全文获取类型
收费全文 | 11294篇 |
免费 | 951篇 |
国内免费 | 1603篇 |
出版年
2024年 | 18篇 |
2023年 | 156篇 |
2022年 | 311篇 |
2021年 | 613篇 |
2020年 | 427篇 |
2019年 | 498篇 |
2018年 | 446篇 |
2017年 | 356篇 |
2016年 | 514篇 |
2015年 | 686篇 |
2014年 | 864篇 |
2013年 | 926篇 |
2012年 | 1067篇 |
2011年 | 1066篇 |
2010年 | 664篇 |
2009年 | 611篇 |
2008年 | 664篇 |
2007年 | 665篇 |
2006年 | 536篇 |
2005年 | 441篇 |
2004年 | 336篇 |
2003年 | 359篇 |
2002年 | 289篇 |
2001年 | 225篇 |
2000年 | 213篇 |
1999年 | 192篇 |
1998年 | 105篇 |
1997年 | 83篇 |
1996年 | 93篇 |
1995年 | 69篇 |
1994年 | 44篇 |
1993年 | 35篇 |
1992年 | 56篇 |
1991年 | 43篇 |
1990年 | 27篇 |
1989年 | 36篇 |
1988年 | 18篇 |
1987年 | 19篇 |
1986年 | 14篇 |
1985年 | 15篇 |
1984年 | 10篇 |
1983年 | 14篇 |
1982年 | 8篇 |
1981年 | 3篇 |
1961年 | 2篇 |
1956年 | 1篇 |
1955年 | 2篇 |
1954年 | 1篇 |
1951年 | 1篇 |
1949年 | 1篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
151.
152.
153.
Zhongli Shi Kaixia Zhang Huimin Zhou Lei Jiang Bing Xie Ruiyuan Wang Wenzhen Xia Yajuan Yin Zhaoyu Gao Dongsheng Cui Rui Zhang Shunjiang Xu 《Aging cell》2020,19(3)
Alzheimer's disease (AD) and cancer have inverse relationship in many aspects. Some tumor suppressors, including miR‐34c, are decreased in cancer but increased in AD. The upstream regulatory pathways and the downstream mechanisms of miR‐34c in AD remain to be investigated. The expression of miR‐34c was detected by RT–qPCR in oxidative stressed neurons, hippocampus of SAMP8 mice, or serum of patients with amnestic mild cognitive impairment (aMCI). Dual luciferase assay was performed to confirm the binding sites of miR‐34c in its target mRNA. The Morris water maze (MWM) was used to evaluate learning and memory in SAMP8 mice administrated with miR‐34c antagomir (AM34c). Golgi staining was used to evaluate the synaptic function and structure. The dramatically increased miR‐34c was mediated by ROS‐JNK‐p53 pathway and negatively regulated synaptotagmin 1 (SYT1) expression by targeting the 3′‐untranslated region (3′‐UTR) of syt1 in AD. The expression of SYT1 protein was reduced by over expression of miR‐34c in the HT‐22 cells and vice versa. Administration of AM34c by the third ventricle injection or intranasal delivery markedly increased the brain levels of SYT1 and ameliorated the cognitive function in SAMP8 mice. The serum miR‐34c was significantly increased in patients with aMCI and might be a predictive biomarker for diagnosis of aMCI. These results indicated that increased miR‐34c mediated synaptic and memory deficits by targeting SYT1 through ROS‐JNK‐p53 pathway and the miR‐34c/SYT1 pathway could be considered as a promising novel therapeutic target for patients with AD. 相似文献
154.
155.
Food Biophysics - In this study, naturally occurring ingredient diosgenin was utilized as an organogelator for structuring canola oil. Results show that stable diosgenin-based organogel can be... 相似文献
156.
157.
Haining Li Bihua Xia Wei Chen Yumeng Zhang Xia Gao Arunachalam Chinnathambi Sulaiman A. Alharbi Yujie Zhao 《Journal of biochemical and molecular toxicology》2020,34(9)
The current work planned to assess the protecting properties of nimbolide against doxorubicin (DOX)‐treated myocardial damage. Myocardial damage was produced with 2.5 mg/kg of DOX given on alternative days (14 days). Thiobarbituric acid reactive substances (TBARS) levels of a lipid peroxidative marker were elevated, whereas reduced body weight, heart weight, blood pressure indices and reduced levels of antioxidants like glutathione‐S‐transferase, superoxide dismutase, catalase, glutathione peroxidase, glutathione, and glutathione reductase were observed in the heart tissue of DOX‐treated animals. DOX‐treated animals showed augmented levels of cardiac markers likes monocyte chemotactic protein‐1, interferon‐gamma, aspartate transferase, creatine kinase, lactate dehydrogenase, creatine kinase‐muscle/brain, heart‐type fatty acid‐binding protein, glycogen phosphorylase isoenzyme BB, transforming growth factor‐β, brain natriuretic peptide, myoglobin, and cTnI in serum. Histopathological assessment confirmed the DOX‐induced cardiotoxicity. Furthermore, DOX‐induced rats showed augmented inflammatory mediators (nuclear factor‐κB [NF‐kB], tumor necrosis factor‐α [TNF‐α], and interleukin‐1β [IL‐1β]) and increased PI3K/Akt signaling proteins (PI3K, p‐Bad/Bad, caspase‐3, and p‐Akt), whereas decreased oxidative markers (HO‐1 and NQO‐1) and p‐PTEN were observed. Nimbolide‐supplemented rats showed reduced activity/levels of cardiac markers and TBARS levels in serum and heart tissue. Levels of enzymatic and nonenzymatic antioxidants were augmented in the heart tissue of nimbolide‐supplemented rats. Nimbolide influence decreased apoptosis, inflammation, and enhanced antioxidant markers through the modulation of p‐Bad/Bad, caspase‐3, PI3K, p‐Akt, TNF‐α, NF‐kB, IL‐1β, HO‐1, NQO‐1, and p‐PTEN markers. The histopathological explanations were observed to be in line with biochemical analysis. Therefore, the finding of current work was that nimbolide has a defensive effect on the myocardium against DOX‐induced cardiac tissue damage. 相似文献
158.
159.
Li X. B. Titlyanov E. A. Titlyanova T. V. Belous O. S. Xia J. Q. Huang H. 《Russian Journal of Marine Biology》2020,46(6):485-492
Russian Journal of Marine Biology - Intensive algal sampling was conducted from 2017 to 2019 in coastal waters of Wuzhizhou Island (South China Sea, China). In total, 183 species of marine... 相似文献
160.