, showed a pronounced dependence on the pH of the parasite cytosol; the flux was low at cytosolic pH values < 7.2 but increased steeply with cytosolic pH at values > 7.2. 36Cl− influx measurements revealed the presence of a Cl− uptake mechanism with characteristics similar to those of the Cl−-dependent H+-equivalent flux. The intracellular concentration of Cl− in the parasite was estimated to be ∼48 mm in situ. The data are consistent with the intraerythrocytic parasite having in its plasma membrane a 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid-sensitive transporter that, under physiological conditions, imports Cl− together with H+-equivalents, resulting in an intracellular Cl− concentration well above that which would occur if Cl− ions were distributed passively in accordance with the parasite''s large, inwardly negative membrane potential. 相似文献
956.
957.
958.
The lowest energy structure for Mn2(BF)(CO)10 is predicted to consist of two Mn(CO)5 groups bridged by a BF group without a manganese-manganese bond. This structure is related to the stable compounds Mn2(μ-BX)(CO)10 (X = Cl, Br) and [(η5-C5H5)Ru(CO)2]2(μ-BF), which have been synthesized and characterized by X-ray crystallography. The following principles determine the lowest energy structures of the Mn2(BF)(CO)n (n = 9, 8, 7, 6) derivatives: (1) two-electron donor bridging μ-BF groups are highly favorable; (2) four-electron donor bridging η2-μ-BF groups are not found and thus appear to be highly unfavorable. Thus the lowest energy structure of Mn2(BF)(CO)9 is a doubly bridged structure with bridging CO and BF groups, in contrast to the experimentally observed unbridged structure of Mn2(CO)10. The lowest energy structures of Mn2(BF)(CO)8 have either a four-electron donor η2-μ-CO group or a two-electron donor bridging BF group. Similarly the lowest energy structures of the more highly unsaturated Mn2(BF)(CO)n (n = 7, 6) are singlet (for n = 7) or triplet (for n = 6) states in which the BF group is a bridging rather than a terminal ligand. 相似文献
959.
960.
Curtis J. Henry Jason M. Grayson Latoya M. Mitchell Marlena M. Westcott Elizabeth M. Hiltbold 《Cellular immunology》2010,264(1):23-31
Listeria monocytogenes infection induces a strong inflammatory response characterized by the production of IL-12 and IFN-γ and protective immunity against this pathogen is dependent on CD8+ T cells (CTL). Recent studies have suggested that these inflammatory cytokines affect the rate of memory CD8+ T cell generation as well as the number of short-lived effector cells generated. The role of the closely related cytokine, IL-23, in this response has not been examined. We hypothesized that IL-12 and IL-23 produced by dendritic cells collectively enhance the generation and function of memory cells. To test this hypothesis, we employed a DC vaccination approach. Mice lacking IL-12 and IL-23 were vaccinated with wild-type (WT), IL-12−/−, or IL-12/23−/− DC and protection to Lm was monitored. Mice vaccinated with WT and IL-12−/− DC were resistant to lethal challenge with Lm. Surprisingly, mice vaccinated with IL-12/23−/− DC exhibited significantly reduced protection when challenged. Protection correlated with the relative size of the memory pools generated. In summary, these data indicate that IL-23 can partially compensate for the lack of IL-12 in the generation protective immunity against Lm. 相似文献