全文获取类型
收费全文 | 28294篇 |
免费 | 2296篇 |
国内免费 | 2223篇 |
专业分类
32813篇 |
出版年
2024年 | 77篇 |
2023年 | 409篇 |
2022年 | 924篇 |
2021年 | 1546篇 |
2020年 | 1018篇 |
2019年 | 1245篇 |
2018年 | 1178篇 |
2017年 | 866篇 |
2016年 | 1234篇 |
2015年 | 1792篇 |
2014年 | 2130篇 |
2013年 | 2232篇 |
2012年 | 2655篇 |
2011年 | 2277篇 |
2010年 | 1411篇 |
2009年 | 1121篇 |
2008年 | 1488篇 |
2007年 | 1239篇 |
2006年 | 1088篇 |
2005年 | 931篇 |
2004年 | 764篇 |
2003年 | 644篇 |
2002年 | 586篇 |
2001年 | 491篇 |
2000年 | 379篇 |
1999年 | 430篇 |
1998年 | 255篇 |
1997年 | 218篇 |
1996年 | 255篇 |
1995年 | 205篇 |
1994年 | 252篇 |
1993年 | 152篇 |
1992年 | 220篇 |
1991年 | 183篇 |
1990年 | 174篇 |
1989年 | 113篇 |
1988年 | 83篇 |
1987年 | 75篇 |
1986年 | 49篇 |
1985年 | 63篇 |
1984年 | 48篇 |
1983年 | 39篇 |
1982年 | 37篇 |
1981年 | 24篇 |
1980年 | 16篇 |
1979年 | 25篇 |
1977年 | 15篇 |
1976年 | 16篇 |
1975年 | 15篇 |
1973年 | 17篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
41.
The lesions induced in Bacillus subtilis deoxyribonucleic acid (DNA) after treating bacterial cells (in vivo) and bacterial DNA (in vitro) with chloramine were studied biologically and physically. Single-strand breaks and a few double-strand scissions (at higher chloramine doses) accompanied loss of DNA-transforming activity in both kinds of treatments. Chloramine was about three times more efficient in vitro than in vivo in inducing DNA single-strand breaks. DNA was slowly chlorinated; the subsequent efficiency of producing DNA breaks was high. Chlorination of cells also reduced activity of endonucleases in cells; however, chlorinated DNA of both treatments was sensitized to cleavage by endonucleases. The procedure of extracting DNA from cells treated with chloramine induced further DNA degradation. Both treatments introduced a small fraction of alkali-sensitive lesions in DNA. DNA chlorinated in vitro showed further reduction in transforming activity as well as further degradation after incubation at 50 C for 5 h whereas DNA extracted from chloramine-treated cells did not show such a heat sensitivity. 相似文献
42.
43.
44.
A subsystem impactor test for pedestrian lower limb injury evaluation has been brought in China New Car Assessment Protocol(CNCAP).Concerning large anthropometr... 相似文献
45.
46.
Qiang Lv Shuang Han Lei Wang Jinchan Xia Peng Li Ruoyang Hu Jinzheng Wang Lei Gao Yuli Chen Yu Wang Jing Du Fang Bao Yong Hu Xingzhi Xu Wei Xiao Yikun He 《Nucleic acids research》2022,50(12):6820
Nitric oxide (NO) is a key player in numerous physiological processes. Excessive NO induces DNA damage, but how plants respond to this damage remains unclear. We screened and identified an Arabidopsis NO hypersensitive mutant and found it to be allelic to TEBICHI/POLQ, encoding DNA polymerase θ. The teb mutant plants were preferentially sensitive to NO- and its derivative peroxynitrite-induced DNA damage and subsequent double-strand breaks (DSBs). Inactivation of TEB caused the accumulation of spontaneous DSBs largely attributed to endogenous NO and was synergistic to DSB repair pathway mutations with respect to growth. These effects were manifested in the presence of NO-inducing agents and relieved by NO scavengers. NO induced G2/M cell cycle arrest in the teb mutant, indicative of stalled replication forks. Genetic analyses indicate that Polθ is required for translesion DNA synthesis across NO-induced lesions, but not oxidation-induced lesions. Whole-genome sequencing revealed that Polθ bypasses NO-induced base adducts in an error-free manner and generates mutations characteristic of Polθ-mediated end joining. Our experimental data collectively suggests that Polθ plays dual roles in protecting plants from NO-induced DNA damage. Since Polθ is conserved in higher eukaryotes, mammalian Polθ may also be required for balancing NO physiological signaling and genotoxicity. 相似文献
47.
Aaron Mendez-Bermudez Liudmyla Lototska Melanie Pousse Florent Tessier Oliver Croce Chrysa
M Latrick Veronica Cherdyntseva Joe Nassour Jiang Xiaohua Yiming Lu Corinne Abbadie Sarantis Gagos Jing Ye Eric Gilson 《Nucleic acids research》2022,50(13):7493
Cellular senescence triggers various types of heterochromatin remodeling that contribute to aging. However, the age-related mechanisms that lead to these epigenetic alterations remain elusive. Here, we asked how two key aging hallmarks, telomere shortening and constitutive heterochromatin loss, are mechanistically connected during senescence. We show that, at the onset of senescence, pericentromeric heterochromatin is specifically dismantled consisting of chromatin decondensation, accumulation of DNA breakages, illegitimate recombination and loss of DNA. This process is caused by telomere shortening or genotoxic stress by a sequence of events starting from TP53-dependent downregulation of the telomere protective protein TRF2. The resulting loss of TRF2 at pericentromeres triggers DNA breaks activating ATM, which in turn leads to heterochromatin decondensation by releasing KAP1 and Lamin B1, recombination and satellite DNA excision found in the cytosol associated with cGAS. This TP53–TRF2 axis activates the interferon response and the formation of chromosome rearrangements when the cells escape the senescent growth arrest. Overall, these results reveal the role of TP53 as pericentromeric disassembler and define the basic principles of how a TP53-dependent senescence inducer hierarchically leads to selective pericentromeric dismantling through the downregulation of TRF2. 相似文献
48.
49.
Lihua Qu Yi Li Chao Chen Tong Yin Qian Fang Yijin Zhao Wenting Lv Ziqi Liu Yangye Chen Li Shen 《Cell death & disease》2022,13(8)
Acute lung injury (ALI) is a potentially life-threatening, devastating disease with an extremely high rate of mortality. The underlying mechanism of ALI is currently unclear. In this study, we aimed to confirm the hub genes associated with ALI and explore their functions and molecular mechanisms using bioinformatics methods. Five microarray datasets available in GEO were used to perform Robust Rank Aggregation (RRA) to identify differentially expressed genes (DEGs) and the key genes were identified via the protein-protein interaction (PPI) network. Lipopolysaccharide intraperitoneal injection was administered to establish an ALI model. Overall, 40 robust DEGs, which are mainly involved in the inflammatory response, protein catabolic process, and NF-κB signaling pathway were identified. Among these DEGs, we identified two genes associated with ALI, of which the CAV-1/NF-κB axis was significantly upregulated in ALI, and was identified as one of the most effective targets for ALI prevention. Subsequently, the expression of CAV-1 was knocked down using AAV-shCAV-1 or CAV-1-siRNA to study its effect on the pathogenesis of ALI in vivo and in vitro. The results of this study indicated that CAV-1/NF-κB axis levels were elevated in vivo and in vitro, accompanied by an increase in lung inflammation and autophagy. The knockdown of CAV-1 may improve ALI. Mechanistically, inflammation was reduced mainly by decreasing the expression levels of CD3 and F4/80, and activating autophagy by inhibiting AKT/mTOR and promoting the AMPK signaling pathway. Taken together, this study provides crucial evidence that CAV-1 knockdown inhibits the occurrence of ALI, suggesting that the CAV-1/NF-κB axis may be a promising therapeutic target for ALI treatment.Subject terms: Cell signalling, Respiratory tract diseases 相似文献
50.