全文获取类型
收费全文 | 9892篇 |
免费 | 873篇 |
国内免费 | 852篇 |
专业分类
11617篇 |
出版年
2024年 | 26篇 |
2023年 | 155篇 |
2022年 | 333篇 |
2021年 | 576篇 |
2020年 | 403篇 |
2019年 | 442篇 |
2018年 | 426篇 |
2017年 | 308篇 |
2016年 | 433篇 |
2015年 | 614篇 |
2014年 | 784篇 |
2013年 | 760篇 |
2012年 | 926篇 |
2011年 | 779篇 |
2010年 | 541篇 |
2009年 | 423篇 |
2008年 | 462篇 |
2007年 | 494篇 |
2006年 | 409篇 |
2005年 | 341篇 |
2004年 | 304篇 |
2003年 | 235篇 |
2002年 | 202篇 |
2001年 | 176篇 |
2000年 | 158篇 |
1999年 | 155篇 |
1998年 | 72篇 |
1997年 | 69篇 |
1996年 | 72篇 |
1995年 | 52篇 |
1994年 | 64篇 |
1993年 | 51篇 |
1992年 | 75篇 |
1991年 | 59篇 |
1990年 | 39篇 |
1989年 | 51篇 |
1988年 | 29篇 |
1987年 | 33篇 |
1986年 | 25篇 |
1985年 | 25篇 |
1984年 | 8篇 |
1983年 | 11篇 |
1982年 | 3篇 |
1981年 | 1篇 |
1980年 | 5篇 |
1979年 | 6篇 |
1978年 | 1篇 |
1970年 | 1篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
41.
42.
Yanfei Jiang Yujie Li Ye Ding Xiaoqian Dai Xiaotao Ma Lei Bao 《Bioscience, biotechnology, and biochemistry》2013,77(9):1493-1503
In our study, it has been detected in vivo and in vitro that GSPE reversed high glucose-induced the increase of ICAM-1 and VCAM-1. It is shown that by western blotting detection, GSPE significantly inhibited the activation of NF-κB induced by high glucose while there was significant decrease of the expression of PKC with GSPE intervention. By adding the NF-κB blocker PDTC and the PKC inhibitor peptide 19–31(10?6 M), no significant difference was found in the levels of VCAM-1 and ICAM-1 among GSPE group, the PKC inhibitor peptide 19–31-added GSPE group and the PDTC-added GSPE group. So the conclusion could be drawn that PKC inhibition must be involved in GSPE decreasing the level of ICAM-1 and VCAM-1.We proved for the first time that GSPE prevented high glucose-induced the increase of ICAM-1 and VCAM-1 by PKC and NF-κB inhibition. These findings show a novel mechanism of the action GSPE preventing endothelial dysfunction, which may have clinical application values. 相似文献
43.
44.
45.
46.
47.
Jingjing Pei Jieru Deng Zuodong Ye Jiaying Wang Hongchao Gou Wenjun Liu 《Autophagy》2016,12(10):1738-1758
A growing number of studies have demonstrated that both macroautophagy/autophagy and apoptosis are important inner mechanisms of cell to maintain homeostasis and participate in the host response to pathogens. We have previously reported that a functional autophagy pathway is trigged by infection of classical swine fever virus (CSFV) and is required for viral replication and release in host cells. However, the interplay of autophagy and apoptosis in CSFV-infected cells has not been clarified. In the present study, we demonstrated that autophagy induction with rapamycin facilitates cellular proliferation after CSFV infection, and that autophagy inhibition by knockdown of essential autophagic proteins BECN1/Beclin 1 or MAP1LC3/LC3 (microtubule-associated protein 1 light chain 3) promotes apoptosis via fully activating both intrinsic and extrinsic mechanisms in CSFV-infected cells. We also found that RIG-I-like receptor (RLR) signaling was amplified in autophagy-deficient cells during CSFV infection, which was closely linked to the activation of the intrinsic apoptosis pathway. Moreover, we discovered that virus infection of autophagy-impaired cells results in an increase in copy number of mitochondrial DNA and in the production of reactive oxygen species (ROS), which plays a significant role in enhanced RLR signaling and the activated extrinsic apoptosis pathway in cultured cells. Collectively, these data indicate that CSFV-induced autophagy delays apoptosis by downregulating ROS-dependent RLR signaling and thus contributes to virus persistent infection in host cells. 相似文献
48.
Hybrid Solar Cells: Enhanced Electro‐Optical Properties of Nanocone/Nanopillar Dual‐Structured Arrays for Ultrathin Silicon/Organic Hybrid Solar Cell Applications (Adv. Energy Mater. 8/2016) 下载免费PDF全文
49.
50.