全文获取类型
收费全文 | 1398篇 |
免费 | 49篇 |
国内免费 | 7篇 |
出版年
2024年 | 1篇 |
2023年 | 7篇 |
2022年 | 17篇 |
2021年 | 28篇 |
2020年 | 32篇 |
2019年 | 24篇 |
2018年 | 30篇 |
2017年 | 36篇 |
2016年 | 24篇 |
2015年 | 41篇 |
2014年 | 91篇 |
2013年 | 75篇 |
2012年 | 66篇 |
2011年 | 122篇 |
2010年 | 63篇 |
2009年 | 85篇 |
2008年 | 88篇 |
2007年 | 85篇 |
2006年 | 86篇 |
2005年 | 63篇 |
2004年 | 57篇 |
2003年 | 31篇 |
2002年 | 24篇 |
2001年 | 14篇 |
2000年 | 14篇 |
1999年 | 22篇 |
1998年 | 22篇 |
1997年 | 18篇 |
1996年 | 12篇 |
1995年 | 22篇 |
1994年 | 16篇 |
1993年 | 15篇 |
1992年 | 18篇 |
1991年 | 10篇 |
1990年 | 10篇 |
1989年 | 12篇 |
1988年 | 8篇 |
1987年 | 10篇 |
1986年 | 6篇 |
1985年 | 9篇 |
1984年 | 8篇 |
1983年 | 5篇 |
1982年 | 9篇 |
1981年 | 8篇 |
1980年 | 2篇 |
1979年 | 3篇 |
1978年 | 3篇 |
1975年 | 1篇 |
1973年 | 1篇 |
排序方式: 共有1454条查询结果,搜索用时 15 毫秒
161.
162.
大鼠肺内NOS之分布及缺氧对其活性的影响 总被引:5,自引:0,他引:5
本文以组织化学方法对大鼠肺内一氧化氮合酶(NOS)进行定位研究,并观察了不同时间(8小时~28天)缺氧时肺内NOS活性的变化。结果显示:①正常大鼠各级支气管、肺泡管和肺泡囊上皮细胞呈NOS强阳性反应;肺血管内膜呈NOS阳性反应。②缺氧8小时,肺血管内膜NOS阳性反应开始降低,并缺氧时间越长,NOS阳性反应越低、③缺氧14天时,肺泡间质和肺血管周围炎性细胞呈NOS阳性反应;缺氧28天时,炎性细胞NOS阳性反应增强。④缺氧对支气管、肺泡管和肺泡囊上皮细胞NOS的活性无明显影响。从而提示一氧化氮不仅对肺具有一定的生理学作用,而且可能参与缺氧时肺的某些病理学过程。 相似文献
163.
Haitao Li Craig Hemann Tamer M. Abdelghany Mohamed A. El-Mahdy Jay L. Zweier 《The Journal of biological chemistry》2012,287(43):36623-36633
Cytoglobin (Cygb) is a recently discovered cytoplasmic heme-binding globin. Although multiple hemeproteins have been reported to function as nitrite reductases in mammalian cells, it is unknown whether Cygb can also reduce nitrite to nitric oxide (NO). The mechanism, magnitude, and quantitative importance of Cygb-mediated nitrite reduction in tissues have not been reported. To investigate this pathway and its quantitative importance, EPR spectroscopy, spectrophotometric measurements, and chemiluminescence NO analyzer studies were performed. Under anaerobic conditions, mixing nitrite with ferrous-Cygb triggered NO formation that was trapped and detected using EPR spin trapping. Spectrophotometric studies revealed that nitrite binding to ferrous-Cygb is followed by formation of ferric-Cygb and NO. The kinetics and magnitude of Cygb-mediated NO formation were characterized. It was observed that Cygb-mediated NO generation increased linearly with the increase of nitrite concentration under anaerobic conditions. This Cygb-mediated NO production greatly increased with acidosis and near-anoxia as occur in ischemic conditions. With the addition of nitrite, soluble guanylyl cyclase activation was significantly higher in normal smooth muscle cells compared with Cygb knocked down cells with Cygb accounting for ∼40% of the activation in control cells and ∼60% in cells subjected to hypoxia for 48 h. Overall, these studies show that Cygb-mediated nitrite reduction can play an important role in NO generation and soluble guanylyl cyclase activation under hypoxic conditions, with this process regulated by pH, oxygen tension, nitrite concentration, and the redox state of the cells. 相似文献
164.
Pino E Wang H McDonald ME Qiang L Farmer SR 《The Journal of biological chemistry》2012,287(22):18351-18358
Obese white adipose tissue is hypoxic but is incapable of inducing compensatory angiogenesis. Brown adipose tissue is highly vascularized, facilitating delivery of nutrients to brown adipocytes for heat production. In this study, we investigated the mechanisms by which white and brown adipocytes respond to hypoxia. Brown adipocytes produced lower amounts of hypoxia-inducible factor 1α (HIF-1α) than white adipocytes in response to low O(2) but induced higher levels of hypoxia-associated genes. The response of white adipocytes to hypoxia required HIF-1α, but its presence alone was incapable of inducing target gene expression under normoxic conditions. In addition to the HIF-1α targets, hypoxia also induced many inflammatory genes. Exposure of white adipocytes to a peroxisome proliferator-activated receptor γ (PPARγ) ligand (troglitazone) attenuated induction of these genes but enhanced expression of the HIF-1α targets. Knockdown of PPARγ in mature white adipocytes prevented the usual robust induction of HIF-1α targets in response to hypoxia. Similarly, knockdown of PPARγ coactivator (PGC) 1β in PGC-1α-deficient brown adipocytes eliminated their response to hypoxia. These data demonstrate that the response of white adipocytes requires HIF-1α but also depends on PPARγ in white cells and the PPARγ cofactors PGC-1α and PGC-1β in brown cells. 相似文献
165.
Fujita N Markova D Anderson DG Chiba K Toyama Y Shapiro IM Risbud MV 《The Journal of biological chemistry》2012,287(20):16975-16986
166.
167.
Müller cells support the integrity of the blood-retinal barrier, whereas their dysfunction under pathological conditions may contribute to retinal edema formation. The apelin peptide, as the endogenous ligand of G protein-coupled receptor APJ, participates in numbers of physiological and pathological processes. Recent studies highlight its emerging role against ischemic injury. Our study aimed to investigate the potential neuroprotection of apelin for primary rat retinal Müller cells under hypoxia or glucose-deprivation (GD) by cell viability, migration and apoptosis, as well as apelin/APJ immunofluorescence labeling and mRNA expression. The results showed that exogenous apelin significantly stimulated Müller cells viability and migration under normal, hypoxic and glucose-free condition, also prevented apoptosis. Apelin immunoreactivities represented weak and diffuse staining in the cytoplasm, along with restricted nuclear APJ expression. They both appeared stronger immunoreactivities after 12h hypoxia. Under hypoxic stress, apelin mRNA expression began to increase at 6h (9.97 folds, p<0.01), and APJ mRNA also up-regulated (2h 6.50 folds, p<0.05; 4h 2.25 folds, p<0.05; 6h 14 folds, p<0.01), whereas they both down-regulated during 4-12h GD. Our results suggested that apelin induced the tolerance of Müller cells to hypoxia and GD. Its administration might be a promising protection for blood-retinal barrier to ischemia. 相似文献
168.
169.
170.
Ramesh Chand Meena Navin Kumar Surendra Nath Amitabha Chakrabarti 《Indian journal of microbiology》2012,52(2):209-214
DNA repair functions are essential for the maintenance of genetic integrity and are regulated in response to both environmental and chemical stressors in mammalian and yeast cells in culture. The inhibitory effect of limited O2 availability on DNA repair functions in general and on homologous recombination (HR) in particular, correlates with increased chromosomal abnormalities in hypoxic cancer cells. Given the above, we have investigated the effects of CoCl2,––a hypoxia mimetic agent on HR and genetic aberrations in Saccharomyces cerevisiae. Our studies demonstrate that both acute and chronic exposure to CoCl2 activated HR and increased genetic aberrations in S. cerevisiae D7 cells. At early time points following addition of CoCl2 to the growth media, cells were briefly arrested in the G1-S boundary concomitant with a transient increase in Rad52-GFP foci formation and induction of low levels of DNA damage. The mode of action of CoCl2 is thus similar to that of DNA synthesis inhibitors, the later are known to induce HR and cause G1-S arrest. We propose that the activation of HR in the presence of the hypoxia mimetic agent may be attributed to the replication stress and/or DNA damage induced by the stressor. 相似文献