全文获取类型
收费全文 | 107篇 |
免费 | 18篇 |
出版年
2021年 | 2篇 |
2020年 | 1篇 |
2017年 | 2篇 |
2016年 | 2篇 |
2015年 | 4篇 |
2014年 | 1篇 |
2013年 | 4篇 |
2012年 | 8篇 |
2011年 | 8篇 |
2010年 | 7篇 |
2009年 | 3篇 |
2008年 | 4篇 |
2007年 | 4篇 |
2006年 | 5篇 |
2005年 | 5篇 |
2004年 | 5篇 |
2003年 | 4篇 |
2002年 | 4篇 |
2001年 | 3篇 |
1999年 | 4篇 |
1998年 | 6篇 |
1997年 | 1篇 |
1996年 | 5篇 |
1995年 | 2篇 |
1994年 | 1篇 |
1993年 | 3篇 |
1992年 | 6篇 |
1991年 | 2篇 |
1990年 | 3篇 |
1984年 | 2篇 |
1982年 | 1篇 |
1981年 | 1篇 |
1977年 | 4篇 |
1976年 | 1篇 |
1975年 | 2篇 |
1972年 | 1篇 |
1971年 | 1篇 |
1953年 | 1篇 |
1925年 | 1篇 |
1904年 | 1篇 |
排序方式: 共有125条查询结果,搜索用时 218 毫秒
91.
CC van Diemen DS Postma M Siedlinski A Blokstra HA Smit HM Boezen 《Respiratory research》2011,12(1):57
Background
An imbalance in Matrix MetalloProteases (MMPs) and Tissue Inhibitors of MMPs (TIMPs) contributes to Chronic Obstructive Pulmonary Disease (COPD) development. Longitudinal studies investigating Single Nucleotide Polymorphisms (SNPs) in MMPs and TIMPs with respect to COPD development and lung function decline in the general population are lacking.Methods
We genotyped SNPs in MMP1 (G-1607GG), MMP2 (-1306 C/T), MMP9 (3 tagging SNPs), MMP12 (A-82G and Asn357Ser) and TIMP1 (Phe124Phe and Ile158Ile) in 1390 Caucasians with multiple FEV1 measurements from a prospective cohort study in the general population. FEV1 decline was analyzed using linear mixed effect models adjusted for confounders. Analyses of the X-chromosomal TIMP1 gene were stratified according to sex. All significant associations were repeated in an independent general population cohort (n = 1152).Results
MMP2 -1306 TT genotype carriers had excess FEV1 decline (-4.0 ml/yr, p = 0.03) compared to wild type carriers. TIMP1 Ile158Ile predicted significant excess FEV1 decline in both males and females. TIMP1 Phe124Phe predicted significant excess FEV1 decline in males only, which was replicated (p = 0.10) in the second cohort. The MMP2 and TIMP1 Ile158Ile associations were not replicated. Although power was limited, we did not find associations with COPD development.Conclusions
We for the first time show that TIMP1 Phe124Phe contributes to excess FEV1 decline in two independent prospective cohorts, albeit not quite reaching conventional statistical significance in the replication cohort. SNPs in MMPs evidently do not contribute to FEV1 decline in the general population. 相似文献92.
Sanchez EJ Munske GR Criswell A Milting H Dunker AK Kang C 《Molecular and cellular biochemistry》2011,349(1-2):195-204
Prolactin (PRL) is known to participate in the lactation-induced maternal bone loss, presumably by inducing the release of receptor activator of nuclear factor-κB ligand (RANKL), a potent osteoclastogenic factor from osteoblasts. Since maternal bone resorption was too massive to be solely explained by RANKL and osteoclasts did not express PRL receptors (PRLR), the involvement of some other osteoblast-derived osteoclastogenic modulators was anticipated. Herein, the authors used quantitative real-time PCR to investigate the mRNA expressions of various osteoclastogenic factors in osteoblast-like UMR106 cells directly exposed to PRL for 48 h. These cells were found to express PRLR and respond to 300 ng/ml PRL by increasing RANKL mRNA expression. This PRL concentration (comparable to plasma PRL levels in lactation) also induced the upregulation of monocyte chemoattractant protein (MCP)-1, cyclooxygenase (Cox)-2, and ephrin-B1, whereas a higher concentration (500 ng/ml) was required to upregulate tumor necrosis factor (TNF)-α and interleukin (IL)-1. However, 100-500 ng/ml PRL affected neither the cell proliferation, the cell viability nor the mRNA expressions of macrophage colony-stimulating factor, IL-6, ephrin type-B receptor 4 and ephrin-B2. In conclusion, besides RANKL overexpression, PRL upregulated the expressions of other osteoclastogenic modulators, i.e., MCP-1, Cox-2, TNF-α, IL-1, and ephrin-B1, thus, further explaining how PRL induced bone loss in lactating mothers. 相似文献
93.
94.
95.
96.
97.
Adaptation of Nitrogen Fixation by Intact Soybean Nodules to Altered Rhizosphere pO(2) 总被引:4,自引:4,他引:0
下载免费PDF全文
![点击此处可从《Plant physiology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
The N2-fixing legume nodule requires O2 for ATP production; however, the O2 sensitivity of nitrogenase dictates a requirement for a low pO2 inside the nodule. The effects of long term exposures to various pO2s on N2[C2H2] fixation were evaluated with intact soybean (Glycine max [L.] Merr., var. Wye) plants. Continuous exposure of their rhizosphere to a pO2 of 0.06 atmospheres initially reduced nitrogenase activity by 37 to 45% with restoration of original activity in 4 to 24 hours and with no further change in tests up to 95 hours; continuous exposure to 0.02 atmosphere of O2 initially reduced nitrogenase activity 72%, with only partial recovery by 95 hours. Similar exposures to a pO2 of 0.32 atmospheres had little effect on N2[C2H2] fixation; a pO2 of 0.89 atmospheres initially reduced nitrogenase activity by 98% with restoration to only 14 to 24% of that of the ambient O2 controls by 95 hours. Re-exposure to ambient pO2 of plants adapted to nonambient pO2s reduced N2[C2H2] fixation to similar magnitudes as the reductions which occurred upon initial exposure to variant pO2 conditions, and a time period was required to readapt to ambient O2. It is concluded that the N2[C2H2]-fixing system of intact soybean plants is able to adapt to a wide range of external pO2s as probably occur in soil. We postulate that this occurs through an undefined mechanism which enables the nodule to maintain an internal pO2 optimal for nitrogenase activity. 相似文献
98.
S K Powers J Lawler D Criswell F K Lieu D Martin 《Journal of applied physiology》1992,72(3):1068-1073
We examined the oxidative and antioxidant enzyme activities in respiratory and locomotor muscles in response to endurance training in young and aging rats. Young adult (4-mo-old) and old (24-mo-old) female Fischer 344 rats were divided into four groups: 1) young trained (n = 12), 2) young untrained (n = 12), 3) old trained (n = 10), and 4) old untrained (n = 6). Both young and old endurance-trained animals performed the same training protocol during 10 wk of continuous treadmill exercise (60 min/day, 5 days/wk). Compared with young untrained animals, the young trained group had significantly elevated (P less than 0.05) activities of 3-hydroxyacyl-CoA dehydrogenase (HADH), glutathione peroxidase (GPX), and citrate synthase (CS) in both the costal diaphragm and the plantaris muscle. In contrast, training had no influence (P greater than 0.05) on the activity of lactate dehydrogenase within the costal diaphragm in young animals. In the aging animals, training did not alter (P greater than 0.05) activities of CS, HADH, GPX, or lactate dehydrogenase in the costal diaphragm but significantly (P less than 0.05) increased CS, HADH, and GPX activities in the plantaris muscle. Furthermore, training resulted in higher activities of CS and HADH in the intercostal muscles in the old trained than in the old untrained animals. Finally, activities of CS, HADH, and GPX were significantly (P less than 0.05) lower in the plantaris in the old untrained than in the young untrained animals; however, CS, HADH, and GPX activities were greater (P less than 0.05) in the costal diaphragm in the old sedentary than in the young untrained animals.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
99.
100.
Scott K. Powers Daniel Martin Michael Cicale Nancy Collop David Huang David Criswell 《European journal of applied physiology and occupational physiology》1992,65(1):37-42
These experiments examined the exercise-induced changes in pulmonary gas exchange in elite endurance athletes and tested the hypothesis that an inadequate hyperventilatory response might explain the large intersubject variability in arterial partial pressure of oxygen (PaO2) during heavy exercise in this population. Twelve highly trained endurance cyclists [maximum oxygen consumption (VO2max) range = 65-77 ml.kg-1.min-1] performed a normoxic graded exercise test on a cycle ergometer to VO2max at sea level. During incremental exercise at VO2max, 5 of the 12 subjects had ideal alveolar to arterial PO2 gradients (PA-aO2) of above 5 kPa (range 5-5.7) and a decline from resting PaO2 (delta PaO2) 2.4 kPa or above (range 2.4-2.7). In contrast, 4 subjects had a maximal exercise PA-aO2 of 4.0-4.3 kPa with delta PaO2 of 0.4-1.3 kPa while the remaining 3 subjects had PA-aO2 of 4.3-5 kPa with delta PaO2 between 1.7 and 2.0 kPa. The correlation between PAO2 and PaO2 at VO2max was 0.17. Further, the correlation between the ratio of ventilation to oxygen consumption vs PaO2 and arterial partial pressure of carbon dioxide vs PaO2 at VO2max was 0.17 and 0.34, respectively. These experiments demonstrate that heavy exercise results in significantly compromised pulmonary gas exchange in approximately 40% of the elite endurance athletes studied. These data do not support the hypothesis that the principal mechanism to explain this gas exchange failure is an inadequate hyperventilatory response. 相似文献