首页 | 本学科首页   官方微博 | 高级检索  
文章检索
  按 检索   检索词:      
出版年份:   被引次数:   他引次数: 提示:输入*表示无穷大
  收费全文   224篇
  免费   10篇
  国内免费   2篇
儿科学   2篇
妇产科学   1篇
基础医学   53篇
口腔科学   4篇
临床医学   6篇
内科学   17篇
皮肤病学   2篇
神经病学   98篇
特种医学   2篇
外科学   3篇
综合类   7篇
预防医学   2篇
眼科学   1篇
药学   16篇
中国医学   3篇
肿瘤学   19篇
  2023年   1篇
  2021年   2篇
  2020年   1篇
  2019年   1篇
  2018年   2篇
  2017年   3篇
  2016年   6篇
  2015年   3篇
  2014年   7篇
  2013年   9篇
  2012年   8篇
  2011年   11篇
  2010年   15篇
  2009年   15篇
  2008年   31篇
  2007年   15篇
  2006年   11篇
  2005年   17篇
  2004年   8篇
  2003年   7篇
  2002年   6篇
  2001年   8篇
  2000年   4篇
  1999年   2篇
  1998年   5篇
  1997年   3篇
  1996年   5篇
  1995年   8篇
  1994年   5篇
  1993年   7篇
  1992年   4篇
  1991年   5篇
  1989年   1篇
排序方式: 共有236条查询结果,搜索用时 15 毫秒
1.
2.
NG2 cells comprise a heterogeneous precursor population but molecular markers distinguishing between the assumed NG2 cell subpopulations are lacking. Previously, we described that a subfraction of the synaptic cell adhesion molecule SynCAM 1 is modified with the glycan polysialic acid (polySia) in NG2 cells. As for its major carrier, the neural cell adhesion molecule NCAM, polySia attenuates SynCAM 1 adhesion. Functions, as well as cellular and subcellular distribution of polySia‐SynCAM 1 are elusive. Using murine glial cultures we now demonstrate that polySia‐SynCAM 1 is confined to the Golgi compartment of a subset of NG2 cells and transiently recruited to the cell surface in response to depolarization. NG2 cells with Golgi‐confined polySia were NCAM‐negative, but positive for markers of oligodendrocyte precursor cells (OPCs). Consistent with previous data on polySia‐SynCAM 1, polySia in Ncam?/? NG2 cells was exclusively attached to N‐glycans and synthesized by ST8SIA2, one out of two mammalian polysialyltransferases. Unexpectedly, Golgi‐confined polySia was also detected in Ncam?/? microglia, but this fraction resided on O‐glycans and was produced by the second polysialyltransferase, ST8SIA4, indicating the presence of yet another polySia carrier in microglia. Searching for this carrier, we identified polysialylated neuropilin‐2, so far only known from dendritic cells and exudate macrophages. Microglia activation by LPS, but not interleukin‐4, caused a transient translocation of Golgi‐localized polySia to the cell surface, resulting in complete depletion. Finally, NO‐production of LPS‐stimulated microglia was attenuated by addition of polySia suggesting that the observed loss of polySia‐neuropilin‐2 is involved in negative feedback regulation of pro‐inflammatory microglia polarization. GLIA 2015;63:1240–1255  相似文献   
3.
4.
Depressive symptoms exist on a continuum, the far end of which is found in depressive disorders. Utilizing the continuous spectrum of depressive symptoms may therefore contribute to the understanding of the biological underpinnings of depression. Gene set enrichment analysis (GSEA) is an important tool for the identification of gene groups linked to complex traits, and was applied in the present study on genome-wide association study (GWAS) data of depression scores and their brain-level structural correlates in healthy young individuals. On symptom level (i.e. depression scores), robust enrichment was identified for two gene sets: NCAM1 Interactions and Collagen Formation. Depression scores were also associated with decreased fractional anisotropy (FA) – a brain white matter property – within the forceps minor and the left superior temporal longitudinal fasciculus. Within each of these tracts, mean FA value of depression score-associated voxels was used as a phenotype in a subsequent GSEA. The NCAM1 Interactions gene set was significantly enriched in these tracts. By linking the NCAM1 Interactions gene set to depression scores and their structural brain correlates in healthy participants, the current study contributes to the understanding of the molecular underpinnings of depressive symptomatology.  相似文献   
5.
6.
Introduction: Recovery after peripheral nerve lesions depends on guiding axons back to their targets. Polysialic acid upregulation by regrowing axons has been proposed recently as necessary for this target selectivity. Methods: We reexamined this proposition using a cross‐reinnervation model whereby axons from obturator motor neurons that do not upregulate polysialic acid regenerated into the distal femoral nerve. Our aim was to assess their target selectivity between pathways to muscle and skin. Results: After simple cross‐repair, obturator motor neurons showed no pathway preference, but the same repair with a shortened skin pathway resulted in selective targeting of these motor neurons to muscle by a polysialic acid–independent mechanism. Conclusion: The intrinsic molecular differences between motor neuron pools can be overcome by manipulation of their access to different peripheral nerve pathways such that obturator motor neurons preferentially project to a terminal nerve branch to muscle despite not upregulating the expression of polysialic acid. Muscle Nerve 47: 364–371, 2013  相似文献   
7.
Background: Antibodies to CD56 label natural killer cells as well as tissues with neural and neuroendocrine differentiation. Despite its apparently limited distribution, other conditions may unexpectedly show strong CD56 expression. Methods: We report three cases to document another setting with strong expression of CD56 in the skin: damaged and/or regenerating muscle fibers. One case of cutaneous lupus erythematosus, one case of lymphomatoid granulomatosis, and one case of a dermal scar adjacent to cutaneous muscle fibers were evaluated with a panel of antibodies, including CD56. Results: All cases showed histopathologic evidence of muscle fiber damage in the setting of lymphocytic infiltration or trauma. All cases showed prominent expression of CD56 by damaged and/or regenerating muscle fibers. The degree of CD56 expression was directly proportional to the proximity to the injury site and inversely proportional to fiber diameter. Conclusions: Even though CD56 is a useful marker for certain cytotoxic lymphomas and neural/neuroendocrine neoplasms, its expression is not limited to these conditions. Our cases highlight another unexpected example of strong CD56 expression in the skin: damaged and/or regenerating muscle fibers. The growing list of CD56‐positive conditions suggests that this marker may not be as specific as initially assumed. Mckay K, McNiff J, Subtil A. Prominent CD56 expression by damaged and regenerating muscle fibers in the skin.  相似文献   
8.
目的:研究长期中等负荷游泳运动对大鼠空间记忆及海马神经黏附分子(NCAM)的影响。方法:雄性SD大鼠40只,随机分为空白对照组(CN组)、水迷宫组(CM组)、运动组(EN组)和运动+水迷宫组(EM组)4组,每组10只。CN组和CM组常规饲养,不加干预;EN组和EM组进行7周中等负荷游泳训练,1次/天,6 d/周。第1次游10 min,此后每日增加5 min,至第2周末达60 min,第3周后每天游120 min,维持该运动量至第7周。每周末测大鼠体重。7周后,CN组和EN组大鼠断头取大脑海马组织,采用real-time PCR和Western blot检测NCAM mRNA和蛋白表达;CM组和EM组大鼠进行Morris水迷宫训练并检测定其定位航行和空间探索能力。结果:1、实验期间,EN组第5、7周末体重均显著低于CN组(P<0.05);EM组第4、5、6、7周末体重显著低于CM组(P<0.05,P<0.01)。2、Morris水迷宫训练后,EM组大鼠平均逃避潜伏期显著低于CM组(P<0.05),而在水迷宫空间探索实验中,EM组大鼠空间探索平均穿越次数较CM组显著增多(P<0.01)。3、EN组海马组织NCAM基因和蛋白表达均显著高于CN组(P<0.01)。结论:7周中等负荷运动缩短大鼠定位航行逃避潜伏期,提高大鼠空间探索穿越次数,长期适宜运动提高大鼠海马NCAM表达,有利于提高大鼠的空间学习记忆能力。  相似文献   
9.
Microglia are tissue macrophages and mediators of innate immune responses in the brain. The protein‐modifying glycan polysialic acid (polySia) is implicated in modulating microglia activity. Cultured murine microglia maintain a pool of Golgi‐confined polySia, which is depleted in response to lipopolysaccharide (LPS)‐induced activation. Polysialylated neuropilin‐2 (polySia‐NRP2) contributes to this pool but further polySia protein carriers have remained elusive. Here, we use organotypic brain slice cultures to demonstrate that injury‐induced activation of microglia initiates Golgi‐confined polySia expression in situ. An unbiased glycoproteomic approach with stem cell‐derived microglia identifies E‐selectin ligand‐1 (ESL‐1) as a novel polySia acceptor. Together with polySia‐NRP2, polySia‐ESL‐1 is also detected in primary cultured microglia, in brain slice cultures and in phorbol ester‐induced THP‐1 macrophages. Induction of stem cell‐derived microglia, activated microglia in brain slice cultures and THP‐1 macrophages by LPS, but not interleukin‐4, causes polySia depletion and, as shown for stem cell‐derived microglia, a metalloproteinase‐dependent release of polySia‐ESL‐1 and polySia‐NRP2. Moreover, soluble polySia attenuates LPS‐induced production of nitric oxide and proinflammatory cytokines. Thus, shedding of polySia‐ESL‐1 and polySia‐NRP2 after LPS‐induced activation of microglia and THP‐1 macrophages may constitute a mechanism for negative feedback regulation. GLIA 2016 GLIA 2016;64:1314–1330  相似文献   
10.
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号