全文获取类型
收费全文 | 1542篇 |
免费 | 80篇 |
国内免费 | 4篇 |
专业分类
耳鼻咽喉 | 16篇 |
儿科学 | 65篇 |
妇产科学 | 40篇 |
基础医学 | 165篇 |
口腔科学 | 46篇 |
临床医学 | 110篇 |
内科学 | 189篇 |
皮肤病学 | 14篇 |
神经病学 | 242篇 |
特种医学 | 97篇 |
外科学 | 173篇 |
综合类 | 186篇 |
预防医学 | 66篇 |
眼科学 | 13篇 |
药学 | 96篇 |
中国医学 | 14篇 |
肿瘤学 | 94篇 |
出版年
2021年 | 41篇 |
2019年 | 26篇 |
2018年 | 44篇 |
2017年 | 17篇 |
2015年 | 19篇 |
2014年 | 26篇 |
2013年 | 22篇 |
2012年 | 37篇 |
2011年 | 45篇 |
2010年 | 41篇 |
2009年 | 33篇 |
2008年 | 44篇 |
2007年 | 39篇 |
2006年 | 55篇 |
2005年 | 51篇 |
2004年 | 44篇 |
2003年 | 37篇 |
2002年 | 35篇 |
2001年 | 40篇 |
2000年 | 42篇 |
1999年 | 51篇 |
1998年 | 41篇 |
1997年 | 39篇 |
1996年 | 34篇 |
1995年 | 28篇 |
1994年 | 45篇 |
1993年 | 18篇 |
1992年 | 25篇 |
1991年 | 29篇 |
1990年 | 35篇 |
1989年 | 42篇 |
1988年 | 46篇 |
1987年 | 43篇 |
1986年 | 37篇 |
1985年 | 29篇 |
1984年 | 26篇 |
1983年 | 22篇 |
1982年 | 18篇 |
1980年 | 13篇 |
1978年 | 14篇 |
1976年 | 17篇 |
1975年 | 15篇 |
1974年 | 22篇 |
1973年 | 13篇 |
1972年 | 15篇 |
1971年 | 17篇 |
1970年 | 23篇 |
1969年 | 12篇 |
1968年 | 15篇 |
1967年 | 17篇 |
排序方式: 共有1626条查询结果,搜索用时 15 毫秒
1.
2.
3.
M. Flint Beal 《Annals of neurology》1995,38(3):357-366
The etiology of neurodegenerative diseases remains enigmatic; however, evidence for defects in energy metabolism, excitotoxicity, and for oxidative damage is increasingly compelling. It is likely that there is a complex interplay between these mechanisms. A defect in energy metabolism may lead to neuronal depolarization, activation of N-methyl-D-aspartate excitatory amino acid-receptors, and increases in intracellular calcium, which are buffered by mitochondria. Mitochondria are the major intracellular source of free radicals, and increased mitochondrial calcium concentrations enhance free radical generation. Mitochondrial DNA is particularly susceptible to oxidative stress, and there is evidence of age-dependent damage and deterioration of respiratory enzyme activities with normal aging. This may contribute to the delayed onset and age dependence of neurodegenerative diseases. There is evidence for increased oxidative damage to macromolecules in amyotrophic lateral sclerosis, Huntington's disease, Parkinson's disease, and Alzheimer's disease. Potential therapeutic approaches include glutamate release inhibitors, excitatory amino acid antagonists, strategies to improve mitochondrial function, free radical scavengers, and trophic factors. All of these approaches appear promising in experimental studies and are now being applied to human studies. 相似文献
4.
5.
6.
7.
8.
9.
HERMAN TOURNAYE RONNY JANSSENS PAUL DEVROEY RK VAN STEIRTEGHEM 《International journal of andrology》1994,17(1):1-8
In order to evaluate the effects of pentoxifylline on sperm motility and longevity, a controlled in-vitro study was conducted on normozoospermic donor semen samples using the Cellsoft automated system for sperm motility analysis. After incubation and selection, pentoxifylline was found to improve the recovery of spermatozoa and to increase their velocity. In the subgroup of progressively motile spermatozoa, curvilinear velocity was also enhanced. It is concluded that pentoxifylline has an effect on the vigour, but not on the pattern, of sperm motion. Pentoxifylline did not improve the motility characteristics of senescent spermatozoa in normozoospermic sperm samples. Sperm survival, as shown by supra-vital staining, and motility longevity both decreased with time after pentoxifylline treatment. 相似文献
10.
High aggregate burden of somatic mtDNA point mutations in aging and Alzheimer's disease brain. 总被引:12,自引:0,他引:12
Michael T Lin David K Simon Colette H Ahn Lauren M Kim M Flint Beal 《Human molecular genetics》2002,11(2):133-145
The mitochondrial theory of aging proposes that mitochondrial DNA (mtDNA) accumulates mutations with age, and that these mutations contribute to physiological decline in aging and degenerative diseases. Although a great deal of indirect evidence supports this hypothesis, the aggregate burden of mtDNA mutations, particularly point mutations, has not been systematically quantified in aging or neurodegenerative disorders. Therefore, we directly assessed the aggregate burden of brain mtDNA point mutations in 17 subjects with Alzheimer's disease (AD), 10 elderly control subjects and 14 younger control subjects, using a PCR-cloning-sequencing strategy. We found that brain mtDNA from elderly subjects had a higher aggregate burden of mutations than brain mtDNA from younger subjects. The average aggregate mutational burden in elderly subjects was 2 x 10(-4) mutations/bp. The bulk of these mutations were individually rare point mutations, 60% of which changed an amino acid. Control experiments ensure that these results were not due to artifacts arising from PCR error, mistaken identification of nuclear pseudogenes or ex vivo oxidation. Cytochrome oxidase activity correlated negatively with increasing mutational burden. These findings significantly bolster the mitochondrial theory of aging. 相似文献