全文获取类型
收费全文 | 47770篇 |
免费 | 4650篇 |
国内免费 | 45篇 |
专业分类
耳鼻咽喉 | 272篇 |
儿科学 | 1625篇 |
妇产科学 | 1441篇 |
基础医学 | 6478篇 |
口腔科学 | 841篇 |
临床医学 | 6305篇 |
内科学 | 8391篇 |
皮肤病学 | 714篇 |
神经病学 | 4279篇 |
特种医学 | 1652篇 |
外国民族医学 | 3篇 |
外科学 | 5532篇 |
综合类 | 1046篇 |
一般理论 | 68篇 |
预防医学 | 6434篇 |
眼科学 | 1066篇 |
药学 | 3487篇 |
1篇 | |
中国医学 | 67篇 |
肿瘤学 | 2763篇 |
出版年
2023年 | 331篇 |
2022年 | 463篇 |
2021年 | 978篇 |
2020年 | 573篇 |
2019年 | 962篇 |
2018年 | 1043篇 |
2017年 | 737篇 |
2016年 | 877篇 |
2015年 | 921篇 |
2014年 | 1278篇 |
2013年 | 1818篇 |
2012年 | 2758篇 |
2011年 | 2757篇 |
2010年 | 1478篇 |
2009年 | 1323篇 |
2008年 | 2364篇 |
2007年 | 2504篇 |
2006年 | 2438篇 |
2005年 | 2309篇 |
2004年 | 2251篇 |
2003年 | 2069篇 |
2002年 | 1919篇 |
2001年 | 1312篇 |
2000年 | 1268篇 |
1999年 | 1132篇 |
1998年 | 535篇 |
1997年 | 453篇 |
1996年 | 421篇 |
1995年 | 364篇 |
1994年 | 395篇 |
1993年 | 384篇 |
1992年 | 869篇 |
1991年 | 817篇 |
1990年 | 792篇 |
1989年 | 689篇 |
1988年 | 713篇 |
1987年 | 677篇 |
1986年 | 629篇 |
1985年 | 675篇 |
1984年 | 544篇 |
1983年 | 436篇 |
1982年 | 282篇 |
1981年 | 306篇 |
1980年 | 261篇 |
1979年 | 477篇 |
1978年 | 349篇 |
1976年 | 271篇 |
1974年 | 291篇 |
1973年 | 269篇 |
1972年 | 272篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
1.
2.
Major depressive disorder and other neuropsychiatric disorders are often managed with long-term use of antidepressant medication. Fluoxetine, an SSRI antidepressant, is widely used as a first-line treatment for neuropsychiatric disorders. However, fluoxetine has also been shown to increase the risk of metabolic diseases such as non-alcoholic fatty liver disease. Fluoxetine has been shown to increase hepatic lipid accumulation in vivo and in vitro. In addition, fluoxetine has been shown to alter the production of prostaglandins which have also been implicated in the development of non-alcoholic fatty liver disease. The goal of this study was to assess the effect of fluoxetine exposure on the prostaglandin biosynthetic pathway and lipid accumulation in a hepatic cell line (H4-II-E-C3 cells). Fluoxetine treatment increased mRNA expression of prostaglandin biosynthetic enzymes (Ptgs1, Ptgs2, and Ptgds), PPAR gamma (Pparg), and PPAR gamma downstream targets involved in fatty acid uptake (Cd36, Fatp2, and Fatp5) as well as production of 15-deoxy-Δ12,14PGJ2 a PPAR gamma ligand. The effects of fluoxetine to induce lipid accumulation were attenuated with a PTGS1 specific inhibitor (SC-560), whereas inhibition of PTGS2 had no effect. Moreover, SC-560 attenuated 15-deoxy-Δ12,14PGJ2 production and expression of PPAR gamma downstream target genes. Taken together these results suggest that fluoxetine-induced lipid abnormalities appear to be mediated via PTGS1 and its downstream product 15d-PGJ2 and suggest a novel therapeutic target to prevent some of the adverse effects of fluoxetine treatment. 相似文献
3.
Christopher Teng JiaDe Yu Jesse Taylor Adam I. Rubin James R. Treat 《Pediatric dermatology》2019,36(5):697-701
Erosive pustular dermatosis of the scalp (EPDS) is an uncommon chronic inflammatory response to scalp trauma that usually resolves with cicatricial alopecia. It most commonly affects elderly patients with a history of actinic damage. Herein, we describe a 16‐year‐old girl with acrofacial dysostosis type 1 presenting after surgery with crusting purulent scalp lesions, whose clinical presentation and histopathologic findings were consistent with EPDS. A review of the literature on EPDS in children is also detailed. 相似文献
4.
James A. Akingbasote Alison J. Foster Ian Wilson Sunil Sarda Huw B. Jones J. Gerry Kenna 《Archives of toxicology》2016,90(4):853-862
Hepatic NADPH-cytochrome P450 oxidoreductase null (HRN?) mice exhibit normal hepatic and extrahepatic biotransformation enzyme activities when compared to wild-type (WT) mice, but express no functional hepatic cytochrome P450 activities. When incubated in vitro with [14C]-diclofenac, liver microsomes from WT mice exhibited extensive biotransformation to oxidative and glucuronide metabolites and covalent binding to proteins was also observed. In contrast, whereas glucuronide conjugates and a quinone-imine metabolite were formed when [14C]-diclofenac was incubated with HRN? mouse liver, only small quantities of P450-derived oxidative metabolites were produced in these samples and covalent binding to proteins was not observed. Livers from vehicle-treated HRN? mice exhibited enhanced lipid accumulation, bile duct proliferation, hepatocellular degeneration and necrosis and inflammatory cell infiltration, which were not present in livers from WT mice. Elevated liver-derived alanine aminotransferase, glutamate dehydrogenase and alkaline phosphatase activities were also observed in plasma from HRN? mice. When treated orally with diclofenac for 7 days, at 30 mg/kg/day, the severities of the abnormal liver histopathology and plasma liver enzyme findings in HRN? mice were reduced markedly. Oral diclofenac administration did not alter the liver histopathology or elevate plasma enzyme activities of WT mice. These findings indicate that HRN? mice are valuable for exploration of the role played by hepatic P450s in drug biotransformation, but poorly suited to investigations of drug-induced liver toxicity. Nevertheless, studies in HRN? mice could provide novel insights into the role played by inflammation in liver injury and may aid the evaluation of new strategies for its treatment. 相似文献
5.
6.
7.
8.
9.
10.
Jenny U. Johansson Nathaniel S. Woodling Qian Wang Maharshi Panchal Xibin Liang Angel Trueba-Saiz Holden D. Brown Siddhita D. Mhatre Taylor Loui Katrin I. Andreasson 《The Journal of clinical investigation》2015,125(1):350-364
Microglia, the innate immune cells of the CNS, perform critical inflammatory and noninflammatory functions that maintain normal neural function. For example, microglia clear misfolded proteins, elaborate trophic factors, and regulate and terminate toxic inflammation. In Alzheimer’s disease (AD), however, beneficial microglial functions become impaired, accelerating synaptic and neuronal loss. Better understanding of the molecular mechanisms that contribute to microglial dysfunction is an important objective for identifying potential strategies to delay progression to AD. The inflammatory cyclooxygenase/prostaglandin E2 (COX/PGE2) pathway has been implicated in preclinical AD development, both in human epidemiology studies and in transgenic rodent models of AD. Here, we evaluated murine models that recapitulate microglial responses to Aβ peptides and determined that microglia-specific deletion of the gene encoding the PGE2 receptor EP2 restores microglial chemotaxis and Aβ clearance, suppresses toxic inflammation, increases cytoprotective insulin-like growth factor 1 (IGF1) signaling, and prevents synaptic injury and memory deficits. Our findings indicate that EP2 signaling suppresses beneficial microglia functions that falter during AD development and suggest that inhibition of the COX/PGE2/EP2 immune pathway has potential as a strategy to restore healthy microglial function and prevent progression to AD. 相似文献