全文获取类型
收费全文 | 45634篇 |
免费 | 6038篇 |
国内免费 | 22101篇 |
出版年
2024年 | 458篇 |
2023年 | 1349篇 |
2022年 | 2215篇 |
2021年 | 2524篇 |
2020年 | 2458篇 |
2019年 | 2920篇 |
2018年 | 2083篇 |
2017年 | 1918篇 |
2016年 | 2175篇 |
2015年 | 2854篇 |
2014年 | 3934篇 |
2013年 | 3585篇 |
2012年 | 4780篇 |
2011年 | 4784篇 |
2010年 | 3835篇 |
2009年 | 3764篇 |
2008年 | 4075篇 |
2007年 | 3813篇 |
2006年 | 3576篇 |
2005年 | 3067篇 |
2004年 | 2445篇 |
2003年 | 2092篇 |
2002年 | 1860篇 |
2001年 | 1627篇 |
2000年 | 1471篇 |
1999年 | 931篇 |
1998年 | 567篇 |
1997年 | 378篇 |
1996年 | 300篇 |
1995年 | 228篇 |
1994年 | 170篇 |
1993年 | 159篇 |
1992年 | 156篇 |
1991年 | 150篇 |
1990年 | 113篇 |
1989年 | 92篇 |
1988年 | 115篇 |
1987年 | 82篇 |
1986年 | 74篇 |
1985年 | 80篇 |
1984年 | 62篇 |
1983年 | 47篇 |
1982年 | 83篇 |
1981年 | 41篇 |
1979年 | 22篇 |
1978年 | 14篇 |
1957年 | 22篇 |
1954年 | 12篇 |
1953年 | 13篇 |
1950年 | 21篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
21.
22.
Mengmeng Zhuang Yuequ Deng Wenwen Zhang Bo Zhu Hao Yan Jiaqi Lou Pan Zhang Qingwei Cui Hao Tang Han Sun Yong Sun 《Cell death & disease》2021,12(6)
Intestinal mucosal injuries are directly or indirectly related to many common acute and chronic diseases. Long non-coding RNAs (lncRNAs) are expressed in many diseases, including intestinal mucosal injury. However, the relationship between lncRNAs and intestinal mucosal injury has not been determined. Here, we investigated the functions and mechanisms of action of lncRNA Bmp1 on damaged intestinal mucosa. We found that Bmp1 was increased in damaged intestinal mucosal tissue and Bmp1 overexpression was able to alleviate intestinal mucosal injury. Bmp1 overexpression was found to influence cell proliferation, colony formation, and migration in IEC-6 or HIEC-6 cells. Moreover, miR-128-3p was downregulated after Bmp1 overexpression, and upregulation of miR-128-3p reversed the effects of Bmp1 overexpression in IEC-6 cells. Phf6 was observed to be a target of miR-128-3p. Furthermore, PHF6 overexpression affected IEC-6 cells by activating PI3K/AKT signaling which was mediated by the miR-128-3p/PHF6 axis. In conclusion, Bmp1 was found to promote the expression of PHF6 through the sponge miR-128-3p, activating the PI3K/AKT signaling pathway to promote cell migration and proliferation.Subject terms: Cell growth, Cell migration 相似文献
23.
Jian‐Yong Guo Yong‐Sheng Wang Tian Chen Xiao‐Xu Jiang Ping Wu Tao Geng Zhong‐Hua Pan Meng‐Ke Shang Cheng‐Xiang Hou Kun Gao Xi‐Jie Guo 《Insect Science》2020,27(3):449-462
Bombyx mori cytoplasmic polyhedrosis virus (BmCPV) is a major pathogen of the economic insect silkworm, Bombyx mori. Virus‐encoded microRNAs (miRNAs) have been proven to play important roles in host–pathogen interactions. In this study we identified a BmCPV‐derived miRNA‐like 21 nt small RNA, BmCPV‐miR‐1, from the small RNA deep sequencing of BmCPV‐infected silkworm larvae by stem‐loop quantitative real‐time PCR (qPCR) and investigated its functions with qPCR and lentiviral expression systems. Bombyx mori inhibitor of apoptosis protein (BmIAP) gene was predicted by both target prediction software miRanda and Targetscan to be one of its target genes with a binding site for BmCPV‐miR‐1 at the 5′ untranslated region. It was found that the expression of BmCPV‐miR‐1 and its target gene BmIAP were both up‐regulated in BmCPV‐infected larvae. At the same time, it was confirmed that BmCPV‐miR‐1 could up‐regulate the expression of BmIAP gene in HEK293T cells with lentiviral expression systems and in BmN cells by transfecting mimics. Furthermore, BmCPV‐miR‐1 mimics could up‐regulate the expression level of BmIAP gene in midgut and fat body in the silkworm. In the midgut of BmCPV‐infected larvae, BmCPV‐miR‐1 mimics could be further up‐regulated and inhibitors could lower the virus‐mediated expression of BmIAP gene. With the viral genomic RNA segments S1 and S10 as indicators, BmCPV‐miR‐1 mimics could up‐regulate and inhibitors down‐regulate their replication in the infected silkworm. These results implied that BmCPV‐miR‐1 could inhibit cell apoptosis in the infected silkworm through up‐regulating BmIAP expression, providing the virus with a better cell circumstance for its replication. 相似文献
24.
25.
26.
27.
28.
Advanced hepatic fibrosis therapy using drug-delivering nanoparticles is a relatively unexplored area. Angiotensin type 1 (AT1) receptor blockers such as losartan can be delivered to hepatic stellate cells (HSC), blocking their activation and thereby reducing fibrosis progression in the liver. In our study, we analyzed the possibility of utilizing drug-loaded vehicles such as hyaluronic acid (HA) micelles carrying losartan to attenuate HSC activation. Losartan, which exhibits inherent lipophilicity, was loaded into the hydrophobic core of HA micelles with a 19.5% drug loading efficiency. An advanced liver fibrosis model was developed using C3H/HeN mice subjected to 20 weeks of prolonged TAA/ethanol weight-adapted treatment. The cytocompatibility and cell uptake profile of losartan-HA micelles were studied in murine fibroblast cells (NIH3T3), human hepatic stellate cells (hHSC) and FL83B cells (hepatocyte cell line). The ability of these nanoparticles to attenuate HSC activation was studied in activated HSC cells based on alpha smooth muscle actin (α-sma) expression. Mice treated with oral losartan or losartan-HA micelles were analyzed for serum enzyme levels (ALT/AST, CK and LDH) and collagen deposition (hydroxyproline levels) in the liver. The accumulation of HA micelles was observed in fibrotic livers, which suggests increased delivery of losartan compared to normal livers and specific uptake by HSC. Active reduction of α-sma was observed in hHSC and the liver sections of losartan-HA micelle-treated mice. The serum enzyme levels and collagen deposition of losartan-HA micelle-treated mice was reduced significantly compared to the oral losartan group. Losartan-HA micelles demonstrated significant attenuation of hepatic fibrosis via an HSC-targeting mechanism in our in vitro and in vivo studies. These nanoparticles can be considered as an alternative therapy for liver fibrosis. 相似文献
29.
30.