全文获取类型
收费全文 | 779篇 |
免费 | 74篇 |
出版年
2022年 | 6篇 |
2021年 | 13篇 |
2020年 | 7篇 |
2019年 | 7篇 |
2018年 | 8篇 |
2017年 | 11篇 |
2016年 | 16篇 |
2015年 | 24篇 |
2014年 | 29篇 |
2013年 | 29篇 |
2012年 | 43篇 |
2011年 | 39篇 |
2010年 | 19篇 |
2009年 | 23篇 |
2008年 | 29篇 |
2007年 | 36篇 |
2006年 | 30篇 |
2005年 | 21篇 |
2004年 | 17篇 |
2003年 | 16篇 |
2002年 | 12篇 |
2001年 | 21篇 |
2000年 | 24篇 |
1999年 | 9篇 |
1998年 | 13篇 |
1996年 | 7篇 |
1992年 | 7篇 |
1991年 | 12篇 |
1990年 | 9篇 |
1989年 | 7篇 |
1988年 | 8篇 |
1987年 | 11篇 |
1986年 | 11篇 |
1985年 | 15篇 |
1984年 | 6篇 |
1982年 | 15篇 |
1981年 | 6篇 |
1980年 | 11篇 |
1978年 | 10篇 |
1974年 | 8篇 |
1973年 | 9篇 |
1972年 | 17篇 |
1971年 | 7篇 |
1970年 | 7篇 |
1969年 | 8篇 |
1966年 | 8篇 |
1940年 | 6篇 |
1922年 | 6篇 |
1920年 | 6篇 |
1917年 | 5篇 |
排序方式: 共有853条查询结果,搜索用时 15 毫秒
31.
Gonzalez-Voyer A Székely T Drummond H 《Evolution; international journal of organic evolution》2007,61(8):1946-1955
In many parentally fed species, siblings compete for food not only by begging and scrambling, but also by violently attacking each other. This aggressive competition has mostly been studied in birds, where it is often combined with dominance subordination, aggressive intimidation, and siblicide. Previous experimental and theoretical studies proposed several life-history, morphological, and behavioral variables that may facilitate the evolution of broodmate aggression, and explain its taxonomic distribution. Here we apply phylogenetic comparative analyses for the first time to test the influence of five hypothesized facilitators of the evolution of broodmate aggression, analyzing 69 species in seven avian families using two quantitative measures of aggression: incidence and intensity. We show that incidence and intensity of aggression increase with long nestling periods and indirect feeding, and small brood size is associated with intense aggression. Large food parcels were not correlated with either the incidence or intensity of aggression. Our study suggests that indirect feeding, long nestling periods, and small broods, possibly in combination with other factors, have tended to favor the evolution of aggressive broodmate competition. 相似文献
32.
Kiseleva E Allen TD Rutherford SA Murray S Morozova K Gardiner F Goldberg MW Drummond SP 《Nature protocols》2007,2(8):1943-1953
This protocol details methods for the isolation of yeast nuclei from budding yeast (Saccharomyces cerevisiae) and fission yeast (Schizosaccharomyces pombe), immuno-gold labeling of proteins and visualization by field emission scanning electron microscopy (FESEM). This involves the removal of the yeast cell wall and isolation of the nucleus from within, followed by subsequent processing for high-resolution microscopy. The nuclear isolation step can be performed in two ways: enzymatic treatment of yeast cells to rupture the cell wall and generate spheroplasts (cells that have partially lost their cell wall and their characteristic shape), followed by isolation of the nuclei by centrifugation or homogenization; and whole cell freezing followed by manual cell rupture and centrifugation. This protocol has been optimized for the visualization of the yeast nuclear envelope (NE), nuclear pore complexes (NPCs) and associated cyto-skeletal structures. Samples once processed for FESEM can be stored under vacuum for weeks, allowing considerable time for image acquisition. 相似文献
33.
34.
We have improved the expression of recombinant human granulocyte-colony-stimulating factor (G-CSF), produced by either pL or trpP expression vectors in Escherichia coli, by altering the sequence at the 5' end of the G-CSF-coding region. Initial attempts to express G-CSF resulted in neither detectable G-CSF mRNA nor protein in the trpP system, and only G-CSF mRNA was detectable in the pL system. We modified both expression vectors to decrease the G + C content of the 5' end of the coding region without altering the predicted amino acid sequence. This resulted in expression of detectable G-CSF mRNA and protein in both systems. Expression reached 17% and 6.5% of the total soluble cellular protein in the pL and trpP expression systems, respectively. The N-terminal sequence of the recombinant G-CSF from the pL system was Met-Thr-Pro-Leu-Gly-Pro-. G-CSF isolated from several human cell lines (including the LD-1 cell line reported here), does not have an N-terminal methionyl residue. Deletion of the threonine codon at the beginning of the coding region for the mature G-CSF resulted in efficient removal of the N-terminal methionine residue during expression in E. coli. 相似文献
35.
Loss of the human DNA mismatch repair pathway confers cross-resistance to structurally unrelated anticancer drugs. Examples include cisplatin, doxorubicin (adriamycin), and specific alkylating agents. We focused on defining the molecular events that link adriamycin to mismatch repair-dependent drug resistance because adriamycin, unlike drugs that covalently modify DNA, can interact reversibly with DNA. We found that adriamycin, nogalamycin, and actinomycin D comprise a class of drugs that reversibly inhibits human mismatch repair in vitro at low micromolar concentrations. The substrate DNA was not covalently modified by adriamycin treatment in a way that prevents repair, and the inhibition was independent of the number of intercalation sites separating the mismatch and the DNA nick used to direct repair, from 10 to 808 base pairs. Over the broad concentration range tested, there was no evidence for recognition of intercalated adriamycin by MutSalpha as if it were an insertion mismatch. Inhibition apparently results from the ability of the intercalated drug to prevent mismatch binding, shown using a defined mobility shift assay, which occurs at drug concentrations that inhibit repair. These data suggest that adriamycin interacts with the mismatch repair pathway through a mechanism distinct from the manner by which covalent DNA lesions are processed. 相似文献
36.
37.
38.
39.
Seatter MJ Drummond R Kanke T Macfarlane SR Hollenberg MD Plevin R 《Cellular signalling》2004,16(1):21-29
C-terminal truncation mutants were made to investigate the role of the C-terminus in coupling proteinase-activated receptor-2 (PAR-2) to various signalling pathways. Membrane expression of the delta15, delta34, delta43, and delta34-43 mutants was similar; however, expression of deltatail was lost, as was agonist-mediated internalisation of deltatail, delta43, and delta34-43. Additionally, trypsin and SLIGKV-stimulated [3H]IP accumulation was abrogated in cells transiently expressing delta43 or delta34-43 truncations, but remained unaffected in cells expressing delta34 or delta15. PAR-2 agonist-stimulated intracellular Ca(2+) mobilisation and PYK-2 activity were also abolished by deltatail, delta43, and delta34-43 mutants. However, trypsin-stimulated stress-activated protein kinases (SAPKs) or extracellular signal-regulated kinase (ERK) activities were unaffected by the delta34-43 mutation, although activity was abrogated following delta43 or deltatail truncations, suggesting that Ca(2+) mobilisation, PYK-2, or receptor internalisation are not requied for activation of SAPKs or ERK. These studies identify a novel sequence within the PAR-2 C-terminus essential for InsP(3) generation and PYK-2 activity but not mitogen-activated protein kinase (MAPK) activation. 相似文献
40.