全文获取类型
收费全文 | 158篇 |
免费 | 1篇 |
出版年
2023年 | 2篇 |
2022年 | 2篇 |
2021年 | 5篇 |
2020年 | 2篇 |
2019年 | 6篇 |
2018年 | 3篇 |
2017年 | 6篇 |
2016年 | 6篇 |
2015年 | 3篇 |
2014年 | 8篇 |
2013年 | 3篇 |
2012年 | 4篇 |
2011年 | 10篇 |
2010年 | 5篇 |
2009年 | 10篇 |
2008年 | 4篇 |
2007年 | 10篇 |
2006年 | 5篇 |
2005年 | 6篇 |
2004年 | 5篇 |
2003年 | 3篇 |
2002年 | 4篇 |
2001年 | 2篇 |
2000年 | 4篇 |
1999年 | 2篇 |
1998年 | 6篇 |
1995年 | 1篇 |
1992年 | 4篇 |
1989年 | 4篇 |
1988年 | 2篇 |
1987年 | 4篇 |
1986年 | 2篇 |
1985年 | 5篇 |
1984年 | 1篇 |
1983年 | 1篇 |
1981年 | 1篇 |
1977年 | 1篇 |
1975年 | 2篇 |
1973年 | 2篇 |
1971年 | 1篇 |
1970年 | 1篇 |
1968年 | 1篇 |
排序方式: 共有159条查询结果,搜索用时 9 毫秒
61.
62.
I. F. Sukhanova L. M. Kozhevnikova G. Yu. Mironova P. V. Avdonin 《Biology Bulletin》2017,44(2):179-186
It has been shown that the Epac1 and Epac2 protein inhibitor ESI-09 has no effect on the amplitude of contraction of aortic rings caused by the influence of serotonin, noradrenaline, or KCl depolarizing solution, but changes the kinetics of the contractile response. It was noted that in the presence of ESI-09 the curve of the relaxation phase in intact and deendothelized vessels moved to the left under the impact of serotonin or KCl and the phase of prolonged tonic contraction, which developed after the exposure to noradrenalin, was canceled. It was found that ESI-09 exerted different effects on the induced growth in the concentration of cytoplasmic Ca2+ in the aortic smooth muscle cells of rats depending on the agonist, whereas the selective inhibitor Epac2 ESI-05 has no effect on vascular contractility and calcium metabolism in the aortic smooth muscle of rats. The cAMP-independent participation of Epac1 in the formation of the contractile response to the influence of vasoconstrictor compounds was revealed. 相似文献
63.
64.
O. N. Sheveleva O. V. Payushina M. N. Kozhevnikova N. N. Butorina V. I. Starostin 《Cell and Tissue Biology》2011,5(6):551-559
Fetal liver stroma consists of different cell populations. We found that the liver of 17- and 20-day rat fetuses contained
skeletal muscle precursors that expressed MyoD. In primary cultures of liver cells from 15-, 17- and 20-day fetuses, spontaneous
myotube formation was observed. The antigenic profile of these myogenic elements assayed by immunocytochemistry and PCR unambiguously
indicated their skeletal muscle nature. Examination of major myogenic gene expression demonstrated that myogenic potencies
cells from liver depended on the stage of fetal development cell cultivation. It was shown that fetal liver MSCs were capable
of myotube formation in induction medium with 5-azacytidine. The results of our study show that 15- to 20-day prenatal rat
liver contains mainly preexisting skeletal muscle precursors expressing MyoD and, probably, inducible muscle precursors. 相似文献
65.
66.
Christine R Keenan Josephine SL Mok Trudi Harris Yuxiu Xia Saad Salem Alastair G Stewart 《Respiratory research》2014,15(1):55
Background
We have previously shown that transforming growth factor-beta (TGF-beta) impairs glucocorticoid (GC) function in pulmonary epithelial cell-lines. However, the signalling cascade leading to this impairment is unknown. In the present study, we provide the first evidence that TGF-beta impairs GC action in differentiated primary air-liquid interface (ALI) human bronchial epithelial cells (HBECs). Using the BEAS-2B bronchial epithelial cell line, we also present a systematic examination of the known pathways activated by TGF-beta, in order to ascertain the molecular mechanism through which TGF-beta impairs epithelial GC action.Methods
GC transactivation was measured using a Glucocorticoid Response Element (GRE)–Secreted embryonic alkaline phosphatase (SEAP) reporter and measuring GC-inducible gene expression by qRT-PCR. GC transrepression was measured by examining GC regulation of pro-inflammatory mediators. TGF-beta signalling pathways were investigated using siRNA and small molecule kinase inhibitors. GRα level, phosphorylation and sub-cellular localisation were determined by western blotting, immunocytochemistry and localisation of GRα–Yellow Fluorescent Protein (YFP). Data are presented as the mean ± SEM for n independent experiments in cell lines, or for experiments on primary HBEC cells from n individual donors. All data were statistically analysed using GraphPad Prism 5.0 (Graphpad, San Diego, CA). In most cases, two-way analyses of variance (ANOVA) with Bonferroni post-hoc tests were used to analyse the data. In all cases, P <0.05 was considered to be statistically significant.Results
TGF-beta impaired Glucocorticoid Response Element (GRE) activation and the GC induction of several anti-inflammatory genes, but did not broadly impair the regulation of pro-inflammatory gene expression in A549 and BEAS-2B cell lines. TGF-beta-impairment of GC transactivation was also observed in differentiated primary HBECs. The TGF-beta receptor (ALK5) inhibitor SB431541 fully prevented the GC transactivation impairment in the BEAS-2B cell line. However, neither inhibitors of the known downstream non-canonical signalling pathways, nor knocking down Smad4 by siRNA prevented the TGF-beta impairment of GC activity.Conclusions
Our results indicate that TGF-beta profoundly impairs GC transactivation in bronchial epithelial cells through activating ALK5, but not through known non-canonical pathways, nor through Smad4-dependent signalling, suggesting that TGF-beta may impair GC action through a novel non-canonical signalling mechanism. 相似文献67.
Natalia A Muraleva Oyuna S Kozhevnikova Anna A Zhdankina Natalia A Stefanova Tatyana V Karamysheva Anzhella Z Fursova 《Cell cycle (Georgetown, Tex.)》2014,13(22):3499-3505
Age-related macular degeneration (AMD), a neurodegenerative and vascular retinal disease, is the leading cause of blindness in the developed world. Accumulating evidence suggests that alterations in the expression of a small heat shock protein (αB-crystallin) are involved in the pathogeneses of AMD. Here we demonstrate that senescence-accelerated OXYS rats—an animal model of the dry form of AMD—develop spontaneous retinopathy against the background of reduced expression of αB-crystallin in the retina at the early preclinical stages of retinopathy (age 20 days) as well as at 4 and 24 months of age, during the progressive stage of the disease. The level of αA-crystallin expression in the retina of OXYS rats at all the ages examined was no different from that in disease-free Wistar rats. Treatment with the mitochondria-targeted antioxidant SkQ1 (plastoquinonyl-decyltriphenylphosphonium) from 1.5 to 4 months of age, 250 nmol/kg, increased the level of αB-crystallin expression in the retina of OXYS rats. SkQ1 slowed the development of retinopathy and reduced histological aberrations in retinal pigment epithelium cells. SkQ1 also attenuated neurodegenerative changes in the photoreceptors and facilitated circulation in choroid blood vessels in the retina of OXYS rats; this improvement was probably linked with the restoration of αB-crystallin expression. 相似文献
68.
69.
70.
Plant and Soil - Nutrient resource utilization is essential for plant community composition and productivity. Previous studies found that an increase in resource diversity causes species losses and... 相似文献