全文获取类型
收费全文 | 19814篇 |
免费 | 966篇 |
国内免费 | 1785篇 |
专业分类
林业 | 1660篇 |
农学 | 1569篇 |
基础科学 | 371篇 |
2497篇 | |
综合类 | 7571篇 |
农作物 | 1309篇 |
水产渔业 | 777篇 |
畜牧兽医 | 4455篇 |
园艺 | 1482篇 |
植物保护 | 874篇 |
出版年
2024年 | 52篇 |
2023年 | 250篇 |
2022年 | 414篇 |
2021年 | 678篇 |
2020年 | 623篇 |
2019年 | 796篇 |
2018年 | 510篇 |
2017年 | 738篇 |
2016年 | 934篇 |
2015年 | 880篇 |
2014年 | 1075篇 |
2013年 | 1255篇 |
2012年 | 1521篇 |
2011年 | 1526篇 |
2010年 | 1347篇 |
2009年 | 1454篇 |
2008年 | 1200篇 |
2007年 | 1314篇 |
2006年 | 1150篇 |
2005年 | 991篇 |
2004年 | 686篇 |
2003年 | 560篇 |
2002年 | 421篇 |
2001年 | 323篇 |
2000年 | 302篇 |
1999年 | 279篇 |
1998年 | 160篇 |
1997年 | 161篇 |
1996年 | 163篇 |
1995年 | 128篇 |
1994年 | 92篇 |
1993年 | 104篇 |
1992年 | 89篇 |
1991年 | 74篇 |
1990年 | 64篇 |
1989年 | 50篇 |
1988年 | 46篇 |
1987年 | 34篇 |
1986年 | 28篇 |
1985年 | 23篇 |
1984年 | 13篇 |
1983年 | 8篇 |
1982年 | 4篇 |
1981年 | 5篇 |
1980年 | 6篇 |
1978年 | 5篇 |
1977年 | 6篇 |
1962年 | 4篇 |
1956年 | 10篇 |
1955年 | 4篇 |
排序方式: 共有10000条查询结果,搜索用时 31 毫秒
991.
AIM To investigate the mechanism of long noncoding RNA (lncRNA) FEZF1-AS1 regulating microRNA-363-3p (miR-363-3p) on the viability and apoptosis of lipopolysaocharide (LPS)-induced vascular endothelial cells. METHODS Human umbilical vein endothelial cells (HUVECs) were cultured in vitro . pcDNA-NC, pcDNA-FEZF1-AS1, anti-miR-NC, anti-miR-363-3p, miR-NC and miR-363-3p mimics were transfected into the HUVECs and LPS stimulation was applied for 24 h. RT-qPCR was used to detect the expression of FEZF1-AS1 and miR-363-3p. The cell viability was measured by MTT assay. The apoptotic rate was analyzed by flow cytometry. The dual-luciferase reporter experiment was used to verify the targeted regulation of FEZF1-AS1 and miR-363-3p. Western blot was used to determined the expression of cyclin D1, Ki67 and cleaved caspase-3. RESULTS Compared with control group, the expression level of FEZF1-AS1 in LPS group was significantly reduced (P <0.05), and the expression level of miR-363-3p was significantly increased (P <0.05). Compared with pcDNA-NC+LPS group, the cell viability in pcDNA-FEZF1-AS1+LPS group was significantly increased (P <0.05), the apoptotic rate was significantly reduced (P <0.05), the protein levels of cyclin D1 and Ki67 were significantly increased (P <0.05), and the protein level of cleaved caspase-3 was significantly reduced (P <0.05). Compared with anti-miR-NC+LPS group, the cell viability in anti-miR-363-3p+LPS group was significantly increased (P <0.05), the apoptotic rate was significantly reduced (P <0.05), the protein levels of cyclin D1 and Ki67 were significantly increased (P <0.05), and the protein level of cleaved caspase-3 was significantly reduced (P <0.05). Dual-luciferase reporter experiment confirmed that FEZF1-AS1 targeted miR-363-3p. Compared with miR-NC+pcDNA-FEZF1-AS1+LPS group, the cell viability in miR-363-3p+pcDNA-FEZF1-AS1+LPS group was significantly reduced (P <0.05), the apoptotic rate was significantly increased (P <0.05), the protein levels of cyclin D1 and Ki67 were significantly reduced (P <0.05), and the protein level of cleaved caspase-3 was significantly increased (P <0.05). CONCLUSION Over-expression of FEZF1-AS1 promotes the viability and inhibits apoptosis of LPS induced vascular endothelial cells by inhibiting the expression of miR-363-3p. 相似文献
992.
MicroRNA-142-3p modulates atherosclerosis-associated endothelial cell apoptosis via targeting Rictor
AIM To investigate the role of microRNA-142-3p (miR-142-3p) in endothelial cell apoptosis during atherosclerosis (AS) and the underlying mechanism. METHODS Human aortic endothelial cells (HAECs) were treated with oxidized low-density lipoprotein (ox-LDL). The expression level of miR-142-3p was detected by RT-qPCR. Apoptosis was determined via flow cytometry (FCM) and caspase-3 activity assay. Prediction of the binding site between miR-142-3p and 3’-UTR of Rictor mRNA was performed by bioinformatics analysis and confirmed by dual-luciferase reporter assay. RESULTS The expression of miR-142-3p was substantially up-regulated during the ox-LDL-elicited apoptosis in HAECs (P <0.05,P <0.01). Forced expression of miR-142-3p exacerbated apoptosis in HAECs whereas inhibition of miR-142-3p partly alleviated apoptotic cell death mediated by ox-LDL. Further analysis identified Rictor as a direct target gene of miR-142-3p, and Rictor knock-down abolished the anti-apoptotic effect of miR-142-3p inhibitor. Moreover, the Akt/endothelial nitric oxide synthase (eNOS) signaling pathway was found to mediate the beneficial effect of miR-142-3p inhibitor on endothelial cells apoptosis. CONCLUSION Down-regulation of miR-142-3p inhibits endothelial cell apoptosis and atherosclerotic development by up-regulating the expression of Rictor and activating the Akt/eNOS signaling pathway. 相似文献
993.
994.
图X称为弱1/2-传递图,如果X是弱边传递但不是弱弧传递的图.图X弱边传递是指自同态幺半群End(X)在边集上的传递作用;而图X弱弧传递是指End(X)在有序边集上的传递作用. 相似文献
995.
阐述了在胶南自然条件下生产无公害绿茶的主要技术,从环境选择、地力改善、肥料施用、病虫害管理等方面进行了详细的论述,为江北无公害绿茶生产提供了良好的借鉴。 相似文献
996.
M Fevrier 《Comparative immunology, microbiology and infectious diseases》1985,8(2):159-170
Antibody response to an antigen involves the co-operation between three types of cells: macrophages, T cells and B cells. The cognate interactions between these cells play a fundamental role in the expression of a specific antibody response, but the last is modulated by antigen-nonspecific soluble factors produced either by macrophages or by T cells. Macrophages elaborate a spectrum of molecules modulating the function of lymphoid cells; among them are IL1 and prostaglandins of the E series, which are respectively enhancer and inhibitor of the antibody response in vitro. These molecules alter T cell and B cell activities through different mechanisms involving activation or inhibition of IL2 production, or alteration of cells surface antigens. However, the cellular events following the fixation of soluble factor on its receptors are not known. 相似文献
997.
998.
999.
1000.
城市污水处理厂H2S气体的产生、危害及预防 总被引:4,自引:0,他引:4
本文主要介绍了城市污水处理厂H2S的产生的根源,对人体的危害和对设备的损害,中毒预防、中毒后急救和治疗措施。只要了解了H2S的性质,采取必要的措施可完全避免H2S对人体造成伤害和对设备造成损害。 相似文献