MRI评估胎儿神经系统畸形

目的探讨MRI诊断胎儿中枢神经系统畸形的价值及其应用指征。方法回顾性分析450例中枢神经系统畸形胎儿的超声和MRI资料,与产后诊断或尸体检查结果进行对照。结果 450例患者共检出神经系统病变594处,包括单纯侧脑室增宽99处、脑积水21处、小脑延髓池增宽59处、Dandy-Walker畸形/小脑发育不良45处、胼胝体发育不良/缺如67处、透明隔增宽6处、脑白质软化15处、室管膜下囊肿/出血30处、颅内出血26处、颅内实质性病变14处、蛛网膜囊肿60处、孔洞脑13处、脑裂14处、积水型无脑畸形3处、脑水肿1处、平滑脑4处、脑组织发育不良3处、全前脑20处、小头畸形8处、头形异常3处、开放性神经管缺陷68处、脑血管畸形5处、透明隔缺如2处、颅底凹陷症1处、枕骨大孔窄1处、囊性松果体1处、脉络丛病变5处。超声正确诊断487处,准确率81.99%(487/594),MRI正确诊断551处,准确率92.76%(551/594)。结论对于胎儿神经系统各种病变,超声和MRI各有优劣,明确MRI应用指征有助于指导合理地选择产前MRI,从而明确诊断。     

The role of DJ-1 in the oxidative stress cell death cascade after stroke

Oxidative stress is closely associated with secondary cell death in many disorders of the central nervous system including stroke,Parkinson’s disease,Alzheimer’s disease.Among many aberrant oxidative stress-associated proteins,DJ-1 has been associated with the oxidative stress cell death cascade primarily in Parkinson’s disease.Although principally expressed in the cytoplasm and nucleus,DJ-1 can be secreted into the serum under pathological condition.Recently,a close pathological association between DJ-1 and oxidative stress in stroke has been implicated.To this end,we and others have demonstrated the important role of mitochondria in neuroprotection for stroke by demonstrating that the translocation of DJ-1 in the mitochondria could potentially mitigate mitochondrial injury.Here,we discuss our recent findings testing the hypothesis that DJ-1 not only functions as a form of intracellular protection from oxidative stress,but that it also utilizes paracrine and/or autocrine cues in order to accomplish extracellular signaling between neighboring neuronal cells,resulting in neuroprotection.This article highlights recent evidence supporting the status of DJ-1 as key anti-oxidative stress therapeutic target for stroke.     

Proteoglycans: Road Signs for Neurite Outgrowth

Proteoglycans in the central nervous system play integral roles as ＂traffic signals＂ for the direction of neurite outgrowth. This attribute of proteoglycans is a major factor in regeneration of the injured central nervous system. In this review, the structures of proteoglycans and the evidence suggesting their involvement in the response following spinal cord injury are presented. The review further describes the methods routinely used to determine the effect proteoglycans have on neurite outgrowth. The effects of proteoglycans on neurite outgrowth are not completely understood as there is disagreement on what component of the molecule is interacting with growing neurites and this ambiguity is chronicled in an historical context. Finally, the most recent findings suggesting possible receptors, interactions, and sulfation patterns that may be important in eliciting the effect of proteoglycans on neurite outgrowth are discussed. A greater understanding of the proteoglycan-neurite interaction is necessary for successfully promoting regeneration in the iniured central nervous system.     

Time dependent integration of matrix metalloproteinases and their targeted substrates directs axonal sprouting and synaptogenesis following central nervous system injury

Over the past two decades, many investigators have reported how extracellular matrix molecules act to regulate neuroplasticity. The majority of these studies involve proteins which are targets of matrix metalloproteinases. Importantly, these enzyme/substrate interactions can regulate degenerative and regenerative phases of synaptic plasticity, directing axonal and dendritic reorganization after brain insult. The present review first summarizes literature support for the prominent role of matrix metalloproteinases during neuroregeneration, followed by a discussion of data contrasting adaptive and maladaptive neuroplasticity that reveals time-dependent metalloproteinase/substrate regulation of postinjury synaptic recovery. The potential for these enzymes to serve as therapeutic targets for enhanced neuroplasticity after brain injury is illustrated with experiments demonstrating that metalloproteinase inhibitors can alter adaptive and maladaptive outcome. Finally, the complexity of metalloproteinase role in reactive synaptogenesis is revealed in new studies showing how these enzymes interact with immune molecules to mediate cellular response in the local regenerative environment, and are regulated by novel binding partners in the brain extracellular matrix. Together, these different examples show the complexity with which metalloproteinases are integrated into the process of neuroregeneration, and point to a promising new angle for future studies exploring how to facilitate brain plasticity.     

In the presence of danger：the extracellular matrix defensive response to central nervous system injury

Glial cells in the central nervous system （CNS） contribute to formation of the extracellular matrix, which provides adhesive sites, signaling molecules, and a diffusion barrier to enhance efficient on and axon potential propagation. In the normal adult CNS, the extracellular matrix （ECM） is relatively stable except in selected regions characterized by dynamic remodeling. However, after trauma such as a spinal cord injury or cortical contusion, the lesion epicenter becomes a focus of acute neuroinflammation. The activation of the surrounding glial cells leads to a dramatic change in the composition of the ECM at the edges of the lesion, creating a perilesion environment dominated by growth inhibitory molecules and restoration of the peripheral/ central nervous system border. An advantage of this response is to limit the invasion of damaging cells and diffusion of toxic molecules into the spared tissue regions, but this occurs at the cost of inhibiting migration of endogenous repair cells and preventing axonal regrowth. The following review was prepared by reading and discussing over 200 research articles in the field published in PubMed and selecting those with significant impact and/or controversial points. This article highlights structural and functional features of the normal adult CNS ECM and then focuses on the reactions of glial cells and changes in the perilesion border that occur following spinal cord or contusive brain injury. Current research strategies directed at modifying the inhibitory perilesion microenvironment without eliminating the protective functions of glial cell activation are discussed.     

A novel mode of retinal regeneration： the merit of a new Xenopus model

<正>Retinal regeneration:The retina is a part of the central nervous system(CNS)and has long attracted neurobiologists as an excellent model organ for the study of CNS regeneration.In classical studies using urodele amphibians like the salamander newt,it has been shown that the retina regenerates after the removal of the whole tissue even in the adulthood.This type of regeneration is considered as an example of"transdifferentiation",since the source of the regenerating retina is the     

1例重度老年性痴呆患者的康复疗养护理

老年性痴呆是一种以进行性认知障碍和记忆能力损害为主的中枢神经系统退行性疾病。按病情发展分为轻度痴呆（能完全自理日常生活）、中度痴呆（部分自理日常生活）和重度痴呆（日常生活完全不能自理）。医学界认为“痴呆症的治疗，重点在于良好的保健护理”。现结合我院护理1例老年性痴呆患者的康复疗养护理，探讨如何提升疗养效果，减慢机能衰退的护理体会。     

颅脑损伤致神经源性肺水肿的呼吸道护理

颅脑损伤并发的神经源性肺水肿（NPE）是继发于各种中枢神经系统损伤所致的突发性颅内压增高引起的急性肺水肿^[1]，多见于重型颅脑损伤患者，其特点为起病急，发展快，易漏诊延误治疗，病死率高。作者对2000年6月至2006年5月收治的36例颅脑损伤所致NPE的护理经验，探讨并总结如下。     

神经干细胞的国内研究进展

神经干细胞是指中枢神经系统中某些特殊部位具有多向分化潜能和自我更新能力的一组细胞群。在特定的条件下可在脑内发生迁移和整合．替代受损的细胞．重建神经功能区和传导通路，随着医学生物学的发展．人们对神经干细胞的研究有了更为深入的进展。神经干细胞被认为是最具潜能的神经替代物，必将为人类的神经科疾病提供更好的治疗前景．