全文获取类型
收费全文 | 1151篇 |
免费 | 90篇 |
国内免费 | 27篇 |
专业分类
耳鼻咽喉 | 7篇 |
儿科学 | 23篇 |
妇产科学 | 25篇 |
基础医学 | 145篇 |
口腔科学 | 22篇 |
临床医学 | 200篇 |
内科学 | 277篇 |
皮肤病学 | 6篇 |
神经病学 | 86篇 |
特种医学 | 101篇 |
外科学 | 170篇 |
综合类 | 30篇 |
一般理论 | 1篇 |
预防医学 | 72篇 |
眼科学 | 19篇 |
药学 | 48篇 |
肿瘤学 | 36篇 |
出版年
2022年 | 8篇 |
2021年 | 16篇 |
2019年 | 11篇 |
2018年 | 14篇 |
2017年 | 11篇 |
2016年 | 12篇 |
2015年 | 11篇 |
2014年 | 16篇 |
2013年 | 26篇 |
2012年 | 39篇 |
2011年 | 31篇 |
2010年 | 21篇 |
2009年 | 25篇 |
2008年 | 28篇 |
2007年 | 42篇 |
2006年 | 62篇 |
2005年 | 66篇 |
2004年 | 34篇 |
2003年 | 34篇 |
2002年 | 30篇 |
2001年 | 36篇 |
2000年 | 49篇 |
1999年 | 44篇 |
1998年 | 31篇 |
1997年 | 16篇 |
1996年 | 25篇 |
1995年 | 21篇 |
1994年 | 26篇 |
1993年 | 11篇 |
1992年 | 32篇 |
1991年 | 35篇 |
1990年 | 35篇 |
1989年 | 37篇 |
1988年 | 32篇 |
1987年 | 31篇 |
1986年 | 31篇 |
1985年 | 39篇 |
1984年 | 22篇 |
1983年 | 20篇 |
1982年 | 10篇 |
1981年 | 13篇 |
1980年 | 9篇 |
1979年 | 12篇 |
1978年 | 10篇 |
1977年 | 14篇 |
1975年 | 9篇 |
1974年 | 9篇 |
1973年 | 8篇 |
1971年 | 10篇 |
1970年 | 8篇 |
排序方式: 共有1268条查询结果,搜索用时 15 毫秒
1.
2.
E. Wieczerzak E. Jankowska S. Rodziewicz‐Motowido A. Giedo J. giewka Z. Grzonka M. Abrahamson A. Grubb D. Brmme 《Chemical biology & drug design》2005,66(Z1):1-11
Abstract: We have designed and synthesized a new series of azapeptides which act as potential inhibitors of cathepsin B and/or cathepsin K. Their structures are based upon the inhibitory sites of natural cysteine protease inhibitors, cystatins. For the synthesized azapeptides, the equilibrium constants for dissociation of inhibitor–enzyme complex, Ki, were determined. Comparison of these values indicated that all of the azainhibitors act much stronger toward cathepsin B. Z‐Arg‐Leu‐His‐Agly‐Ile‐Val‐OMe ( 7 ) proved to be approximately 500 times more potent for cathepsin B than for cathepsin K. To be able to explain the obtained experimental values we used the molecular dynamics procedures to analyze the interactions between cathepsin B and compound 7 . We also determined the structure of the most potent and selective cathepsin B azainhibitor by means of NMR studies and theoretical calculations. In this report, we describe SAR studies of azapeptide inhibitors indicating the influence of the conformational flexibility of the examined compounds on inhibition of cathepsins B and K. 相似文献
3.
4.
5.
6.
7.
8.
9.
M Bjarnadottir B S Wulff M Sameni B F Sloane D Keppler A Grubb M Abrahamson 《Molecular pathology》1998,51(6):317-326
AIM: To study the cellular transport of L68Q cystatin C, the cystatin variant causing amyloidosis and brain haemorrhage in patients suffering from hereditary cystatin C amyloid angiopathy (HCCAA). METHODS: Expression vectors for wild-type and L68Q cystatin C were constructed and used to transfect mouse NIH/3T3 cells. Stable cell clones were isolated after cotransfection with pSV2neo. Clones expressing human wild-type and L68Q cystatin C were compared with respect to secreted cystatin C by enzyme linked immunosorbent assay (ELISA), and for intracellular cystatin C by western blotting and immunofluorescence cytochemistry. Colocalisation studies in cells were performed by double staining with antibodies against human cystatin C and marker proteins for lysosomes, the Golgi apparatus, or the endoplasmic reticulum, and evaluated by confocal microscopy. RESULTS: Concentrations of human cystatin C secreted from transfected NIH/3T3 cells were similar to those secreted from human cells in culture. In general, clones expressing the gene encoding L68Q cystatin C secreted slightly lower amounts of the protein than clones expressing wild-type human cystatin C. Both immunofluorescence cytochemistry and western blotting experiments showed an increased accumulation of cystatin C in cells expressing the gene encoding L68Q cystatin C compared with cells expressing the gene for the wild-type protein. The intracellularly accumulating L68Q cystatin C was insoluble and located mainly in the endoplasmic reticulum. CONCLUSIONS: The cellular transport of human cystatin C is impeded by the pathogenic amino acid substitution Leu68-->Gln. The resulting intracellular accumulation and increased localised concentration of L68Q cystatin C might be an important event in the molecular pathophysiology of amyloid formation and brain haemorrhage in patients with HCCAA. 相似文献
10.