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111.
Two approaches towards the synthesis of phosphine ligated half-sandwich complexes [(ηx-CxHx)M(PR3)2GaI2]n containing diiodogallyl ligands have been investigated. Insertion of ‘GaI’ into the Mo-I bond of (η7-C7H7)Mo(CO)2I has been shown to yield the crystallographically characterized dimeric complex [(η7-C7H7)Mo(CO)2GaI2]2 (2). Attempts to substitute the carbonyl ligands by the phosphine ligand dppe [dppe = bis(diphenylphosphino)ethane] have been shown instead to yield the sparingly soluble complex [(η7-C7H7)Mo(CO)2GaI2]2(μ-dppe) (3) in which the phosphine bridges two [(η7-C7H7)Mo(CO)2GaI2] units via a pair of P → Ga donor/acceptor bonds. By contrast, attempts to insert ‘GaI’ directly into the metal-halogen bond of phosphine ligated complexes such as (η5-C5H5)Ru(PPh3)2Cl or (η5-C5H5)Ru(dppe)Cl have been shown to result in the formation of the tetraiodogallate species(η5-C5H5)Ru(PPh3)2(μ-I)GaI3 (5) and [(η5-C5H5)Ru(dppe)]+[GaI4]− (7). 相似文献
112.
Flagellar assembly proceeds in a sequential manner, beginning at the base and concluding with the filament. A critical aspect of assembly is that gene expression is coupled to assembly. When cells transition from a nonflagellated to a flagellated state, gene expression is sequential, reflecting the manner in which the flagellum is made. A key mechanism for establishing this temporal hierarchy is the sigma(28)-FlgM checkpoint, which couples the expression of late flagellar (P(class3)) genes to the completion of the hook-basal body. In this work, we investigated the role of FliZ in coupling middle flagellar (P(class2)) gene expression to assembly in Salmonella enterica serovar Typhimurium. We demonstrate that FliZ is an FlhD(4)C(2)-dependent activator of P(class2)/middle gene expression. Our results suggest that FliZ regulates the concentration of FlhD(4)C(2) posttranslationally. We also demonstrate that FliZ functions independently of the flagellum-specific sigma factor sigma(28) and the filament-cap chaperone/FlhD(4)C(2) inhibitor FliT. Furthermore, we show that the previously described ability of sigma(28) to activate P(class2)/middle gene expression is, in fact, due to FliZ, as both are expressed from the same overlapping P(class2) and P(class3) promoters at the fliAZY locus. We conclude by discussing the role of FliZ regulation with respect to flagellar biosynthesis based on our characterization of gene expression and FliZ's role in swimming and swarming motility. 相似文献
113.
114.
Flagellar gene expression is temporally regulated in response to the assembly state of the growing flagellum. The key mechanism for enforcing this temporal hierarchy in Salmonella enterica serovar Typhimurium is the sigma(28)-FlgM checkpoint, which couples the expression of the late flagellar (P(class3)) genes to the completion of the hook-basal body. This checkpoint is triggered when FlgM is secreted from the cell. In addition to the sigma(28)-FlgM checkpoint, a number of other regulatory mechanisms respond to the secretion of late proteins. In this work, we examined how middle (P(class2)) and late (P(class3)) gene expression is affected by late protein secretion. Dynamic analysis of flagellar gene expression identified a novel mechanism where induction of P(class2) activity is delayed either when late protein secretion is abolished or when late protein secretion is increased. Using a number of different approaches, we were able to show that this mechanism did not involve any known flagellar regulator. Furthermore, the changes in P(class2) activity were not correlated with the associated changes in P(class3) activity, which was found to be proportional to late protein secretion rates. Our data indicate that both P(class2) and P(class3) promoters are continuously regulated in response to assembly and late protein secretion rates. These results suggest that flagellar regulation is more complex than previously thought. 相似文献
115.
Anthony Ricciardi Tim M. Blackburn James T. Carlton Jaimie T.A. Dick Philip E. Hulme Josephine C. Iacarella Jonathan M. Jeschke Andrew M. Liebhold Julie L. Lockwood Hugh J. MacIsaac Petr Pyšek David M. Richardson Gregory M. Ruiz Daniel Simberloff William J. Sutherland David A. Wardle David C. Aldridge 《Trends in ecology & evolution》2017,32(11):809-810
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117.
Numerous reports have described a steady overall increase in resistance among clinical isolates of the Bacteroides fragilis group to several antimicrobial agents, particularly clindamycin. Determination of resistance rates is significantly influenced by the number of isolates of each species within the B. fragilis group tested. Historically, the B. fragilis species has remained the most susceptible to most antimicrobials when compared to non-B. fragilis species. This study compares the effect of a gradually changing ratio of blood isolates of B. fragilis to non-B. fragilis species tested by broth micro-dilution over a 12-year period on selected antimicrobial agents. In 1987, the ratio of blood isolates of B. fragilis to non-B. fragilis was 68% to 32%; in 1991 it was 59% to 41%; and in 1999 it was 51% to 49%. Both metronidazole and imipenem showed the least changes because of their inherent high activity against all species. For clindamycin, decreases in susceptibility ranged from 84% to 64% for B. fragilis compared to 58% to 67% for non-B. fragilis species. Ampicillin-sulbactam showed a decrease in susceptibility in B. fragilis and non-B. fragilis species, but was highest in 1999 when the ratio of non-B. fragilis species was the highest. Overall resistance rates to cefoxitin varied from 8% to 25% during the testing years and was consistently higher among the non-B. fragilis species. These comparisons indicate that the ratio of B. fragilis group species isolated from the blood has changed over the last 12 years and has appreciably affected the resistance rates to some commonly used anti-anaerobic agents. Whether the noted changes in species isolation rates are a result of selective antibiotic pressure or other factors is yet to be determined. 相似文献
118.
Apoptosis in response to TRAIL or TNF requires the activation of initiator caspases, which then activate the effector caspases that dismantle cells and cause death. However, little is known about the dynamics and regulatory logic linking initiators and effectors. Using a combination of live-cell reporters, flow cytometry, and immunoblotting, we find that initiator caspases are active during the long and variable delay that precedes mitochondrial outer membrane permeabilization (MOMP) and effector caspase activation. When combined with a mathematical model of core apoptosis pathways, experimental perturbation of regulatory links between initiator and effector caspases reveals that XIAP and proteasome-dependent degradation of effector caspases are important in restraining activity during the pre-MOMP delay. We identify conditions in which restraint is impaired, creating a physiologically indeterminate state of partial cell death with the potential to generate genomic instability. Together, these findings provide a quantitative picture of caspase regulatory networks and their failure modes. 相似文献
119.
Positions of multiple insertions in SSU rDNA of lichen-forming fungi 总被引:11,自引:3,他引:8
Lichen-forming fungi, in symbiotic associations with algae, frequently have
nuclear small subunit ribosomal DNA (SSU rDNA) longer than the 1,800
nucleotides typical for eukaryotes. The lichen-forming ascomycetous fungus
Lecanora dispersa contains insertions at eight distinct positions of its
SSU rDNA; the lichen-forming fungi Calicium tricolor and Porpidia
crustulata each contain one insertion. Insertions are not limited to fungi
that form lichens; the lichen ally Mycocalicium albonigrum also contains
two insertions. Of the 11 insertion positions now reported for
lichen-forming fungi and this ally, 6 positions are known only from
lichen-forming fungi. Including the 4 newly reported in this study,
insertions are now known from at least 17 positions among all reported SSU
rDNA sequences. Insertions, most of which are Group I introns, are reported
in fungal and protistan lineages and occur at corresponding positions in
genomes as phylogenetically distant as the nuclei of fungi, green algae,
and red algae. Many of these positions are exposed in the mature rRNA
tertiary structure and may be subject to independent insertion of introns.
Insertion of introns, accompanied by their sporadic loss, accounts for the
scattered distribution of insertions observed within the SSU rDNA of these
diverse organisms.
相似文献
120.
The extent of polylactosamine glycosylation of MDCK LAMP-2 is determined by its Golgi residence time 总被引:2,自引:1,他引:1
The increased polylactosamine glycosylation of LAMP-2 in MDCK cells
cultured for 1 day relative to cells cultured for 3 days has been
correlated with its slower rate of Golgi transit (Nabi and Rodriguez-
Boulan, 1993, Mol. Biol. Cell., 4, 627-635). To determine if the
differential polylactosamine glycosylation of LAMP-2 is a consequence of
glycosyltransferase expression levels, the activities of beta1- 6GlcNAc-TV,
beta1-3GlcNAc-T(i), beta1-2GlcNAc-TI, beta1, 4Gal-T, alpha2- 6sialyl-T, and
alpha2-3sialyl-T were assayed and no significant differences in the
activities of these enzymes in 1 and 3 day cell extracts were detected.
During MDCK epithelial polarization, the Golgi apparatus undergoes
morphological changes and apiconuclear Golgi networks were more evident in
3 day cells. Treatment with nocodazole disrupted Golgi networks and
generated numerous Golgi clusters in both 1 day and 3 day cells. In the
presence of nocodazole the differential migration of LAMP-2 in 1 and 3 day
MDCK cells was maintained and could be eliminated by treatment with
endo-beta-galactosidase, indicating that gross Golgi morphology did not
influence the extent of LAMP-2 polylactosamine glycosylation. Nocodazole
treatment did, however, result in the faster migration of LAMP-2 which was
not due to modification of core N-glycans as the precursor form of the
glycoprotein migrated with an identical molecular size. Following
incubation at 20 degrees C, which prevents the exit of proteins from the
trans-Golgi network, the molecular size of LAMP-2 increased to a similar
extent in both 1 and 3 day MDCK cells. Extending the time of incubation at
20 degrees C did not influence the size of LAMP-2, demonstrating that its
glycosylation is modified not by its retention within the Golgi but rather
by its equivalent slower Golgi passage at the lower temperature in both 1
and 3 day cells. An identical effect was observed in nocodazole treated
cells, demonstrating that Golgi residence time determines the extent of
LAMP-2 polylactosamine glycosylation, even in isolated Golgi clusters.
相似文献