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1.
Charles L. Nunn Peter H. Thrall Kelly Stewart Alexander H. Harcourt 《Evolutionary ecology》2008,22(4):519-543
Emerging infectious diseases threaten a wide diversity of animals, and important questions remain concerning disease emergence
in socially structured populations. We developed a spatially explicit simulation model to investigate whether—and under what
conditions—disease-related mortality can impact rates of pathogen spread in populations of polygynous groups. Specifically,
we investigated whether pathogen-mediated dispersal (PMD) can occur when females disperse after the resident male dies from
disease, thus carrying infections to new groups. We also examined the effects of incubation period and virulence, host mortality
and rates of background dispersal, and we used the model to investigate the spread of the virus responsible for Ebola hemorrhagic
fever, which currently is devastating African ape populations. Output was analyzed using regression trees, which enable exploration
of hierarchical and non-linear relationships. Analyses revealed that the incidence of disease in single-male (polygynous)
groups was significantly greater for those groups containing an average of more than six females, while the total number of
infected hosts in the population was most sensitive to the number of females per group. Thus, as expected, PMD occurs in polygynous
groups and its effects increase as harem size (the number of females) increases. Simulation output further indicated that
population-level effects of Ebola are likely to differ among multi-male–multi-female chimpanzees and polygynous gorillas,
with larger overall numbers of chimpanzees infected, but more gorilla groups becoming infected due to increased dispersal
when the resident male dies. Collectively, our results highlight the importance of social system on the spread of disease
in wild mammals. 相似文献
2.
3.
Threonine is a precursor of glycine in the rat, but the metabolic pathway involved is unclear. To elucidate this pathway, the biosynthesis of glycine, and of aminoacetone, from L-threonine were studied in rat liver mitochondrial preparations of differing integrities. In the absence of added cofactors, intact mitochondria formed glycine and aminoacetone in approximately equal amounts from 20 mM L-threonine, but exogenous NAD+ decreased and CoA increased the ratio of glycine to aminoacetone formed. In intact and freeze-thawed mitochondria, the ratio of glycine to aminoacetone formed was markedly sensitive to the concentration of L-threonine, glycine being the major product at low L-threonine concentrations. Disruption of mitochondrial integrity by sonication (1 min) decreased the ratio of glycine to aminoacetone formed, and in 20000 X g supernatant fractions from sonicated (3 min) mitochondria, aminoacetone was the major product. The main non-nitogenous two-carbon compound detected when intact mitochondria catabolized L-threonine to glycine was acetate, which was probably derived from deacylation of acetyl-CoA. These results suggest that glycine formation from L-threonine in rat liver mitochondria occurred primarily by the coupled activities of threonine dehydrogenase and 2-amino-3-oxobutyrate CoA-ligase, the extent of coupling between the enzymes being dependent upon a close physical relationship and upon the flux through the dehydrogenase reaction. In vivo glycine synthesis would predominate, and aminoacetone would be a minor product. 相似文献
4.
Nucleotide sequence of the Methylobacterium extorquens AM1 moxF and moxJ genes involved in methanol oxidation 总被引:10,自引:0,他引:10
The nucleotide sequence has been determined for two genes involved in methanol oxidation in the facultative methylotroph, Methylobacterium extorquens AM1. The two genes are moxF, encoding the 66-kDa subunit of the methanol dehydrogenase and moxJ, located immediately downstream from moxF, which encodes a 30-kDa protein with unknown function. This information completes the sequence of the 5.86-kb XhoI-SalI fragment containing the moxFJGI region in M. extorquens AM1, and the structure of this gene cluster is presented. Evidence is presented that moxJ is also present in Paracoccus denitrificans. The aa sequence of MoxJ has provided little information concerning its function, but it does appear to contain a signal sequence suggesting a periplasmic location. 相似文献
5.
Molecular cloning of a malyl coenzyme A lyase gene from Pseudomonas sp. strain AM1, a facultative methylotroph 总被引:22,自引:21,他引:1 下载免费PDF全文
A genomic library containing HindIII partial digests of Pseudomonas sp. strain AM1 DNA was constructed in the broad-host-range cosmid pVK100. PCT57, a Pseudomonas sp. strain AM1 methanol mutant deficient in malyl coenzyme A lyase activity, was complemented to a methanol-positive phenotype by mobilization of the pVK100 library into PCT57 recipients with the ColE1/RK2 mobilizing plasmid pRK2013. Six different complemented isolates all contained a recombinant plasmid carrying the same 19.6-kilobase-pair Pseudomonas sp. strain AM1 DNA insert. Subcloning and complementation analysis demonstrated that the gene deficient in PCT57 (mcl-1) was located in a 1.6-kilobase-pair region within a 7.4-kilobase-pair EcoRI-HindIII fragment. 相似文献
6.
Mutations in the consensus ATP-binding sites of XcpR and PilB eliminate extracellular protein secretion and pilus biogenesis in Pseudomonas aeruginosa. 总被引:12,自引:4,他引:8 下载免费PDF全文
The process of extracellular secretion in Pseudomonas aeruginosa requires specialized machinery which is widely distributed among bacteria that actively secrete proteins to the extracellular medium. One of the components of this machinery is the product of the xcpR gene, which is homologous to pilB, a gene encoding a protein essential for the biogenesis of type IV pili. Both XcpR and PilB are characterized by the presence of a conserved ATP-binding motif (Walker sequence). The codons of highly conserved glycine residues within the Walker sequences of xcpR and pilB were altered to encode a serine, and the effects of these substitutions were examined. Bacteria expressing mutant XcpR or PilB were unable to secrete exotoxin A or assemble pili, respectively. In addition, high-level expression of mutant XcpR in wild-type P. aeruginosa led to a pleiotropic extracellular secretion defect, resulting in the periplasmic accumulation of enzymes that are normally secreted from the cell. These studies show that the putative ATP-binding sites of XcpR and PilB are essential for their functions in protein secretion and assembly of pili, respectively. Moreover, the observed dominant negative phenotype of mutant XcpR suggests that this protein functions as a multimer or, alternatively, interacts with another essential component of the extracellular protein secretion machinery. 相似文献
7.
Cleavage, methylation, and localization of the Pseudomonas aeruginosa export proteins XcpT, -U, -V, and -W. 总被引:9,自引:2,他引:7 下载免费PDF全文
Four components of the apparatus of extracellular protein secretion of Pseudomonas aeruginosa, Xcpt, -U, -V, and -W (XcpT-W), are synthesized as precursors with short N-terminal leader peptides that share sequence similarity with the pilin subunit of this organism. A specialized leader peptidase/methylase, product of the pilD gene, has been shown to cleave the leader peptide from prepilin and to methylate the N-terminal phenylalanine of the mature pilin. Antibodies were prepared against XcpT-W and used to purify each of these proteins. Sequence analysis of XcpT-W has shown that these proteins, like mature pilin, contain N-methylphenylalanine as the N-terminal amino acid. Analysis of cellular fractions from wild-type and pilD mutant strains of P. aeruginosa showed that the precursor forms of XcpT-W are located predominantly in the bacterial inner membrane, and their localization is not altered after PilD-mediated removal of the leader sequence. These studies demonstrate that the biogenesis of the apparatus of extracellular protein secretion and that of type IV pili share a requirement for PilD. This bifunctional enzyme, acting in the inner membrane, cleaves the leader peptides from precursors of pilins and XcpT-W and subsequently methylates the amino group of the N-terminal phenylalanine of each of its substrates. 相似文献
8.
Fc receptors on mouse effector cells mediating natural cytotoxicity against tumor cells. 总被引:6,自引:0,他引:6
R B Herberman S Bartram J S Haskill M Nunn H T Holden W H West 《Journal of immunology (Baltimore, Md. : 1950)》1977,119(1):322-326
Mouse effector cells mediating natural cytotoxicity against tumor cells have been previously thought to be lymphocytes that lack any detectable cell surface markers. The present study presents evidence for receptors for the Fc portion of IgG on these cells. By adsorption of cytotoxic spleen cells on monolayers of sheep erythrocytes (E) plus IgG antibodies to sheep erythrocytes (EA), 50 to 96% of the total cytotoxic reactivity could be removed. Parallel adsorption of cells on E monolayers or on EA monolayers coated with protein A, to block the Fc portion of IgG, resulted in little or no depletion of cytotoxic activity. The presence of Fc receptors on the NK cells was confirmed by combining EA rosette formation with velocity sedimentation at unit gravity. Peak cytotoxicity occurred at the same sedimentation velocity as the peak of Fc-positive cells. After EA rosette formation, there was a shift to a higher sedimentation velocity in the Fc-positive cells and in the natural cytotoxic activity. The increase in sedimentation velocity of NK activity that was observed in these experiments indicated that most of the cells had only bound a small number (three or four) of antibody-coated erythrocytes. Together, these data indicate that cells with Fc receptors account for most of the total lytic activity of normal mouse spleen cells. 相似文献
9.
10.
Mutants of Escherichia coli K-12 constitutive for fatty acid degradation (fadR) showed an increased rate of utilization of exogenous acetate. Acetate transport, oxidation, and incorporation into macromolecules was approximately fivefold greater in fadR mutants than fadR+ strains during growth on succinate as a carbon source. This effect was due to the elevated levels of glyoxylate shunt enzymes in fadR mutants, since (i) similar results were seen with mutants constitutive for the glyoxylate shunt enzymes (iclR), (ii) induction of the glyoxylate shunt in fadR+ strains by growth on acetate or oleate increased the rate of acetate utilization to levels comparable to those in fadR mutants, and (iii) fadR and fadR+ derivatives of mutants defective for the glyoxylate shunt enzymes showed equivalent rates of acetate utilization under these conditions. These results suggest that the operation of the glyoxylate shunt may play a significant role in the utilization of exogenous acetate by fadR mutants. 相似文献