全文获取类型
收费全文 | 20750篇 |
免费 | 1559篇 |
国内免费 | 1篇 |
出版年
2022年 | 106篇 |
2021年 | 222篇 |
2020年 | 171篇 |
2019年 | 179篇 |
2018年 | 358篇 |
2017年 | 293篇 |
2016年 | 537篇 |
2015年 | 913篇 |
2014年 | 906篇 |
2013年 | 1240篇 |
2012年 | 1480篇 |
2011年 | 1465篇 |
2010年 | 876篇 |
2009年 | 722篇 |
2008年 | 1248篇 |
2007年 | 1228篇 |
2006年 | 1159篇 |
2005年 | 1098篇 |
2004年 | 1018篇 |
2003年 | 933篇 |
2002年 | 878篇 |
2001年 | 421篇 |
2000年 | 420篇 |
1999年 | 383篇 |
1998年 | 196篇 |
1997年 | 171篇 |
1996年 | 140篇 |
1995年 | 159篇 |
1994年 | 141篇 |
1993年 | 106篇 |
1992年 | 230篇 |
1991年 | 233篇 |
1990年 | 210篇 |
1989年 | 164篇 |
1988年 | 176篇 |
1987年 | 146篇 |
1986年 | 142篇 |
1985年 | 126篇 |
1984年 | 115篇 |
1983年 | 97篇 |
1982年 | 94篇 |
1981年 | 118篇 |
1979年 | 110篇 |
1978年 | 103篇 |
1977年 | 82篇 |
1976年 | 96篇 |
1975年 | 80篇 |
1974年 | 90篇 |
1973年 | 79篇 |
1971年 | 80篇 |
排序方式: 共有10000条查询结果,搜索用时 0 毫秒
41.
Sabrina Forveille Heng Zhou Allan Sauvat Lucillia Bezu Kevin Müller Peng Liu Laurence Zitvogel Gérard Pierron ?ystein Rekdal Oliver Kepp Guido Kroemer 《Cell cycle (Georgetown, Tex.)》2015,14(21):3506-3512
The oncolytic peptide LTX-315 has been designed for killing human cancer cells and turned out to stimulate anti-cancer immune responses when locally injected into tumors established in immunocompetent mice. Here, we investigated the question whether LTX-315 induces apoptosis or necrosis. Transmission electron microscopy or morphometric analysis of chromatin-stained tumor cells revealed that LTX-315 failed to induce apoptotic nuclear condensation and rather induced a necrotic phenotype. Accordingly, LTX-315 failed to stimulate the activation of caspase-3, and inhibition of caspases by means of Z-VAD-fmk was unable to reduce cell killing by LTX-315. In addition, 2 prominent inhibitors of regulated necrosis (necroptosis), namely, necrostatin-1 and cycosporin A, failed to reduce LTX-315-induced cell death. In conclusion, it appears that LTX-315 triggers unregulated necrosis, which may contribute to its pro-inflammatory and pro-immune effects. 相似文献
42.
Mathieu Lefèvre Daniel J. Felmlee Marie Parnot Thomas F. Baumert Catherine Schuster 《PloS one》2014,9(4)
Hepatitis C virus (HCV) is a major cause of liver disease worldwide and HCV infection represents a major health problem. HCV associates with host lipoproteins forming host/viral hybrid complexes termed lipoviral particles. Apolipoprotein E (apoE) is a lipoprotein component that interacts with heparan sulfate proteoglycans (HSPG) to mediate hepatic lipoprotein uptake, and may likewise mediate HCV entry. We sought to define the functional regions of apoE with an aim to identify critical apoE binding partners involved in HCV infection. Using adenoviral vectors and siRNA to modulate apoE expression we show a direct correlation of apoE expression and HCV infectivity, whereas no correlation exists with viral protein expression. Mutating the HSPG binding domain (HSPG-BD) of apoE revealed key residues that are critical for mediating HCV infection. Furthermore, a novel synthetic peptide that mimics apoE’s HSPG-BD directly and competitively inhibits HCV infection. Genetic knockdown of the HSPG proteins syndecan (SDC) 1 and 4 revealed that SDC4 principally mediates HCV entry. Our data demonstrate that HCV uses apoE-SDC4 interactions to enter hepatoma cells and establish infection. Targeting apoE-SDC interactions could be an alternative strategy for blocking HCV entry, a critical step in maintaining chronic HCV infection. 相似文献
43.
Four main molecular forms of acetylcholinesterase (AChE) can be solubilized from newborn rat superior cervical ganglia (SCG), homogenized in the presence of a high-ionic-strength, detergent-containing medium. These forms, respectively referred to as 16, 10, 6.5, and 4 S, are characterized by their sedimentation coefficients. Their relative proportions in SCG are notably different in vivo during postnatal maturation, and in culture. The 16-S AChE appears to be mainly neuronal in origin, is maintained in culture independently of original presynaptic in vivo elements, and its cellular pool is not depleted in the presence of tetrodotoxin (TTX). 相似文献
44.
Administration of choline chloride i.p. to rats causes a dose-dependent increase in the brain concentration of the neurotransmitter, acetylcholine (ACh). This increase is maximal (22% after a 60-mg/kg dose) 40 minutes after injection. These observations suggest that precursor availability may influence brain ACh synthesis, just as brain tryptophan and tyrosine levels have previously been shown to control the synthesis of brain serotonin and catecholamines. 相似文献
45.
46.
47.
48.
49.
50.