全文获取类型
收费全文 | 71846篇 |
免费 | 4884篇 |
国内免费 | 201篇 |
专业分类
耳鼻咽喉 | 529篇 |
儿科学 | 2091篇 |
妇产科学 | 1166篇 |
基础医学 | 9841篇 |
口腔科学 | 1505篇 |
临床医学 | 7540篇 |
内科学 | 15233篇 |
皮肤病学 | 981篇 |
神经病学 | 6872篇 |
特种医学 | 2232篇 |
外国民族医学 | 1篇 |
外科学 | 10051篇 |
综合类 | 878篇 |
一般理论 | 72篇 |
预防医学 | 6408篇 |
眼科学 | 1737篇 |
药学 | 4910篇 |
1篇 | |
中国医学 | 80篇 |
肿瘤学 | 4803篇 |
出版年
2023年 | 377篇 |
2022年 | 523篇 |
2021年 | 1399篇 |
2020年 | 840篇 |
2019年 | 1365篇 |
2018年 | 1662篇 |
2017年 | 1239篇 |
2016年 | 1357篇 |
2015年 | 1583篇 |
2014年 | 2368篇 |
2013年 | 3214篇 |
2012年 | 5239篇 |
2011年 | 5374篇 |
2010年 | 3004篇 |
2009年 | 2672篇 |
2008年 | 4878篇 |
2007年 | 5338篇 |
2006年 | 5241篇 |
2005年 | 4976篇 |
2004年 | 4767篇 |
2003年 | 4311篇 |
2002年 | 4208篇 |
2001年 | 578篇 |
2000年 | 404篇 |
1999年 | 638篇 |
1998年 | 900篇 |
1997年 | 754篇 |
1996年 | 636篇 |
1995年 | 608篇 |
1994年 | 490篇 |
1993年 | 466篇 |
1992年 | 348篇 |
1991年 | 312篇 |
1990年 | 266篇 |
1989年 | 256篇 |
1988年 | 264篇 |
1987年 | 216篇 |
1986年 | 232篇 |
1985年 | 243篇 |
1984年 | 309篇 |
1983年 | 325篇 |
1982年 | 384篇 |
1981年 | 370篇 |
1980年 | 345篇 |
1979年 | 199篇 |
1978年 | 241篇 |
1977年 | 191篇 |
1976年 | 133篇 |
1975年 | 102篇 |
1974年 | 105篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
41.
42.
43.
44.
45.
Peter R. McNally DO John C. Lemon MD John S. Goff MD Stephen R. Freeman MD 《Digestive diseases and sciences》1993,38(2):369-373
Summary A case of a 31-year-old female with congenital esophageal stenosis presenting with symptoms of chest pain caused by esophageal dysmotility is described. The involved segment in congenital esophageal stenosis has a characteristic thickening of the muscularis propria layer, as seen by EUS examination. In these patients, symptoms of dysphagia can be managed with esophageal dilation and noncardiac esophageal chest pain responds to pharmacotherapy with diltiazem.The opinions and assertions contained herein are the private ones of the authors and are not to be construed as official policy or reflecting the views of the Army or the Department of Defense. 相似文献
46.
H. Ronald Zielke Marian J. Jackson J. Tyson Tildon Stephen R. Max 《Molecular and chemical neuropathology / sponsored by the International Society for Neurochemistry and the World Federation of Neurology and research groups on neurochemistry and cerebrospinal fluid》1993,19(3):219-233
The effect of aluminum on the metabolism of glutamate and glutamine in astrocytes was studied to provide information about a possible biochemical mechanism for aluminum neurotoxicity and its potential contribution to neurodegenerative disease. Exposure of cultured rat brain astrocytes for 3–4 d to 5–7.5 mM aluminum lactate increased glutamine synthetase activity by 100–300% and diminished glutaminase activity by 50–85%. Increased glutamine synthetase enzyme activity was accompanied by an elevated level of glutamine synthetase mRNA. Alterations in glutaminase and glutamine synthetase following aluminum exposure caused increased intracellular glutamine levels, decreased intracellular glutamate levels, and increased conversion of glutamate to glutamine and the release of the latter into the extracellular space. The results of these changes may alter the availability of neurotransmitter glutamate in vivo and may be a mechanism for the aluminum neurotoxicity observed in individuals exposed to the metal during dialysis procedures and other situations. 相似文献
47.
Jeffrey A. Gray Stephen N. Mitchell Michael H. Joseph Grigory A. Grigoryan Sharon Dawe Helen Hodges 《Drug development research》1994,31(1):3-17
Data are reviewed, largely from experiments in the authors'laboratory, that suggest three modes of action of systemic nicotine in producing three different types of effect upon behavior and cognitive function. (1) Preexposure of a stimulus without consequence makes it harder subsequently to form associations to that stimulus, a form of selective attention known as latent inhibition. Latent inhibition is blocked by nicotine, an effect that is apparently mediated by a nicotine-induced increase in dopamine release in the nucleus accumbens. (2) A single dose of nicotine proactively increases the partial reinforcement extinction effect measured several weeks later: that is, resistance to extinction is decreased by nicotine in animals that have been trained on a continuous reinforcement schedule, and increased in animals trained on a partial reinforcement schedule. This effect appears to be due to increased synthesis of tyrosine hydroxylase in the cell bodies of noradrenergic neurons in the locus coeruleus, followed by axonal transport to the hippocampus and increased synthesis and release of noradrenaline in that structure. (3) Nicotine improves vigilance in animals with cognitive deficits due to destruction of the forebrain cholinergic projection system, either as a consequence of excitotoxic lesions of the nuclei of origin of this system or after prolonged alcohol consumption; and also in human subjects with Alzheimer's disease (in which this system undergoes degeneration). This effect is most likely due to an action at denervated cholinergic synapses in the hippocampus and neocortex. © 1994 Wiley-Liss, Inc. 相似文献
48.
49.
50.
Amy C Y Lo Alvin K H Cheung Victor K L Hung Chung-Man Yeung Qing-Yu He Jen-Fu Chiu Stephen S M Chung Sookja K Chung 《Journal of cerebral blood flow and metabolism》2007,27(8):1496-1509
Previously, we reported that transgenic mice overexpressing endothelin-1 in astrocytes showed more severe neurological deficits and increased infarct after transient focal ischemia. In those studies, we also observed increased level of aldose reductase (AR), the first and rate-limiting enzyme of the polyol pathway, which has been implicated in osmotic and oxidative stress. To further understand the involvement of the polyol pathway, the mice with deletion of enzymes in the polyol pathway, AR, and sorbitol dehydrogenase (SD), which is the second enzyme in this pathway, were challenged with similar cerebral ischemic injury. Deletion of AR-protected animals from severe neurological deficits and large infarct, whereas similar protection was not observed in mice with SD deficiency. Most interestingly, AR(-/-) brains showed lowered expression of transferrin and transferrin receptor with less iron deposition and nitrotyrosine accumulation. The protection against oxidative stress in AR(-/-) brain was also associated with less poly(adenosine diphosphate-ribose) polymerase (PARP) and caspase-3 activation. Pharmacological inhibition of AR by Fidarestat also protected animals against cerebral ischemic injury. These findings are the first to show that AR contributes to iron- and transferrin-related oxidative stress associated with cerebral ischemic injury, suggesting that inhibition of AR but not SD may have therapeutic potential against cerebral ischemic injury. 相似文献