全文获取类型
收费全文 | 9755篇 |
免费 | 712篇 |
国内免费 | 842篇 |
出版年
2024年 | 14篇 |
2023年 | 125篇 |
2022年 | 360篇 |
2021年 | 638篇 |
2020年 | 362篇 |
2019年 | 476篇 |
2018年 | 468篇 |
2017年 | 320篇 |
2016年 | 450篇 |
2015年 | 687篇 |
2014年 | 797篇 |
2013年 | 786篇 |
2012年 | 931篇 |
2011年 | 860篇 |
2010年 | 500篇 |
2009年 | 451篇 |
2008年 | 499篇 |
2007年 | 416篇 |
2006年 | 327篇 |
2005年 | 267篇 |
2004年 | 236篇 |
2003年 | 242篇 |
2002年 | 200篇 |
2001年 | 148篇 |
2000年 | 115篇 |
1999年 | 129篇 |
1998年 | 73篇 |
1997年 | 69篇 |
1996年 | 63篇 |
1995年 | 50篇 |
1994年 | 38篇 |
1993年 | 25篇 |
1992年 | 39篇 |
1991年 | 22篇 |
1990年 | 21篇 |
1989年 | 37篇 |
1988年 | 14篇 |
1987年 | 8篇 |
1986年 | 9篇 |
1985年 | 21篇 |
1984年 | 4篇 |
1983年 | 8篇 |
1982年 | 2篇 |
1981年 | 2篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
111.
Disabled‐2 (Dab2) and PAR‐3 (partitioning defective 3) are reported to play critical roles in maintaining retinal microvascular endothelial cells biology by regulating VEGF‐VEGFR‐2 signaling. The role of Dab2 and PAR‐3 in glomerular endothelial cell (GEnC) is unclear. In this study, we found that, no matter whether with vascular endothelial growth factor (VEGF) treatment or not, decreased expression of Dab2 could lead to cell apoptosis by preventing activation of VEGF‐VEGFR‐2 signaling in GEnC, accompanied by reduced membrane VEGFR‐2 expression. And silencing of PAR‐3 gene expression caused increased apoptosis of GEnC by inhibiting activation of VEGF‐VEGFR‐2 signaling and membrane VEGFR‐2 expression. In our previous research, we found that the silencing of syndecan‐1 gene expression inhibited VEGF‐VEGFR‐2 signaling by modulating internalization of VEGFR‐2. And our further research demonstrated that downregulation of syndecan‐1 lead to no significant change in the expression of Dab2 and PAR‐3 both at messenger RNA and protein levels in GEnC, while phosphorylation of Dab2 was significantly increased in GEnC transfected with Dab2 small interfering RNA (siRNA) compared with control siRNA. Atypical protein kinase C (aPKC) could induce phosphorylation of Dab2, thus negatively regulating VEGF‐VEGFR‐2 signaling. And we found that decreased expression of syndecan‐1 lead to activation of aPKC, and aPKC inhibitor treatment could block phosphorylation of Dab2 in GEnC. Besides, aPKC inhibitor treatment could activate VEGF‐VGEFR‐2 signaling in GEnC transfected with syndecan‐1 siRNA in a dose‐dependent manner. In conclusion, we speculated that phosphorylation of Dab2 is involved in preventing activation of VEGF‐VEGFR‐2 signaling in GEnC transfected with syndecan‐1 siRNA. This provides a new target for the therapy of GEnC injury and kidney disease. 相似文献
112.
Ming‐Yuan Du Jia‐Xi Duan Chen‐Yu Zhang Hui‐Hui Yang Xin‐Xin Guan Wen‐Jing Zhong Yan‐Zhe Liu Zi‐Ming Li Yu‐Rui Cheng Yong Zhou Cha‐Xiang Guan 《Cell biology international》2020,44(1):98-107
Idiopathic pulmonary fibrosis (IPF) is a progressive disease characterized by excessive deposition of extracellular matrix (ECM) and chronic inflammation with limited therapeutic options. Psoralen, a major active component extracted from Psoralea corylifolia L. seed, has several biological effects. However, the role of psoralen in IPF is still unclear. Here, we hypothesized that psoralen played an essential role in IPF in the inhibition of fibroblast proliferation and inflammatory response. A murine model of IPF was established by injecting bleomycin (BLM) intratracheally, and psoralen was administered for 14 days from the 7th to 21st day after BLM injection. Our results demonstrated that psoralen treatment reduced body weight loss and improved the survival rate of mice with IPF. Histological and immunofluorescent examination showed that psoralen alleviated BLM‐induced lung parenchymal inflammatory and fibrotic alteration. Furthermore, psoralen inhibited proliferation and collagen synthesis of mouse fibroblasts and partially reversed BLM‐induced expression of α‐smooth muscle actin at both the tissue and cell level. Moreover, psoralen decreased the expression of transforming growth factor‐β1, interleukin‐1β, and tumor necrosis factor‐α in the lungs of BLM‐stimulated mice. Our results reveale for the first time that psoralen exerts therapeutic effects against IPF in a BLM‐induced murine model. 相似文献
113.
114.
Jie Dong Jun Lei Nada A. Elsayed Ji Yeon Lee Na Shin Quan Na Anna Chudnovets Bei Jia Xiaohong Wang Irina Burd 《Developmental neurobiology》2020,80(5-6):149-159
Fetuses exposed to an inflammatory environment are predisposed to long‐term adverse neurological outcomes. However, the mechanism by which intrauterine inflammation (IUI) is responsible for abnormal fetal brain development is not fully understood. The mechanistic target of rapamycin (mTOR) signaling pathway is closely associated with fetal brain development. We hypothesized that mTOR signaling might be involved in fetal brain injury and malformation when fetuses are exposed to the IUI environment. A well‐established IUI model was utilized by intrauterine injection of lipopolysaccharide (LPS) to explore the effect of IUI on mTOR signaling in mouse fetal brains. We found that microglia activation in LPS fetal brains was increased, as demonstrated by elevated Iba‐1 protein level and immunofluorescence density. LPS fetal brains also showed reduced neuronal cell counts, decreased cell proliferation demonstrated by low Ki67‐positive density, and elevated neuron apoptosis evidenced by high expression of cleaved Caspase 3. Furthermore, we found that mTOR signaling in LPS fetal brains was elevated at 2 hr after LPS treatment, declined at 6 hr and showed overall inhibition at 24 hr. In summary, our study revealed that LPS‐induced IUI leads to increased activation of microglia cells, neuronal damage, and dynamic alterations in mTOR signaling in the mouse fetal brain. Our findings indicate that abnormal changes in mTOR signaling may underlie the development of future neurological complications in offspring exposed to prenatal IUI. 相似文献
115.
116.
117.
118.
119.