全文获取类型
收费全文 | 58119篇 |
免费 | 4440篇 |
国内免费 | 1657篇 |
出版年
2024年 | 54篇 |
2023年 | 281篇 |
2022年 | 291篇 |
2021年 | 1392篇 |
2020年 | 971篇 |
2019年 | 1189篇 |
2018年 | 1522篇 |
2017年 | 1294篇 |
2016年 | 2002篇 |
2015年 | 3038篇 |
2014年 | 3578篇 |
2013年 | 3906篇 |
2012年 | 4973篇 |
2011年 | 4758篇 |
2010年 | 3084篇 |
2009年 | 2767篇 |
2008年 | 3711篇 |
2007年 | 3539篇 |
2006年 | 3085篇 |
2005年 | 2883篇 |
2004年 | 2638篇 |
2003年 | 2319篇 |
2002年 | 2018篇 |
2001年 | 1528篇 |
2000年 | 1409篇 |
1999年 | 1145篇 |
1998年 | 525篇 |
1997年 | 449篇 |
1996年 | 326篇 |
1995年 | 265篇 |
1994年 | 249篇 |
1993年 | 203篇 |
1992年 | 358篇 |
1991年 | 322篇 |
1990年 | 286篇 |
1989年 | 247篇 |
1988年 | 193篇 |
1987年 | 172篇 |
1986年 | 137篇 |
1985年 | 114篇 |
1984年 | 86篇 |
1983年 | 92篇 |
1982年 | 72篇 |
1981年 | 60篇 |
1980年 | 59篇 |
1979年 | 79篇 |
1978年 | 56篇 |
1977年 | 53篇 |
1976年 | 45篇 |
1974年 | 65篇 |
排序方式: 共有10000条查询结果,搜索用时 62 毫秒
31.
32.
Blocking of acidosis-mediated apoptosis by a reduction of lactate dehydrogenase activity through antisense mRNA expression. 总被引:3,自引:0,他引:3
D Jeong T S Kim J W Lee K T Kim H J Kim I H Kim I Y Kim 《Biochemical and biophysical research communications》2001,289(5):1141-1149
Lactic acid produced from the cells is a potential cause of extra- and intracellular acidification. Due to scarce technical tools, lactic acid that leads to acidification could not be reduced and direct evidence of the relationship between metabolic lactate and apoptosis has not yet been elucidated. In this study, we designed a cellular pH regulation system in CHO cells by a reduction of lactate dehydrogenase (LDH) activity through LDH antisense mRNA expression. This inhibited lactate production and, therefore, acidification of the cytosol. Under HCO3(-)-buffered growth conditions, both the parent CHO cells and the engineered CHO cells maintained their extracellular pH and intracellular pH fairly well. However, upon acidification of the cytosol, only the parent CHO cells underwent apoptosis under HCO3(-)-free conditions. In fact, we observed a number of apoptosis-related events only in control cells, including mitochondrial dysfunction, cytochrome c release, and an increase in caspase-3 enzymatic activity. 相似文献
33.
34.
Shinsaku Tokuda Young Hak Kim Hisako Matsumoto Shigeo Muro Toyohiro Hirai Michiaki Mishima Mikio Furuse 《PloS one》2015,10(12)
The relationship between chronic inflammation and cancer is well known. The inflammation increases the permeability of blood vessels and consequently elevates pressure in the interstitial tissues. However, there have been only a few reports on the effects of hydrostatic pressure on cultured cells, and the relationship between elevated hydrostatic pressure and cell properties related to malignant tumors is less well understood. Therefore, we investigated the effects of hydrostatic pressure on the cultured epithelial cells seeded on permeable filters. Surprisingly, hydrostatic pressure from basal to apical side induced epithelial stratification in Madin-Darby canine kidney (MDCK) I and Caco-2 cells, and cavities with microvilli and tight junctions around their surfaces were formed within the multi-layered epithelia. The hydrostatic pressure gradient also promoted cell proliferation, suppressed cell apoptosis, and increased transepithelial ion permeability. The inhibition of protein kinase A (PKA) promoted epithelial stratification by the hydrostatic pressure whereas the activation of PKA led to suppressed epithelial stratification. These results indicate the role of the hydrostatic pressure gradient in the regulation of various epithelial cell functions. The findings in this study may provide clues for the development of a novel strategy for the treatment of the carcinoma. 相似文献
35.
36.
37.
The formation of R-prime plasmids was selected in crosses involving soybean microsymbionts with genomic Tn5 insertions and carrying plasmid pJB3JI (with one IS2) copy as donors and Escherichia coli HB101 as recipient. Whereas the parent plasmid was 60 kb, recombinant plasmids between 76 kb and 121 kb were obtained. Restriction and Southern analyses confirmed the mobilization of Tn5 on four R-primes from Bradyrhizobium japonicum I-110 and on an R-prime plasmid from Rhizobium fredii HH303. The largest R-prime plasmid was obtained from the rescue of two symbiotically defective R. fredii mutant strains that required adenosine.Non-standard abbreviation TDP
transposon donor pool
Scientific article number A-4728 and contribution number 7724 of the Maryland Agricultural Experiment Station 相似文献
38.
Compression wood (CW) contains higher quantities of β-1-4-galactan than does normal wood (NW). However, the physiological
roles and ultrastructural distribution of β-1-4-galactan during CW formation are still not well understood. The present work
investigated deposition of β-1-4-galactan in differentiating tracheids of Cryptomeria japonica during CW formation using an immunological probe (LM5) combined with immunomicroscopy. Our immunolabeling studies clearly
showed that differences in the distribution of β-1-4-galactan between NW (and opposite wood, OW) and CW are initiated during
the formation of the S1 layer. At this stage, CW was strongly labeled in the S1 layer, whereas no label was observed in the S1 layer of NW and OW. Immunogold labeling showed that β-1-4-galactan in the S1 layer of CW tracheids significantly decreased during the formation of the S2 layer. Most β-1-4-galactan labeling was present in the outer S2 region in mature CW tracheids, and was absent in the inner S2 layer that contained helical cavities in the cell wall. In addition, delignified CW tracheids showed significantly more labeling
of β-1-4-galactan in the secondary cell wall, suggesting that lignin is likely to mask β-1-4-galactan epitopes. The study
clearly showed that β-1-4-galactan in CW was mainly deposited in the outer portion of the secondary cell wall, indicating
that its distribution may be spatially consistent with lignin distribution in CW tracheids of Cryptomeria japonica. 相似文献
39.
Mengmeng Zhuang Yuequ Deng Wenwen Zhang Bo Zhu Hao Yan Jiaqi Lou Pan Zhang Qingwei Cui Hao Tang Han Sun Yong Sun 《Cell death & disease》2021,12(6)
Intestinal mucosal injuries are directly or indirectly related to many common acute and chronic diseases. Long non-coding RNAs (lncRNAs) are expressed in many diseases, including intestinal mucosal injury. However, the relationship between lncRNAs and intestinal mucosal injury has not been determined. Here, we investigated the functions and mechanisms of action of lncRNA Bmp1 on damaged intestinal mucosa. We found that Bmp1 was increased in damaged intestinal mucosal tissue and Bmp1 overexpression was able to alleviate intestinal mucosal injury. Bmp1 overexpression was found to influence cell proliferation, colony formation, and migration in IEC-6 or HIEC-6 cells. Moreover, miR-128-3p was downregulated after Bmp1 overexpression, and upregulation of miR-128-3p reversed the effects of Bmp1 overexpression in IEC-6 cells. Phf6 was observed to be a target of miR-128-3p. Furthermore, PHF6 overexpression affected IEC-6 cells by activating PI3K/AKT signaling which was mediated by the miR-128-3p/PHF6 axis. In conclusion, Bmp1 was found to promote the expression of PHF6 through the sponge miR-128-3p, activating the PI3K/AKT signaling pathway to promote cell migration and proliferation.Subject terms: Cell growth, Cell migration 相似文献
40.