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131.
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Species may survive under contemporary climate change by either shifting their range or adapting locally to the warmer conditions. Theoretical and empirical studies recently underlined that dispersal, the central mechanism behind these responses, may depend on the match between an individuals’ phenotype and local environment. Such matching habitat choice is expected to induce an adaptive gene flow, but it now remains to be studied whether this local process could promote species’ responses to climate change. Here, we investigate this by developing an individual‐based model including either random dispersal or temperature‐dependent matching habitat choice. We monitored population composition and distribution through space and time under climate change. Relative to random dispersal, matching habitat choice induced an adaptive gene flow that lessened spatial range loss during climate warming by improving populations’ viability within the range (i.e. limiting range fragmentation) and by facilitating colonization of new habitats at the cold margin. The model even predicted range contraction under random dispersal but range expansion under optimal matching habitat choice. These benefits of matching habitat choice for population persistence mostly resulted from adaptive immigration decision and were greater for populations with larger dispersal distance and higher emigration probability. We also found that environmental stochasticity resulted in suboptimal matching habitat choice, decreasing the benefits of this dispersal mode under climate change. However population persistence was still better under suboptimal matching habitat choice than under random dispersal. Our results highlight the urgent need to implement more realistic mechanisms of dispersal such as matching habitat choice into models predicting the impacts of ongoing climate change on biodiversity. 相似文献
133.
Katherine L. Helbig Robert J. Lauerer Jacqueline C. Bahr Ivana A. Souza Candace T. Myers Betül Uysal Niklas Schwarz Maria A. Gandini Sun Huang Boris Keren Cyril Mignot Alexandra Afenjar Thierry Billette de Villemeur Delphine Héron Caroline Nava Stéphanie Valence Julien Buratti Christina R. Fagerberg Heather C. Mefford 《American journal of human genetics》2019,104(3):562
134.
Yuki Takegawa Makoto Nakamura Shin Nakamura Takumi Noguchi Julien Sellés A. William Rutherford Alain Boussac Miwa Sugiura 《BBA》2019,1860(4):297-309
The monomeric chlorophyll, ChlD1, which is located between the PD1PD2 chlorophyll pair and the pheophytin, PheoD1, is the longest wavelength chlorophyll in the heart of Photosystem II and is thought to be the primary electron donor. Its central Mg2+ is liganded to a water molecule that is H-bonded to D1/T179. Here, two site-directed mutants, D1/T179H and D1/T179V, were made in the thermophilic cyanobacterium, Thermosynechococcus elongatus, and characterized by a range of biophysical techniques. The Mn4CaO5 cluster in the water-splitting site is fully active in both mutants. Changes in thermoluminescence indicate that i) radiative recombination occurs via the repopulation of *ChlD1 itself; ii) non-radiative charge recombination reactions appeared to be faster in the T179H-PSII; and iii) the properties of PD1PD2 were unaffected by this mutation, and consequently iv) the immediate precursor state of the radiative excited state is the ChlD1+PheoD1? radical pair. Chlorophyll bleaching due to high intensity illumination correlated with the amount of 1O2 generated. Comparison of the bleaching spectra with the electrochromic shifts attributed to ChlD1 upon QA? formation, indicates that in the T179H-PSII and in the WT*3-PSII, the ChlD1 itself is the chlorophyll that is first damaged by 1O2, whereas in the T179V-PSII a more red chlorophyll is damaged, the identity of which is discussed. Thus, ChlD1 appears to be one of the primary damage site in recombination-mediated photoinhibition. Finally, changes in the absorption of ChlD1 very likely contribute to the well-known electrochromic shifts observed at ~430?nm during the S-state cycle. 相似文献
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137.
Violette Azzoni Julien Wicinski Manon Macario Martin Castagn Pascal Finetti Katerina Ambrosova Clia D. Rouault Arnaud Serg Anne Farina Emilie Agavnian Sergiu Coslet Emmanuelle Josselin Arnaud Guille Jos Adelaide Emmanouil Zacharioudakis Rmy Castellano Francois Bertucci Daniel Birnbaum Raphael Rodriguez Emmanuelle Charafe-Jauffret Christophe Ginestier 《Cell death & disease》2022,13(2)
Replication stress (RS) has a pivotal role in tumor initiation, progression, or therapeutic resistance. In this study, we depicted the mechanism of breast cancer stem cells’ (bCSCs) response to RS and its clinical implication. We demonstrated that bCSCs present a limited level of RS compared with non-bCSCs in patient samples. We described for the first time that the spatial nuclear location of BMI1 protein triggers RS response in breast cancers. Hence, in bCSCs, BMI1 is rapidly located to stalled replication forks to recruit RAD51 and activate homologous-recombination machinery, whereas in non-bCSCs BMI1 is trapped on demethylated 1q12 megasatellites precluding effective RS response. We further demonstrated that BMI1/RAD51 axis activation is necessary to prevent cisplatin-induced DNA damage and that treatment of patient-derived xenografts with a RAD51 inhibitor sensitizes tumor-initiating cells to cisplatin. The comprehensive view of replicative-stress response in bCSC has profound implications for understanding and improving therapeutic resistance.Subject terms: Breast cancer, Cancer stem cells 相似文献
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139.
Sequence and structure of the mouse gene coding for the largest neurofilament subunit 总被引:17,自引:0,他引:17
We have determined the complete nucleotide sequence of the mouse gene encoding the neurofilament NF-H protein. The C-terminal domain of NF-H is very rich in charged amino acids (aa) and contains a 3-aa sequence, Lys-Ser-Pro, that is repeated 51 times within a stretch of 368 aa. The location of this serine-rich repeat in the phosphorylated domain of NF-H indicates that it represents the major protein kinase recognition site. The nfh gene shares two common intron positions with the nfl and nfm genes, but has an additional intron that occurs at a location equivalent to one of the introns in non-neuronal intermediate filament-coding genes. This additional nfh intron may have been acquired via duplication of a primordial intermediate filament gene. 相似文献
140.
The molecular mechanisms of toxicity associated with cytoplasmic accumulation of TAR DNA binding protein-43(TDP-43),a pathological feature of many neurodegenera... 相似文献