全文获取类型
收费全文 | 5058篇 |
免费 | 433篇 |
国内免费 | 364篇 |
专业分类
5855篇 |
出版年
2024年 | 16篇 |
2023年 | 67篇 |
2022年 | 167篇 |
2021年 | 273篇 |
2020年 | 192篇 |
2019年 | 241篇 |
2018年 | 238篇 |
2017年 | 172篇 |
2016年 | 224篇 |
2015年 | 330篇 |
2014年 | 406篇 |
2013年 | 388篇 |
2012年 | 471篇 |
2011年 | 437篇 |
2010年 | 245篇 |
2009年 | 246篇 |
2008年 | 269篇 |
2007年 | 222篇 |
2006年 | 177篇 |
2005年 | 153篇 |
2004年 | 120篇 |
2003年 | 132篇 |
2002年 | 119篇 |
2001年 | 82篇 |
2000年 | 74篇 |
1999年 | 56篇 |
1998年 | 29篇 |
1997年 | 37篇 |
1996年 | 38篇 |
1995年 | 44篇 |
1994年 | 33篇 |
1993年 | 27篇 |
1992年 | 28篇 |
1991年 | 22篇 |
1990年 | 18篇 |
1989年 | 14篇 |
1988年 | 8篇 |
1987年 | 8篇 |
1986年 | 9篇 |
1985年 | 3篇 |
1984年 | 6篇 |
1983年 | 5篇 |
1982年 | 2篇 |
1981年 | 1篇 |
1980年 | 1篇 |
1975年 | 1篇 |
1973年 | 1篇 |
1971年 | 1篇 |
1970年 | 1篇 |
1967年 | 1篇 |
排序方式: 共有5855条查询结果,搜索用时 15 毫秒
101.
Focal adhesion kinase (FAK) functions as a key enzyme in the integrin-mediated adhesion-signalling pathway. Here, we aimed to investigate the effects of FAK on adhesion of human dental pulp (HDP) cells. We transfected lentiviral vectors to silence or overexpress FAK in HDP cells ex vivo. Early cell adhesion, cell survival and focal contacts (FCs)-related proteins (FAK and paxillin) were examined. By using immunofluorescence, the formation of FCs and cytoskeleton was detected, respectively. We found that both adhesion and survival of HDP cells were suppressed by FAK inhibition. However, FAK overexpression slightly inhibited cell adhesion and exhibited no change in cell survival compared with the control. A thick rim of cytoskeleton accumulated and smaller dot-shaped FCs appeared in FAK knockdown cells. Phosphorylation of paxillin (p-paxillin) was inhibited in FAK knockdown cells, verifying that the adhesion was inhibited. Less cytoskeleton and elongated FCs were observed in FAK-overexpressed cells. However, p-paxillin had no significant difference compared with the control. In conclusion, the data suggest that FAK maintains cell adhesion, survival and cytoskeleton formation, but excessive FAK has no positive effects on these aspects. 相似文献
102.
103.
104.
The inhibitory effect of two chemokine decoy receptors (CDRs), DARC and D6, on breast cancer metastasis is mainly due to their ability to sequester pro-malignant chemokines. We hypothesized that genetic variants in the DARC and CCBP2 (encoding D6) genes may be associated with breast cancer progression. In the present study, we evaluated the genetic contributions of DARC and CCBP2 to metastatic potential, indicated by lymph node metastasis (LNM). Ten single-nucleotide polymorphisms (SNPs) (potentially functional SNPs and block-based tagging SNPs) in DARC and CCBP2 were genotyped in 785 breast cancer patients who had negative lymph nodes and 678 patients with positive lymph nodes. Two non-synonymous SNPs, rs12075 (G42D) in DARC and rs2228468 (S373Y) in CCBP2, were observed to be associated with LNM in univariate analysis and remained significant after adjustment for conventional clinical risk factors, with odds ratios (ORs) of 0.54 (95% confidence interval [CI], 0.37 to 0.79) and 0.78 (95% CI, 0.62 to 0.98), respectively. Additional functional experiments revealed that both of these significant SNPs could affect metastasis of breast cancer in xenograft models by differentially altering the chemokine sequestration ability of their corresponding proteins. Furthermore, heterozygous GD genotype of G42D on human erythrocytes had a significantly stronger chemokine sequestration ability than homozygous GG of G42D ex vivo. Our data suggest that the genetic variants in the CDR genes are probably associated with the varied metastatic potential of breast cancer. The underlying mechanism, though it needs to be further investigated, may be that CDR variants could affect the chemokine sequestration ability of CDR proteins. 相似文献
105.
106.
Lin Wang Yong Song Hui Wang Ke Liu Zhe Shao Zhengjun Shang 《Journal of cellular and molecular medicine》2020,24(7):4011-4022
This study aimed to explore new therapeutic targets to improve the survival rate of patients with oral squamous cell carcinoma (OSCC).MiR-210-3p, EphrinA3 and EMT related indices were evaluated in OSCC tissues and cell lines. In addition, the relationship between differential EphrinA3 expression and tumour progression was explored through molecular biology techniques, in vitro functional experiments and tumour xenotransplantation models. The expression of EphrinA3 (rs = −0.719, P < .05) and E-cadherin (rs = −0.856, P < .05) was negatively correlated with the pathological grading in OSCC tissues. Protein clustering shows EphrinA3 may be associated with tumour progression. EphrinA3 also can regulate the biological behaviour of oral cancer cells. And it regulates the EMT by the PI3K/AKT signalling pathway. MiR-210-3p targeted the gen EFNA3. Up-regulation of miR-210-3p expression can decrease the expression of EphrinA3 and further to influence the biological behaviour of OSCC. The miR-210-3p-EphrinA3-PI3K/AKT signalling axis plays an important role in the progress of OSCC. EphrinA3 may serve as a novel target for oral cancer treatment. 相似文献
107.
Yan Jia Huanhuan Jin Liyuan Gao Xiang Yang Feixia Wang Hai Ding Anping Chen Shanzhong Tan Feng Zhang Jiangjuan Shao Shijun Wang Shizhong Zheng 《Journal of cellular and molecular medicine》2020,24(9):5304-5316
A growing number of studies recognize that long non‐coding RNAs (lncRNAs) are essential to mediate multiple tumorigenic processes, including hepatic tumorigenesis. However, the pathological mechanism of lncRNA‐regulated liver cancer cell growth remains poorly understood. In this study, we identified a novel function lncRNA, named polo‐like kinase 4 associated lncRNA (lncRNA PLK4, GenBank Accession No. RP11‐50D9.3), whose expression was dramatically down‐regulated in hepatocellular carcinoma (HCC) tissues and cells. Interestingly, talazoparib, a novel and highly potent poly‐ADP‐ribose polymerase 1/2 (PARP1/2) inhibitor, could increase lncRNA PLK4 expression in HepG2 cells. Importantly, we showed that talazoparib‐induced lncRNA PLK4 could function as a tumour suppressor gene by Yes‐associated protein (YAP) inactivation and induction of cellular senescence to inhibit liver cancer cell viability and growth. In summary, our findings reveal the molecular mechanism of talazoparib‐induced anti‐tumor effect, and suggest a potential clinical use of talazoparib‐targeted lncRNA PLK4/YAP‐dependent cellular senescence for the treatment of HCC. 相似文献
108.
Dong Cai Bingke Liu Dehua Zhu Duo Chen Mengjie Lu Junming Cao Yanhu Wang Wenhao Huang Yong Shao Haoran Tu Wei Han 《Liver Transplantation》2020,10(19)
Lithium–sulfur batteries are a promising high energy output solution for substitution of traditional lithium ion batteries. In recent times research in this field has stepped into the exploration of practical applications. However, their applications are impeded by cycling stability and short life‐span mainly due to the notorious polysulfide shuttle effect. In this work, a multifunctional sulfur host fabricated by grafting highly conductive Co3Se4 nanoparticles onto the surface of an N‐doped 3D carbon matrix to inhibit the polysulfide shuttle and improve the sulfur utilization is proposed. By regulating the carbon matrix and the Co3Se4 distribution, N‐CN‐750@Co3Se4‐0.1 m with abundant polar sites is experimentally and theoretically shown to be a good LiPSs absorbent and a sulfur conversion accelerator. The S/N‐CN‐750@Co3Se4‐0.1 m cathode shows excellent sulfur utilization, rate performance, and cyclic durability. A prolonged cycling test of the as‐fabricated S/N‐CN‐750@Co3Se4‐0.1 m cathode is carried out at 0.2 C for more than 5 months which delivers a high initial capacity of 1150.3 mAh g?1 and retains 531.0 mAh g?1 after 800 cycles with an ultralow capacity reduction of 0.067% per cycle, maintaining Coulombic efficiency of more than 99.3%. The reaction details are characterized and analyzed by ex situ measurements. This work highly emphasizes the potential capabilities of transition‐metal selenides in lithium–sulfur batteries. 相似文献
109.
Oyundari Amartuvshin Chi‐Hung Lin Shao‐Chun Hsu Shih‐Han Kao Alvin Chen Wei‐Chun Tang Han‐Lin Chou Dong‐Lin Chang Yen‐Yang Hsu Bai‐Shiou Hsiao Elham Rastegari Kun‐Yang Lin Yu‐Ting Wang Chi‐Kuang Yao Guang‐Chao Chen Bi‐Chang Chen Hwei‐Jan Hsu 《Aging cell》2020,19(8)
Changes in mitochondrial dynamics (fusion and fission) are known to occur during stem cell differentiation; however, the role of this phenomenon in tissue aging remains unclear. Here, we report that mitochondrial dynamics are shifted toward fission during aging of Drosophila ovarian germline stem cells (GSCs), and this shift contributes to aging‐related GSC loss. We found that as GSCs age, mitochondrial fragmentation and expression of the mitochondrial fission regulator, Dynamin‐related protein (Drp1), are both increased, while mitochondrial membrane potential is reduced. Moreover, preventing mitochondrial fusion in GSCs results in highly fragmented depolarized mitochondria, decreased BMP stemness signaling, impaired fatty acid metabolism, and GSC loss. Conversely, forcing mitochondrial elongation promotes GSC attachment to the niche. Importantly, maintenance of aging GSCs can be enhanced by suppressing Drp1 expression to prevent mitochondrial fission or treating with rapamycin, which is known to promote autophagy via TOR inhibition. Overall, our results show that mitochondrial dynamics are altered during physiological aging, affecting stem cell homeostasis via coordinated changes in stemness signaling, niche contact, and cellular metabolism. Such effects may also be highly relevant to other stem cell types and aging‐induced tissue degeneration. 相似文献
110.
Wen Yongdiao Liu Shaobin Zhang Haifeng Xu Yan Yu Qiming Wang Lingling Frezza Fabrizio 《Plasmonics (Norwell, Mass.)》2020,15(4):1141-1149
Plasmonics - Herein, an integrated multifunctional design for simultaneous perfect absorption and polarization conversion is proposed that worked in the Ku band: the proposed structure consisted of... 相似文献