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31.
BACKGROUND: Amyloidoma (tumoral amyloidosis) is the rarest form of central nervous system (CNS) amyloidosis. CASE: A 51-year-old woman presented with recurrent right-sided otitis media and hearing loss. Computed tomography and magnetic resonance imaging revealed a mass in the right temporal lobe. Cytologic findings at the time of stereotactic biopsy for suspected glioma were compatible with amyloidoma. Subsequent histologic and electron microscopic findings confirmed the diagnosis of amyloidoma. Auxiliary testing ruled out systemic amyloidosis and plasma cell dyscrasia. CONCLUSION: To our knowledge, this is the first report on the cytologic findings in a case of CNS amyloidoma.  相似文献   
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The mesenchyme is a remarkably plastic tissue in the embryo. Recent studies have led to the discovery of mesenchymal cells in the adult organism that can differentiate in vitro into unexpected directions, beyond the well-known ability of the mesenchyme to give rise to mesodermal derivatives. These studies highlighted the plastic nature of the mesenchyme, also beyond the embryonic developmental stage. This review discusses the possible functions of the mesenchyme in the adult and the reason for the maintenance of plasticity throughout mammalian life. The properties of the mesenchymal cells clearly exemplify the stem state concept; cells, whether early or late in the differentiation cascade, may assume a stem state that entails high plasticity.  相似文献   
34.
The island rule and a research agenda for studying ecogeographical patterns   总被引:7,自引:4,他引:3  
We are currently experiencing a resurgence of interest in ecogeographical rules, which describe general trends in morphology and related traits along geographical gradients. In order to develop a more comprehensive understanding of the generality and underlying causal mechanisms for these patterns, we recommend a new, more integrated research agenda. In particular, we recommend studies that simultaneously consider different clines in morphology, geographical ranges and diversity as intricately related phenomena; all being ecological, evolutionary and biogeographical responses of organisms to selection regimes that vary non-randomly over space and time, and among species with different ecological and evolutionary histories.  相似文献   
35.
Human activities have elevated the extinction of natural populations as well as the invasion of new areas by non-native species. These dual processes of invasion and extinction may change the richness and similarity of communities, but the form these changes take is likely to depend on the manner in which invasions and extinctions occur and the spatial scale at which the changes are measured. Here, we explore the influence of differing patterns of extinction and invasion on the similarity and richness of a meta-community. In particular, we model simple stochastic processes analogous to realistic modes of human-mediated introduction of non-native species and range expansion by native species. We show that different modes of invasion and extinction can produce very different changes in diversity, and that the relative magnitude of these changes depends both on where in the meta-community diversity is measured and the degree of initial species aggregation. At any spatial scale of measurement, changes in the richness and similarity of communities following invasion and extinction are not necessarily strongly coupled: relatively large increases in richness may or may not also be associated with relatively large increases in similarity among communities. Thus, in real systems, the influence of human-induced invasions and extinctions on diversity will depend on both the precise mode of these processes (especially invasion), and how species populations are distributed across space.  相似文献   
36.
The tumor-suppressor protein p53 is among the most effective of the cell's natural defenses against cancer. In response to cellular stress, p53 binds as a tetramer to diverse DNA targets containing two decameric half-sites, thereby activating the expression of genes involved in cell-cycle arrest or apoptosis. Here we present high-resolution crystal structures of sequence-specific complexes between the core domain of human p53 and different DNA half-sites. In all structures, four p53 molecules self-assemble on two DNA half-sites to form a tetramer that is a dimer of dimers, stabilized by protein-protein and base-stacking interactions. The protein-DNA interface varies as a function of the specific base sequence in correlation with the measured binding affinities of the complexes. The new data establish a structural framework for understanding the mechanisms of specificity, affinity, and cooperativity of DNA binding by p53 and suggest a model for its regulation by regions outside the sequence-specific DNA binding domain.  相似文献   
37.
As the climate warms, boreal tree species are expected to be gradually replaced by temperate species within the southern boreal forest. Warming will be accompanied by changes in above- and below-ground consumers: large moose (Alces alces) replaced by smaller deer (Odocoileus virginianus) above-ground, and small detritivores replaced by larger exotic earthworms below-ground. These shifts may induce a cascade of ecological impacts across trophic levels that could alter the boreal to temperate forest transition. Deer are more likely to browse saplings of temperate tree species, and European earthworms favour seedlings of boreal tree species more than temperate species, potentially hindering the ability of temperate tree species to expand northwards. We hypothesize that warming-induced changes in consumers will lead to novel plant communities by changing the filter on plant species success, and that above- and below-ground cascades of trophic interactions will allow boreal tree species to persist during early phases of warming, leading to an abrupt change at a later time. The synthesis of evidence suggests that consumers can modify the climate change-induced transition of ecosystems.  相似文献   
38.
ABSTRACT: BACKGROUND: Insulin resistance (IR) is the major driving force behind development and progression of atherosclerosis in patients with nonalcoholic fatty liver disease (NAFLD). Therefore, correction of IR is a relevant therapeutic target. We performed the current trial to evaluate whether 12- month metformin therapy improves vascular stiffness in patients with NAFLD and to assess if this improvement is associated with change in glucose control, insulin resistance or circulating adiponectin. METHODS: In randomized, placebo controlled study, 63 patients with NAFLD were assigned to one of two groups: Group 1 received daily metformin; Group 2 received placebo. Central aortic augmentation index (AI) was performed using SphygmoCor (version 7.1, AtCor Medical, Sydney, Australia) at baseline, at 4-and 12-month treatment period. Metabolic parameters, insulin resistance markers and serum adiponectin levels were determined. RESULTS: In placebo group: AI did not improve during the treatment period. Liver function and adiponectin levels did not change during the study. In multiple linear regression analysis, the independent predictors of arterial stiffness improvement were metformin treatment and increase in circulating adiponectin levels. Among metformin treated patients: AI decreased significantly during the study. ALP and ALT decreased during initial 4-month treatment period, however raised to the pretreatment levels after 12 months. Serum adiponectin level tended to increase during treatment period with metformin. CONCLUSIONS: Metformin treatment was associated with significant decrease in AI during one year treatment in NAFLD patients. These beneficial vascular effects was associated with exposure to metformin per se as well as change in adiponectin levels suggesting that metformin may mediate its vascular effects via glicemic control-independent mechanisms.  相似文献   
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Myocardial infarction (MI) is a common complex disease with a genetic component. While several single nucleotide polymorphisms (SNPs) have been reported to be associated with risk of MI, they do not fully explain the observed genetic component of MI. We have been investigating the association between MI and SNPs that are located in genes and have the potential to affect gene function or expression. We have previously published studies that tested about 12,000 SNPs for association with risk of MI, early-onset MI, or coronary stenosis. In the current study we tested 17,576 SNPs that could affect gene function or expression. In order to use genotyping resources efficiently, we staged the testing of these SNPs in three case-control studies of MI. In the first study (762 cases, 857 controls) we tested 17,576 SNPs and found 1,949 SNPs that were associated with MI (P<0.05). We tested these 1,949 SNPs in a second study (579 cases and 1159 controls) and found that 24 SNPs were associated with MI (1-sided P<0.05) and had the same risk alleles in the first and second study. Finally, we tested these 24 SNPs in a third study (475 cases and 619 controls) and found that 5 SNPs in 4 genes (ENO1, FXN (2 SNPs), HLA-DPB2, and LPA) were associated with MI in the third study (1-sided P<0.05), and had the same risk alleles in all three studies. The false discovery rate for this group of 5 SNPs was 0.23. Thus, we have identified 5 SNPs that merit further examination for their potential association with MI. One of these SNPs (in LPA), has been previously shown to be associated with risk of cardiovascular disease in other studies.  相似文献   
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