全文获取类型
收费全文 | 427篇 |
免费 | 41篇 |
国内免费 | 2篇 |
专业分类
儿科学 | 39篇 |
妇产科学 | 1篇 |
基础医学 | 54篇 |
口腔科学 | 12篇 |
临床医学 | 41篇 |
内科学 | 79篇 |
皮肤病学 | 5篇 |
神经病学 | 7篇 |
特种医学 | 53篇 |
外科学 | 36篇 |
综合类 | 8篇 |
预防医学 | 18篇 |
眼科学 | 57篇 |
药学 | 31篇 |
肿瘤学 | 29篇 |
出版年
2022年 | 1篇 |
2021年 | 2篇 |
2020年 | 2篇 |
2019年 | 5篇 |
2018年 | 8篇 |
2017年 | 9篇 |
2016年 | 11篇 |
2015年 | 14篇 |
2014年 | 20篇 |
2013年 | 14篇 |
2012年 | 10篇 |
2011年 | 9篇 |
2010年 | 10篇 |
2009年 | 23篇 |
2008年 | 11篇 |
2007年 | 10篇 |
2006年 | 18篇 |
2005年 | 12篇 |
2004年 | 7篇 |
2003年 | 13篇 |
2002年 | 10篇 |
2001年 | 19篇 |
2000年 | 11篇 |
1999年 | 5篇 |
1998年 | 21篇 |
1997年 | 28篇 |
1996年 | 27篇 |
1995年 | 15篇 |
1994年 | 25篇 |
1993年 | 15篇 |
1992年 | 7篇 |
1991年 | 9篇 |
1990年 | 6篇 |
1989年 | 10篇 |
1988年 | 7篇 |
1987年 | 5篇 |
1986年 | 5篇 |
1985年 | 5篇 |
1984年 | 3篇 |
1983年 | 4篇 |
1982年 | 3篇 |
1981年 | 3篇 |
1980年 | 6篇 |
1977年 | 1篇 |
1976年 | 5篇 |
1975年 | 1篇 |
1974年 | 2篇 |
1972年 | 1篇 |
1969年 | 1篇 |
1966年 | 1篇 |
排序方式: 共有470条查询结果,搜索用时 15 毫秒
11.
Comprehensive mutational scanning of the p53 coding region by two- dimensional gene scanning 总被引:2,自引:0,他引:2
A comprehensive mutational scanning test for the p53 coding region based on
multiplex PCR and two-dimensional DNA electrophoresis was designed and
evaluated. In a 2-step multiplex PCR, the p53 coding region (exons 2-11)
was amplified as a single 8646-bp fragment by long- distance PCR in step
one. This fragment served as a template for the subsequent co-amplification
of the individual exons in two multiplex groups in step two. The multiplex
products were then separated, first on the basis of size in non-denaturant
polyacrylamide gels and then on the basis of sequence by denaturing
gradient gel electrophoresis (DGGE). Primers for optimal PCR, melting
behavior and 2-D gel distribution were designed using a recently developed
computer program. The resulting two-dimensional gene scanning (TDGS) test
was evaluated by screening, in a blinded fashion, 29 coded DNA samples from
Li- Fraumeni syndrome patients with previously identified germline
mutations. All mutations were correctly detected. This assay provides an
accurate, cost-effective and non-radioactive method for simultaneous
mutational scanning of all p53 coding exons.
相似文献
12.
13.
Association of granulocyte-macrophage colony-stimulating factor with the crystalloid granules of human eosinophils 总被引:3,自引:1,他引:3
Levi-Schaffer F; Lacy P; Severs NJ; Newman TM; North J; Gomperts B; Kay AB; Moqbel R 《Blood》1995,85(9):2579-2586
We have previously shown that normal-density human peripheral blood eosinophils transcribe and translate mRNA for granulocyte-macrophage colony-stimulating factor (GM-CSF) and that the intracellular distribution was granular as assessed by light microscopy immunocytochemistry. The present study was conducted to confirm this apparent association between GM-CSF and the crystalloid granule using a subcellular fractionation method for human eosinophils and immunogold electron microscopy (EM). Highly purified (> 99%, by negative selection using anti-CD16 immunomagnetic microbeads) human peripheral blood eosinophils were obtained from four asthmatic subjects (not taking systemic medication), homogenized and density fractionated (5 x 10(7) cells/subject) on linear Nycodenz gradients. Twenty-four fractions were collected from each cell preparation and analyzed for marker enzyme activities as well as total protein. Dot blot analysis with specific monoclonal antibodies (MoAbs) was used to detect the eosinophil granule proteins major basic protein (MBP) and eosinophil cationic protein (ECP). An anti-CD9 MoAb was used as an eosinophil plasma membrane marker. Lactate dehydrogenase (LDH) was used as a cytosolic marker. Immunoreactivity for GM-CSF was detected by a specific enzyme-linked immunosorbent assay using a polyclonal antihuman GM-CSF antibody and confirmed by dot blot. GM-CSF coeluted with the cellular fractions containing granule markers (MBP, ECP, eosinophil peroxidase, hexosaminidase, and arylsulphatase), but not those containing cytoplasm (LDH+) or membrane (CD9+) markers. EM examination of pooled fractions associated with the peak of GM-CSF immunoreactivity confirmed that they contained crystalloid and small granules, but not plasma membrane. In addition, quantification, using immunogold labeling with an anti/GM-CSF MoAb, indicated preferential localization of gold particles over the eosinophil granule cores of intact cells. Thus, our results indicate that GM-CSF resides as a granule-associated, stored mediator in unstimulated human eosinophils. 相似文献
14.
S Desai T Diener BJ-K Tan NJ Lowry C Talukdar WM Chrusch S Wiebe 《The Canadian Journal of Infectious Diseases & Medical Microbiology》2014,25(4):227-228
The present article reports a case involving an immunocompetent, previously well child who, despite two previous doses of inactivated poliovirus vaccine, developed severe flaccid paralysis consistent with polio after receiving oral polio vaccine. 相似文献
15.
16.
17.
18.
Neuropeptide Y Attenuates Stress‐Induced Bone Loss Through Suppression of Noradrenaline Circuits 下载免费PDF全文
PA Baldock S Lin L Zhang T Karl Y Shi F Driessler A Zengin B Hörmer NJ Lee IPL Wong EJD Lin RF Enriquez B Stehrer MJ During E Yulyaningsih S Zolotukhin ST Ruohonen E Savontaus A Sainsbury H Herzog 《Journal of bone and mineral research》2014,29(10):2238-2249
Chronic stress and depression have adverse consequences on many organ systems, including the skeleton, but the mechanisms underlying stress‐induced bone loss remain unclear. Here we demonstrate that neuropeptide Y (NPY), centrally and peripherally, plays a critical role in protecting against stress‐induced bone loss. Mice lacking the anxiolytic factor NPY exhibit more anxious behavior and elevated corticosterone levels. Additionally, following a 6‐week restraint, or cold‐stress protocol, Npy‐null mice exhibit three‐fold greater bone loss compared to wild‐type mice, owing to suppression of osteoblast activity. This stress‐protective NPY pathway acts specifically through Y2 receptors. Centrally, Y2 receptors suppress corticotropin‐releasing factor expression and inhibit activation of noradrenergic neurons in the paraventricular nucleus. In the periphery, they act to control noradrenaline release from sympathetic neurons. Specific deletion of arcuate Y2 receptors recapitulates the Npy‐null stress response, coincident with elevated serum noradrenaline. Importantly, specific reintroduction of NPY solely in noradrenergic neurons of otherwise Npy‐null mice blocks the increase in circulating noradrenaline and the stress‐induced bone loss. Thus, NPY protects against excessive stress‐induced bone loss, through Y2 receptor‐mediated modulation of central and peripheral noradrenergic neurons. © 2014 American Society for Bone and Mineral Research. 相似文献
19.
20.