全文获取类型
收费全文 | 2704篇 |
免费 | 199篇 |
国内免费 | 18篇 |
专业分类
耳鼻咽喉 | 11篇 |
儿科学 | 109篇 |
妇产科学 | 43篇 |
基础医学 | 319篇 |
口腔科学 | 71篇 |
临床医学 | 311篇 |
内科学 | 853篇 |
皮肤病学 | 25篇 |
神经病学 | 201篇 |
特种医学 | 54篇 |
外科学 | 343篇 |
综合类 | 32篇 |
预防医学 | 221篇 |
眼科学 | 24篇 |
药学 | 135篇 |
中国医学 | 8篇 |
肿瘤学 | 161篇 |
出版年
2023年 | 17篇 |
2022年 | 36篇 |
2021年 | 74篇 |
2020年 | 44篇 |
2019年 | 78篇 |
2018年 | 83篇 |
2017年 | 55篇 |
2016年 | 57篇 |
2015年 | 64篇 |
2014年 | 105篇 |
2013年 | 143篇 |
2012年 | 192篇 |
2011年 | 223篇 |
2010年 | 120篇 |
2009年 | 107篇 |
2008年 | 179篇 |
2007年 | 203篇 |
2006年 | 160篇 |
2005年 | 162篇 |
2004年 | 142篇 |
2003年 | 126篇 |
2002年 | 132篇 |
2001年 | 27篇 |
2000年 | 18篇 |
1999年 | 21篇 |
1998年 | 31篇 |
1997年 | 35篇 |
1996年 | 19篇 |
1995年 | 9篇 |
1994年 | 11篇 |
1993年 | 16篇 |
1992年 | 16篇 |
1991年 | 10篇 |
1990年 | 11篇 |
1989年 | 9篇 |
1988年 | 7篇 |
1987年 | 11篇 |
1986年 | 14篇 |
1985年 | 8篇 |
1984年 | 9篇 |
1983年 | 10篇 |
1982年 | 12篇 |
1981年 | 9篇 |
1980年 | 14篇 |
1979年 | 8篇 |
1978年 | 8篇 |
1976年 | 6篇 |
1975年 | 8篇 |
1968年 | 6篇 |
1965年 | 5篇 |
排序方式: 共有2921条查询结果,搜索用时 15 毫秒
51.
52.
Wang Y Marling SJ Zhu JG Severson KS DeLuca HF 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(22):8501-8504
The development of experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis, has been studied in mice that were (i) vitamin D-deficient, (ii) minus the vitamin D receptor, (iii) minus a vitamin D 25-hydroxylase, and (iv) minus the vitamin D 25-hydroxyvitamin D-1α-hydroxylase. EAE development was markedly suppressed in mice lacking the vitamin D receptor and partially suppressed in vitamin D-insufficient mice. However, the absence of either of the two key hydroxylases (i.e., 25-hydroxylase and 1α-hydroxylase) neither inhibits nor enhances the development of EAE. These results indicate that vitamin D and the vitamin D receptor are required for the development of EAE. The results also suggest that 1,25-dihydroxyvitamin D(3) may not play a role in this autoimmune response. 相似文献
53.
Stewart JD Marchan R Lesjak MS Lambert J Hergenroeder R Ellis JK Lau CH Keun HC Schmitz G Schiller J Eibisch M Hedberg C Waldmann H Lausch E Tanner B Sehouli J Sagemueller J Staude H Steiner E Hengstler JG 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(21):8155-8160
Metastasis from primary tumors remains a major problem for tumor therapy. In the search for markers of metastasis and more effective therapies, the tumor metabolome is relevant because of its importance to the malignant phenotype and metastatic capacity of tumor cells. Altered choline metabolism is a hallmark of cancer. More specifically, a decreased glycerophosphocholine (GPC) to phosphocholine (PC) ratio was reported in breast, ovarian, and prostate cancers. Improved strategies to exploit this altered choline metabolism are therefore required. However, the critical enzyme cleaving GPC to produce choline, the initial step in the pathway controlling the GPC/PC ratio, remained unknown. In the present work, we have identified the enzyme, here named EDI3 (endometrial differential 3). Purified recombinant EDI3 protein cleaves GPC to form glycerol-3-phosphate and choline. Silencing EDI3 in MCF-7 cells decreased this enzymatic activity, increased the intracellular GPC/PC ratio, and decreased downstream lipid metabolites. Downregulating EDI3 activity inhibited cell migration via disruption of the PKCα signaling pathway, with stable overexpression of EDI3 showing the opposite effect. EDI3 was originally identified in our screening study comparing mRNA levels in metastasizing and nonmetastasizing endometrial carcinomas. Both Kaplan-Meier and multivariate analyses revealed a negative association between high EDI3 expression and relapse-free survival time in both endometrial (P < 0.001) and ovarian (P = 0.029) cancers. Overall, we have identified EDI3, a key enzyme controlling GPC and choline metabolism. Because inhibition of EDI3 activity corrects the GPC/PC ratio and decreases the migration capacity of tumor cells, it represents a possible target for therapeutic intervention. 相似文献
54.
55.
56.
57.
58.
59.