全文获取类型
收费全文 | 2316篇 |
免费 | 165篇 |
国内免费 | 112篇 |
专业分类
2593篇 |
出版年
2024年 | 5篇 |
2023年 | 22篇 |
2022年 | 66篇 |
2021年 | 122篇 |
2020年 | 88篇 |
2019年 | 83篇 |
2018年 | 75篇 |
2017年 | 64篇 |
2016年 | 107篇 |
2015年 | 136篇 |
2014年 | 154篇 |
2013年 | 190篇 |
2012年 | 194篇 |
2011年 | 179篇 |
2010年 | 114篇 |
2009年 | 90篇 |
2008年 | 114篇 |
2007年 | 109篇 |
2006年 | 90篇 |
2005年 | 68篇 |
2004年 | 64篇 |
2003年 | 57篇 |
2002年 | 61篇 |
2001年 | 39篇 |
2000年 | 37篇 |
1999年 | 30篇 |
1998年 | 13篇 |
1997年 | 15篇 |
1996年 | 17篇 |
1995年 | 17篇 |
1994年 | 11篇 |
1993年 | 12篇 |
1992年 | 23篇 |
1991年 | 17篇 |
1990年 | 14篇 |
1989年 | 9篇 |
1988年 | 13篇 |
1987年 | 11篇 |
1986年 | 12篇 |
1985年 | 5篇 |
1984年 | 4篇 |
1983年 | 5篇 |
1982年 | 4篇 |
1980年 | 5篇 |
1975年 | 4篇 |
1973年 | 4篇 |
1971年 | 3篇 |
1969年 | 3篇 |
1968年 | 2篇 |
1967年 | 2篇 |
排序方式: 共有2593条查询结果,搜索用时 0 毫秒
111.
112.
Shin KH Kim RH Kang MK Kim RH Kim SG Lim PK Yochim JM Baluda MA Park NH 《DNA Repair》2007,6(6):830-840
Many studies have suggested the involvement of wild-type (wt) p53 in the repair of DNA double-strand breaks (DSBs) via DNA end-joining (EJ) process. To investigate this possibility, we compared the capacity and fidelity of DNA EJ in RKO cells containing wt p53 and RKO cells containing no p53 (RKO cells with p53 knockdown). The p53 knockdown cells showed lower fidelity of DNA EJ compared to the control RKO cells. The DNA end-protection assay revealed the association of a protein complex including heterogeneous nuclear ribonucleoprotein G (hnRNP G) with the DNA ends in RKO cells containing wt p53, but not with the DNA ends in RKO cells with p53 knockdown. Depletion of endogenous hnRNP G notably diminished the fidelity of EJ in RKO cells expressing wt p53. Moreover, an ectopic expression of hnRNP G significantly enhanced the fidelity of DNA EJ and the protection of DNA ends in human cancer cells lacking hnRNP G protein or containing mutant hnRNP G. Finally, using recombinant hnRNP G proteins, we demonstrated the hnRNP G protein is able to bind to and protect DNA ends from degradation of nucleases. Our results suggest that wt p53 modulates DNA DSB repair by, in part, inducing hnRNP G, and the ability of hnRNP G to bind and protect DNA ends may contribute its ability to promote the fidelity of DNA EJ. 相似文献
113.
Zhu Jing Zeng Zhaofu Xiong Mengqing Mo Huaheng Jin Meng Hu Ke 《Sleep and biological rhythms》2022,20(3):421-429
Sleep and Biological Rhythms - The relationship between plasma orexin A (OXA) levels and cognitive function in patients with obstructive sleep apnea (OSA) remains unclear. This study aimed to... 相似文献
114.
115.
ZhouWu Shu XiaoCong Zhang Li Zheng GuoNing Zeng You Mo Min Yu Xin Zhang XueRui Tan 《Journal of cellular biochemistry》2019,120(5):7211-7221
116.
117.
118.
Xue Min Mengyun Cai Tong Shao Ziyang Xu Zhaofu Liao Dongliang Liu Mengyuan Zhou Weipeng Wu Yulan Zhou Miaohua Mo Shun Xu Xinguang Liu Xingdong Xiong 《Aging cell》2022,21(1)
Circular RNAs (circRNAs) have been established to be involved in numerous processes in the human genome, but their function in vascular aging remains largely unknown. In this study, we aimed to characterize and analyze the function of a circular intronic RNA, ciPVT1, in endothelial cell senescence. We observed significant downregulation of ciPVT1 in senescent endothelial cells. In proliferating endothelial cells, ciPVT1 knockdown induced a premature senescence‐like phenotype, inhibited proliferation, and led to an impairment in angiogenesis. An in vivo angiogenic plug assay revealed that ciPVT1 silencing significantly inhibited endothelial tube formation and decreased hemoglobin content. Conversely, overexpression of ciPVT1 in old endothelial cells delayed senescence, promoted proliferation, and increased angiogenic activity. Mechanistic studies revealed that ciPVT1 can sponge miR‐24‐3p to upregulate the expression of CDK4, resulting in enhanced Rb phosphorylation. Moreover, enforced expression of ciPVT1 reversed the senescence induction effect of miR‐24‐3p in endothelial cells. In summary, the present study reveals a pivotal role for ciPVT1 in regulating endothelial cell senescence and may have important implications in the search of strategies to counteract the development of age‐associated vascular pathologies. 相似文献
119.
120.
Feng Guo Chengchun Tang Bo Huang Lifei Gu Jun Zhou Zongyang Mo Chang Liu Yuqing Liu 《Molecules and cells》2022,45(3):122
The aim of this study was to investigating whether lncRNA H19 promotes myocardial fibrosis by suppressing the miR-29a-3p/miR-29b-3p-VEGFA/TGF-β axis. Patients with atrial fibrillation (AF) and healthy volunteers were included in the study, and their biochemical parameters were collected. In addition, pcDNA3.1-H19, si-H19, and miR-29a/b-3p mimic/inhibitor were transfected into cardiac fibroblasts (CFs), and proliferation of CFs was detected by MTT assay. Expression of H19 and miR-29a/b-3p were detected using real-time quantitative polymerase chain reaction, and expression of α-smooth muscle actin (α-SMA), collagen I, collagen II, matrix metalloproteinase-2 (MMP-2), and elastin were measured by western blot analysis. The dual luciferase reporter gene assay was carried out to detect the sponging relationship between H19 and miR-29a/b-3p in CFs. Compared with healthy volunteers, the level of plasma H19 was significantly elevated in patients with AF, while miR-29a-3p and miR-29b-3p were markedly depressed (P < 0.05). Serum expression of lncRNA H19 was negatively correlated with the expression of miR-29a-3p and miR-29b-3p among patients with AF (rs = –0.337, rs = –0.236). Moreover, up-regulation of H19 expression and down-regulation of miR-29a/b-3p expression facilitated proliferation and synthesis of extracellular matrix (ECM)-related proteins. SB431542 and si-VEGFA are able to reverse the promotion of miR-29a/b-3p on proliferation of CFs and ECM-related protein synthesis. The findings of the present study suggest that H19 promoted CF proliferation and collagen synthesis by suppressing the miR-29a-3p/miR-29b-3p-VEGFA/TGF-β axis, and provide support for a potential new direction for the treatment of AF. 相似文献