全文获取类型
收费全文 | 2963篇 |
免费 | 240篇 |
国内免费 | 315篇 |
出版年
2024年 | 6篇 |
2023年 | 51篇 |
2022年 | 119篇 |
2021年 | 172篇 |
2020年 | 129篇 |
2019年 | 132篇 |
2018年 | 168篇 |
2017年 | 101篇 |
2016年 | 136篇 |
2015年 | 197篇 |
2014年 | 226篇 |
2013年 | 222篇 |
2012年 | 269篇 |
2011年 | 258篇 |
2010年 | 164篇 |
2009年 | 129篇 |
2008年 | 167篇 |
2007年 | 161篇 |
2006年 | 124篇 |
2005年 | 85篇 |
2004年 | 87篇 |
2003年 | 51篇 |
2002年 | 73篇 |
2001年 | 45篇 |
2000年 | 31篇 |
1999年 | 41篇 |
1998年 | 32篇 |
1997年 | 30篇 |
1996年 | 17篇 |
1995年 | 15篇 |
1994年 | 13篇 |
1993年 | 12篇 |
1992年 | 17篇 |
1991年 | 5篇 |
1990年 | 5篇 |
1989年 | 6篇 |
1988年 | 7篇 |
1987年 | 4篇 |
1986年 | 1篇 |
1985年 | 4篇 |
1984年 | 2篇 |
1983年 | 3篇 |
1980年 | 1篇 |
排序方式: 共有3518条查询结果,搜索用时 15 毫秒
131.
132.
Sheng Niu Jia Wang Bin Bai Lili Wu Anqi Zheng Qian Chen Pei Du Pengcheng Han Yanfang Zhang Yunfei Jia Chengpeng Qiao Jianxun Qi Wenxia Tian HongWei Wang Qihui Wang George Fu Gao 《The EMBO journal》2022,41(1)
Correction to: The EMBO Journal (2021) 40: e107786. DOI 10.15252/embj.2021107786 | Published online 8 June 2021The authors would like to add three references to the paper: Starr et al and Zahradník et al also reported that the Q498H or Q498R mutation has enhanced binding affinity to ACE2; and Liu et al reported on the binding of bat coronavirus to ACE2.Starr et al and Zahradník et al have now been cited in the Discussion section, and the following sentence has been corrected from:“According to our data, the SARS‐CoV‐2 RBD with Q498H increases the binding strength to hACE2 by 5‐fold, suggesting the Q498H mutant is more ready to interact with human receptor than the wildtype and highlighting the necessity for more strict control of virus and virus‐infected animals”.to“Here, according to our data and two recently published papers, the SARS‐CoV‐2 RBD with Q498H or Q498R increases the binding strength to hACE2 (Starr et al, 2020; Zahradník et al, 2021), suggesting the mutant with Q498H or Q498R is more ready to interact with human receptor than the wild type and highlighting the necessity for more strict control of virus and virus‐infected animals”.The Liu et al citation has been added to the following sentence:“In another paper published by our group recently, RaTG13 RBD was found to bind to hACE2 with much lower binding affinity than SARS‐CoV‐2 though RaTG13 displays the highest whole‐genome sequence identity (96.2%) with the SARS‐CoV‐2 (Liu et al, 2021)”.Additionally, the authors have added the GISAID accession IDs to the sequence names of the SARS‐CoV‐2 in two human samples (Discussion section). To make identification unambiguous, the sequence names have been updated from “SA‐lsf‐27 and SA‐lsf‐37” to “GISAID accession ID: EPI_ISL_672581 and EPI_ISL_672589”.Lastly, the authors declare in the Materials and Methods section that all experiments employed SARS‐CoV‐2 pseudovirus in cultured cells. These experiments were performed in a BSL‐2‐level laboratory and approved by Science and Technology Conditions Platform Office, Institute of Microbiology, Chinese Academy of Sciences.These changes are herewith incorporated into the paper. 相似文献
133.
Chia-chen Chang Daniel T. C. Cox Qiao Fan Thi Phuong Le Nghiem Claudia L. Y. Tan Rachel Rui Ying Oh Brenda B. Lin Danielle F. Shanahan Richard A. Fuller Kevin J. Gaston L. Roman Carrasco 《PLoS biology》2022,20(2)
Nature experiences have been linked to mental and physical health. Despite the importance of understanding what determines individual variation in nature experience, the role of genes has been overlooked. Here, using a twin design (TwinsUK, number of individuals = 2,306), we investigate the genetic and environmental contributions to a person’s nature orientation, opportunity (living in less urbanized areas), and different dimensions of nature experience (frequency and duration of public nature space visits and frequency and duration of garden visits). We estimate moderate heritability of nature orientation (46%) and nature experiences (48% for frequency of public nature space visits, 34% for frequency of garden visits, and 38% for duration of garden visits) and show their genetic components partially overlap. We also find that the environmental influences on nature experiences are moderated by the level of urbanization of the home district. Our study demonstrates genetic contributions to individuals’ nature experiences, opening a new dimension for the study of human–nature interactions.Nature experiences have been linked to mental and physical health. This twin study reveals genetic influences on an individual’s orientation towards nature and nature experiences, opening a new dimension to understanding human-nature interactions. 相似文献
134.
绿原酸是灰毡毛忍冬生长发育过程中产生的重要的次级代谢产物,而CCoA OMT是绿原酸合成过程中的关键基因.为进一步揭示灰毡毛忍冬LmCCoA OMT基因的功能,本研究利用RACE技术克隆LmC-CoA OMT全长基因,通过生物信息学进行分析,并在大肠杆菌中表达该蛋白.此外,通过RT-qPCR和HPLC的方法研究CCoA... 相似文献
135.
136.
137.
Shigang Qiao Lei Hong Yongming Zhu Jun Zha An Wang Jia Qiu Wei Li Chen Wang Jianzhong An Huiling Zhang 《Cell death & disease》2022,13(2)
Receptor-interacting protein kinase 1 (RIPK1) and 3 (RIPK3) are critical regulators of programmed necrosis or necroptosis. However, the role of the RIPK1/RIPK3 signaling pathway in myocardial fibrosis and related diabetic cardiomyopathy is still unclear. We hypothesized that RIPK1/RIPK3 activation mediated myocardial fibrosis by impairing the autophagic flux. To this end, we established in vitro and in vivo models of type 2 diabetes mellitus with high glucose fat (HGF) medium and diet respectively. HGF induced myocardial fibrosis, and impaired cardiac diastolic and systolic function by activating the RIPK1/RIPK3 pathway, which increased the expression of autophagic related proteins such as LC3-II, P62 and active-cathepsin D. Inhibition of RIPK1 or RIPK3 alleviated HGF-induced death and fibrosis of cardiac fibroblasts by restoring the impaired autophagic flux. The autophagy blocker neutralized the effects of the RIPK1 inhibitor necrostatin-1 (Nec-1) and RIPK3 inhibitor GSK872 (GSK). RIPK1/RIPK3 inhibition respectively decreased the levels of RIPK3/p-RIPK3 and RIPK1/p-RIPK1. P62 forms a complex with RIPK1-RIPK3 and promotes the binding of RIPK1 and RIPK3, silencing of RIPK1 decreased the association of RIPK1 with P62 and the binding of P62 to LC3. Furthermore, inhibition of both kinases in combination with a low dose of Nec-1 and GSK in the HGF-treated fibroblasts significantly decreased cell death and fibrosis, and restored the autophagic flux. In the diabetic rat model, Nec-1 (1.65 mg/kg) treatment for 4 months markedly alleviated myocardial fibrosis, downregulated autophagic related proteins, and improved cardiac systolic and diastolic function. In conclusion, HGF induces myocardial fibrosis and cardiac dysfunction by activating the RIPK1-RIPK3 pathway and by impairing the autophagic flux, which is obviated by the pharmacological and genetic inhibition of RIPK1/RIPK3.Subject terms: Necroptosis, Diabetes complications 相似文献
138.
139.
Yi Xiao Fang Liu Qinghong Kong Xinting Zhu Haijuan Wang Sanhua Li Nian Jiang Changyan Yu Liu Yun 《Aging cell》2022,21(3)
Metformin, a widely prescribed first‐line drug for the treatment of type II diabetes mellitus, has been shown to extend lifespan and delay the onset of age‐related diseases. The precisely mechanisms by which these effects are realized remain elusive. We find that metformin exposure is restricted to adults, which is sufficient to extend lifespan. However, limiting metformin exposure to the larvae has no significant effect on Caenorhabditis elegans longevity. Here, we show that after metformin treatment, the level of S‐adenosylmethionine (SAM) is reduced in adults but not in the larvae. Potential mechanisms by which reduced SAM might increase lifespan include altering the histone methylation. However, the molecular connections between metformin, SAM limitation, methyltransferases, and healthspan‐associated phenotypes are unclear. Through genetic screening of C. elegans, we find that metformin promotes the healthspan through an H3K4 methyltransferase/demethylase complex to downregulate the targets, including mTOR and S6 kinase. Thus, our studies provide molecular links between meformin, SAM limitation, histone methylation, and healthspan and elucidate the mode action of metformin‐regulated healthspan extension will boost its therapeutic application in the treatment of human aging and age‐related diseases. 相似文献
140.
目前,有关同义密码子使用偏性对蛋白质折叠的影响研究中,样本蛋白均来源于不同的物种。考虑到同义密码子使用偏性的物种差异性,选取枯草杆菌的核蛋白为研究对象。首先,将每条核蛋白按二级结构截取为α螺旋片段、β折叠片段和无规卷曲(α-β混合)片段,并计算其蛋白质折叠速率。然后,整理每个片段相应的核酸序列信息,计算其同义密码子使用度。在此基础上,分析枯草芽孢杆菌核蛋白的同义密码子使用偏性与蛋白质折叠速率的相关性。发现对于不同二级结构的肽链片段,都有部分密码子的使用偏性与其对应的肽链折叠速率显著相关。进一步分析发现,与肽链片段折叠速率显著相关的密码子绝大部分为枯草杆菌全序列或核蛋白序列的每一组同义密码子中使用度最高的密码子。结果表明,在蛋白质的折叠过程中,枯草芽孢杆菌的同义密码子使用偏性起着重要作用。 相似文献