全文获取类型
收费全文 | 5905篇 |
免费 | 385篇 |
国内免费 | 18篇 |
专业分类
耳鼻咽喉 | 49篇 |
儿科学 | 173篇 |
妇产科学 | 147篇 |
基础医学 | 852篇 |
口腔科学 | 86篇 |
临床医学 | 617篇 |
内科学 | 1319篇 |
皮肤病学 | 118篇 |
神经病学 | 562篇 |
特种医学 | 93篇 |
外科学 | 556篇 |
综合类 | 51篇 |
一般理论 | 3篇 |
预防医学 | 746篇 |
眼科学 | 104篇 |
药学 | 402篇 |
中国医学 | 32篇 |
肿瘤学 | 398篇 |
出版年
2024年 | 13篇 |
2023年 | 88篇 |
2022年 | 132篇 |
2021年 | 275篇 |
2020年 | 162篇 |
2019年 | 218篇 |
2018年 | 233篇 |
2017年 | 171篇 |
2016年 | 141篇 |
2015年 | 207篇 |
2014年 | 232篇 |
2013年 | 339篇 |
2012年 | 513篇 |
2011年 | 475篇 |
2010年 | 297篇 |
2009年 | 254篇 |
2008年 | 391篇 |
2007年 | 355篇 |
2006年 | 357篇 |
2005年 | 340篇 |
2004年 | 303篇 |
2003年 | 253篇 |
2002年 | 228篇 |
2001年 | 33篇 |
2000年 | 27篇 |
1999年 | 34篇 |
1998年 | 34篇 |
1997年 | 16篇 |
1996年 | 27篇 |
1995年 | 27篇 |
1994年 | 16篇 |
1993年 | 17篇 |
1992年 | 6篇 |
1991年 | 12篇 |
1990年 | 6篇 |
1989年 | 8篇 |
1988年 | 11篇 |
1987年 | 6篇 |
1986年 | 7篇 |
1985年 | 5篇 |
1984年 | 5篇 |
1983年 | 4篇 |
1982年 | 4篇 |
1980年 | 4篇 |
1979年 | 4篇 |
1976年 | 4篇 |
1974年 | 3篇 |
1973年 | 4篇 |
1971年 | 2篇 |
1961年 | 1篇 |
排序方式: 共有6308条查询结果,搜索用时 15 毫秒
151.
152.
153.
154.
Arranz A Doxaki C Vergadi E Martinez de la Torre Y Vaporidi K Lagoudaki ED Ieronymaki E Androulidaki A Venihaki M Margioris AN Stathopoulos EN Tsichlis PN Tsatsanis C 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(24):9517-9522
Activated macrophages are described as classically activated or M1 type and alternatively activated or M2 type, depending on their response to proinflammatory stimuli and the expression of genetic markers including iNOS, arginase1, Ym1, and Fizz1. Here we report that Akt kinases differentially contribute to macrophage polarization, with Akt1 ablation giving rise to an M1 and Akt2 ablation resulting in an M2 phenotype. Accordingly, Akt2(-/-) mice were more resistant to LPS-induced endotoxin shock and to dextran sulfate sodium (DSS)-induced colitis than wild-type mice, whereas Akt1(-/-) mice were more sensitive. Cell depletion and reconstitution experiments in a DSS-induced colitis model confirmed that the effect was macrophage-dependent. Gene-silencing studies showed that the M2 phenotype of Akt2(-/-) macrophages was cell autonomous. The microRNA miR-155, whose expression was repressed in naive and in LPS-stimulated Akt2(-/-) macrophages, and its target C/EBPβ appear to play a key role in this process. C/EBPβ, a hallmark of M2 macrophages that regulates Arg1, was up-regulated upon Akt2 ablation or silencing. Overexpression or silencing of miR-155 confirmed its central role in Akt isoform-dependent M1/M2 polarization of macrophages. 相似文献
155.
156.
Muñoz F Del Río N Sóñora C Tiscornia I Marco A Hernández A 《European journal of oral sciences》2012,120(2):104-112
Enamel defects in the permanent teeth of patients with coeliac disease (CD) are often reported as an atypical manifestation, sometimes being suggestive of an undiagnosed atypical disease. We proposed to explore the pathogenesis of these oral defects, which are poorly studied. Sequence analyses of proteins from gluten (gliadins) and of proline-rich enamel proteins (amelogenin and ameloblastin) suggested the presence of common antigenic motifs. Therefore, we analyzed, by ELISA and western blotting, the reactivity of sera from patients with CD against gliadin and enamel-derived peptides. Correlation analyses between the levels of specific antibodies against gliadin and enamel derived peptides and inhibition experiments confirmed the presence of cross-reactive antibodies. Immunoblot analysis revealed that the most prominent component in enamel matrix derivative (of approximately 18.6 kDa), identified by an amelogenin-specific antibody, is recognized by sera from patients with CD; in addition, several fractions of pure gliadin were recognized by amelogenin-specific antibody. In agreement, sera from mice immunized with enamel matrix-derived proteins generated antibodies that recognized a peptide (of approximately 21.2 kDa) derived from gliadin. In conclusion, antibodies against gliadin generated in patients with CD can react in vitro with a major enamel protein. The involvement of anti-gliadin serum in the pathogenesis of enamel defects in children with untreated CD can be hypothesized on the basis of these novel results. 相似文献
157.
158.
159.