全文获取类型
收费全文 | 74篇 |
免费 | 3篇 |
国内免费 | 1篇 |
专业分类
耳鼻咽喉 | 1篇 |
基础医学 | 9篇 |
口腔科学 | 2篇 |
临床医学 | 5篇 |
内科学 | 17篇 |
皮肤病学 | 2篇 |
神经病学 | 13篇 |
特种医学 | 12篇 |
外科学 | 9篇 |
预防医学 | 5篇 |
药学 | 3篇 |
出版年
2023年 | 1篇 |
2022年 | 2篇 |
2021年 | 5篇 |
2020年 | 1篇 |
2019年 | 3篇 |
2018年 | 3篇 |
2016年 | 2篇 |
2015年 | 1篇 |
2014年 | 8篇 |
2013年 | 4篇 |
2012年 | 2篇 |
2011年 | 8篇 |
2010年 | 1篇 |
2009年 | 2篇 |
2008年 | 3篇 |
2007年 | 5篇 |
2006年 | 4篇 |
2005年 | 3篇 |
2004年 | 7篇 |
2003年 | 4篇 |
2002年 | 6篇 |
1999年 | 1篇 |
1998年 | 1篇 |
1996年 | 1篇 |
排序方式: 共有78条查询结果,搜索用时 15 毫秒
11.
D. Cristopher Bragg Rick B. Meeker Barbara A. Duff Robert V. English Mary B. Tompkins 《Brain research》1999,816(2):154
The neurotoxic effects of the feline immunodeficiency virus (FIV) and FIV envelope proteins were measured in primary cultures of feline cortical neurons. Envelope protein from the FIV-PPR strain promoted neuronal swelling and death, whereas envelope protein from the FIV-34TF10 isolate produced intermediate or negligible toxicity. No effect was observed in control cultures treated with envelope protein from the Epstein–Barr virus. A concentration–effect curve showed that FIV-PPR protein produced maximal toxicity at 200 pM protein and decreased toxicity at higher concentrations, which is consistent with previous reports of the HIV-1 surface glycoprotein, gp120. These effects required the presence of low concentrations of glutamate. Using the natural host cells as targets, the effects of envelope protein and infectious virions were directly compared. All of the toxic activity could be attributed to non-infectious interactions between the viral envelope and target cells. Addition of 1 μM tetrodotoxin failed to block the effects of FIV-PPR in the presence of 20 μM glutamate. Toxicity would appear to involve two steps in which the envelope protein first sensitizes neurons through non-synaptic interactions (TTX insensitive) thereby setting the stage for enhanced synaptic activation via glutamate receptors (TTX sensitive). 相似文献
12.
13.
Proteolytic host cell enzymes in gingival crevice fluid 总被引:7,自引:0,他引:7
Veli-Jukka Uitto Christopher M. Overall & Cristopher McCulloch 《Periodontology 2000》2003,31(1):77-104
14.
15.
Orekhova EV Stroganova TA Prokofyev AO Nygren G Gillberg C Elam M 《Neuroscience letters》2008,434(2):218-223
Unusual reactions to auditory stimuli are often observed in autism and may relate to ineffective inhibitory modulation of sensory input (sensory gating). A previous study of P50 sensory gating did not reveal abnormalities in high-functioning school age children [C. Kemner, B. Oranje, M.N. Verbaten, H. van Engeland, Normal P50 gating in children with autism, J. Clin. Psychiatry 63 (2002) 214-217]. Sensory gating deficit may, however, characterize younger children with autism or be a feature of retarded children with autism, reflecting imbalance of neuronal excitation/inhibition in these cohorts. We applied a paired clicks paradigm to study P50 sensory gating, and its relation to IQ and EEG gamma spectral power (as a putative marker of cortical excitability), in young (3-8 years) children with autism (N=21) and age-matched typically developing children (N=21). P50 suppression in response to the second click was normal in high-functioning children with autism, but significantly (p<0.03) reduced in those with mental retardation. P50 gating improved with age in both typically developing children and those with autism. Higher ongoing EEG gamma power corresponded to lower P50 suppression in autism (p<0.02), but not in control group. The data suggest that ineffective inhibitory control of sensory processing is characteristic for retarded children with autism and may reflect excitation/inhibition imbalance in this clinical group. 相似文献
16.
17.
18.
Broyles CD 《Toxicology and applied pharmacology》2011,254(2):215-220
Discourse speak is a powerful communication shorthand between individuals in the same discourse group. Discourse speak consists of both jargon, the unique—but understood—terminology used in the discourse group, and a member's own personally subjective vocabulary, wording that is commonly used in the discourse group but has no true consensus-based meaning. It is my observation that sometimes when scientists write, they generally focus solely on content (the pedant's stance), and, consequently, can fail to consciously consider audience, and, by extension, they fail to anticipate that their publication may reach beyond their own discourse group. If scientists do not consciously consider their intended audience and do not adapt their language for “outsiders” who might be part of the audience, the usefulness of the publication becomes limited because the intended meaning can be lost. Thus, as explained in the subsequent commentary, effective communication in the sciences not only involves defendable science but, also, a conscious perception of audience through a deliberate recognition of one's own discourse speak. 相似文献
19.
20.
Early onset torsion dystonia is a movement disorder inherited as an autosomal dominant syndrome with reduced penetrance. Symptoms appear to result from altered neuronal circuitry within the brain with no evidence of neuronal loss. Most cases are caused by loss of a glutamic acid residue in the AAA+ chaperone protein, torsinA, encoded in the DYT1 gene. In this study, torsinA was found to move in conjunction with vimentin in three cell culture paradigms-recovery from microtubule depolymerization, expression of a dominant-negative form of kinesin light chain and respreading after trypsinization. Co-immune precipitation studies revealed association between vimentin and torsinA in a complex including other cytoskeletal elements, actin and tubulin, as well as two proteins previously shown to interact with torsinA-the motor protein, kinesin light chain 1, and the nuclear envelope protein, LAP1. Morphologic and functional differences related to vimentin were noted in primary fibroblasts from patients carrying this DYT1 mutation as compared with controls, including an increased perinuclear concentration of vimentin and a delayed rate of adhesion to the substratum. Overexpression of mutant torsinA inhibited neurite extension in human neuroblastoma cells, with torsinA and vimentin immunoreactivity enriched in the perinuclear region and in cytoplasmic inclusions. Collectively, these studies suggest that mutant torsinA interferes with cytoskeletal events involving vimentin, possibly by restricting movement of these particles/filaments, and hence may affect development of neuronal pathways in the brain. 相似文献