神经营养因子与人工耳蜗的实验研究

综述了在听觉神经系统中，神经营养因子与听力损伤、电刺激、突触疲劳的关系；介绍了神经营养因子保护听觉的分子机制，及神经营养因子在人工耳蜗研究中的应用前景和意义。     

基于少次相干平均和样本熵的视听诱发脑电特征提取

针对脑电信号的非平稳性和非线性,采用少次相干平均结合样本熵的方法对视听诱发脑电信号进行特征提取.首先,对预处理后的脑电信号进行15次相干平均,获得视觉、听觉及视听觉诱发脑电的时域特征信号;然后,将该特征信号做为原始信号输入,构成m维矢量序列,计算相关导联在靶刺激、非靶刺激和自发脑电状态的样本熵值;最后,比较分析单一视觉、听觉和视听刺激下,不同状态脑电样本熵值,文中阐明了视听觉诱发下,大脑认知的复杂性和信息耦合性.结果显示:只进行少次相干平均即可有效提取视听刺激模式下脑电的样本熵特征量,减少了因长时间视觉刺激引起神经疲劳导致的误差.同时,靶刺激的出现可使脑电样本熵值增大,表明中枢神经系统与外周刺激发生信息耦合,导致了大脑系统复杂性的提高.该研究可以应用于神经认知科学和脑-机交互系统中.     

足下垂助行仪

IDC为讯丰通开发出一款帮助足下垂患者重新行走的医疗设备。这款助行仪通过电子脉冲刺激瓣肖因运动神经元损伤或疾病引起的足下垂。该仪器包含—款功能性电刺激（FES）神经修复仪器,绑于病患腿部。该神经修复仪发送电流刺激至神经元,刺激腿部肌肉,辅助病患行走。     

突发强刺激下神经肌肉反应的下意识优先效应

目的 验证并量化突发性强感觉刺激下的神经肌肉下意识反应优先效应.方法 36名大学生分别完成弱声及突发性强声刺激条件下的听觉简单反应、音调辨别反应和音调选择反应任务,并以表面肌电图监测被试相关肌肉电活动.结果 突发性强声刺激下的肌电活动潜伏期远短于各种反应时间（较简单反应时快322±39ms）,且强声刺激显著干扰各种听觉反应任务,对简单反应时的延滞达224±123 ms.结论 研究证实了突发性强听觉刺激下神经肌肉反应的下意识优先效应,突发性强声刺激对各种反应时任务均造成显著干扰.研究结果提示突发性强刺激条件下的表面肌电信号或可作为车辆主动性防撞系统的控制输入.     

神经肌肉刺激仪校准方法研究

<正>一、引言神经肌肉刺激仪不仅具有医用设备的属性,还进一步具有医用计量器具的属性,而相关医用行业标准无法满足神经和肌肉刺激器计量技术指标的管理需求。因此,本文主要从神经肌肉刺激仪的计量技术指标入手,研究神经肌肉刺激仪的校准方法,通过合理利用相关设备对神经肌肉刺激仪的计量性能指标进行较全面的校准。二、技术参数与校准标准要求神经肌肉刺激仪的主要参数有:中频载波频率:2k Hz~8k Hz;低频调制频率:1Hz~150Hz;最大输出电     

磁刺激作用下哺乳动物有髓神经强度-时间关系的研究

磁刺激是一种利用强磁场激活神经的方法。本文将功能电刺激广泛使用的哺乳动物有髓神经纤维CRRSS模型用于磁刺激，利用该模型计算了传播跨膜动作电位沿神经的分布和时间历程，以及用电容初始充电电压表示的给定脉冲宽度的阈值刺激强度，并通过引入一组可变宽度的放电电流脉冲，确定了强度－时间关系曲线。该模型在磁刺激作用下的结果如时值得与电刺激作用下得出的结果是一致的。     

中枢神经再生材料研究进展

首先介绍了目前中枢神经再生面临的问题和应对策略,然后系统地综述了脑再生和脊髓再生修复材料的发展。研究发现,成人中枢神经系统内存的神经干细胞和具有特定分化方向的前体细胞具有潜在的、巨大的修复功能;生物支架材料与神经干细胞的联合使用能够较好地控制细胞微环境,有望提高细胞移植后的存活状况,促进中枢神经再生。最后,结合现在中枢神经再生的研究热点——神经干细胞,阐述了中枢神经再生材料调控干细胞的研究进展和潜能,为联合应用生物材料与干细胞促进中枢再生提供了参考。     

黄连的药用分析

现代药理研究表明,黄连具有抗菌、降压及扩血管、舒张平滑肌,降血糖、抑制鼻咽癌细胞、保护胃黏膜及镇吐、促进大鼠胃溃疡愈合、保护中枢神经细胞等作用。     

FNS技术

本文介绍了功能性神经肌肉电刺激(FNS)基本原理,针对的其中的几个关键问题,提出了研究的方案,并对FNS测控实验结果进行了分析.     

磁性纳米颗粒介导的电磁神经治疗的最新进展

目的 介绍磁性纳米颗粒的性质和生物医学应用,以及通过磁性纳米颗粒介导的电磁神经刺激治疗的最新进展.为今后优化刺激参数、提高磁神经刺激效率提供参考.方法 总结近年来国内外对磁性纳米颗粒的研究进展,并重点分析基于磁性纳米颗粒的神经磁刺激方法及效果.结果 磁性纳米颗粒具有成像、靶向给药、磁热疗等生物医学应用,以磁性纳米颗粒为基础进行神经磁刺激的类型可分为磁热刺激、磁电刺激及磁机械力刺激三种.这种刺激方式安全、高效且精准性高,能够改善传统磁刺激方式的缺陷.结论 磁性纳米颗粒性质独特,是近年来研究最多、发展速度最快的纳米材料之一.利用磁性纳米颗粒介导的神经磁刺激具有广阔的应用前景.     

Microthrombus‐Targeting Micelles for Neurovascular Remodeling and Enhanced Microcirculatory Perfusion in Acute Ischemic Stroke

Reperfusion injury exists as the major obstacle to full recovery of neuron functions after ischemic stroke onset and clinical thrombolytic therapies. Complex cellular cascades including oxidative stress, neuroinflammation, and brain vascular impairment occur within neurovascular units, leading to microthrombus formation and ultimate neuron death. In this work, a multitarget micelle system is developed to simultaneously modulate various cell types involved in these events. Briefly, rapamycin is encapsulated in self‐assembled micelles that are consisted of reactive oxygen species (ROS)‐responsive and fibrin‐binding polymers to achieve micelle retention and controlled drug release within the ischemic lesion. Neuron survival is reinforced by the combination of micelle facilitated ROS elimination and antistress signaling pathway interference under ischemia conditions. In vivo results demonstrate an overall remodeling of neurovascular unit through micelle polarized M2 microglia repair and blood–brain barrier preservation, leading to enhanced neuroprotection and blood perfusion. This strategy gives a proof of concept that neurovascular units can serve as an integrated target for ischemic stroke treatment with nanomedicines.     

Ischemia‐reperfusion injury. A phenomenon,that also occurs in the bone

Ischemia‐reperfusion injury of the bone occurs due to traumatic and non‐traumatic alterations affecting blood supply to the bone. It is likely to occur also upon insertion of an implant. Ischemia‐reperfusion injury of the bone has been studied by interruption of blood supply in situ, in limb replantation/transplantation models, in revascularized bone grafts and non‐vascularized bone fragments, as well as in isolated cultured cells. All cells of the bone are affected, including osteoblasts, osteocytes, osteoclasts, chondrocytes, and bone marrow cells. Critical ischemia times for induction of bone cell death, either in the ischemic period or following reperfusion, are in the range of 3 to 7 h. These critical ischemia times are significantly increased by decreasing the temperature from 37 °C to 0–4 °C. Anoxia is the most likely trigger of cell injury in the ischemic phase. In the reperfusion phase, reactive oxygen species are decisively involved in the injurious process. In general, however, the available information on the mechanism of ischemia‐reperfusion injury of the bone is relatively sparse. On the other hand, there are clear similarities to the mechanisms of ischemia‐reperfusion injury known from other organs, and there is a clear potential for protection against ischemia‐reperfusion injury of the bone.     

Triboelectric nanogenerators stimulated electroacupuncture (EA) treatment for promoting the functional recovery after spinal cord injury

Electroacupuncture (EA), as a particular type of electrostimulation treatment, has an extensive application in the field of biomedicine. Triboelectric nanogenerator (TENG) has sparked significant concern attributed to the high electrical output with low cost, whose electrical signals can also be directly usable for electrical stimulation. Here we propose a Chinese medicine EA treatment with the assistance of TENG technology, in which a bidirectional continuous current from a soft-contact freestanding rotary TENG (FR-TENG) is applied to two effective acupoints of rats by inserting electric needles. The TENG-driven EA treatment promotes the performance of gait 2 weeks after as well as the Basso–Beattie–Bresnahan (BBB) score. This elevation last as long as 4 weeks post injury. Moreover, the TENG-driven EA treatment enhances neuron survival in the ventral horn and inhibits astrocyte activation in the lesion site. Therefore, the TENG-driven EA treatment provides a significant neuroprotection effect on spinal cord contusion in rats. Our studies not only demonstrate the possibility of the TENG-driven EA treatment for traumatic central nervous system injuries but also provide an experimental basis for the prevention and treatment of diseases by traditional Chinese medicine treatment.     

Spectroscopic imaging for detection of ischemic injury in rat kidneys by use of changes in intrinsic optical properties

It is currently impossible to consistently predict kidney graft viability and function before and after transplantation. We explored optical spectroscopy to assess the degree of ischemic damage in kidney tissue. Tunable UV laser excitation was used to record autofluorescence images, at different spectral ranges, of injured and contralateral control rat kidneys to reveal the excitation conditions that offered optimal contrast. Autofluorescence and near-infrared cross-polarized light-scattering imaging were both used to monitor changes in intensity and spectral characteristics, as a function of exposure time to ischemic injury. These two modalities provided different temporal behaviors, arguably arising from two different mechanisms providing direct correlation of intrinsic optical signatures to ischemic injury time.     

Monitoring hydrogen peroxide in the extracellular space of the brain with amperometric microsensors

Interest in the detection of hydrogen peroxide in living brain tissue is growing for several reasons. Peroxide and other reactive oxygen species are implicated in neurodegenerative disorders and appear to have neuromodulatory functions in the brain. Also, there is a need to measure peroxide levels as a companion to measurements with amperometric sensors that rely on enzymes to generate peroxide for the detection of glutamate, choline, and glucose. Herein, we report on measurements performed in the brain of anesthetized rats with carbon fiber amperometric sensors coated with a cross-linked redox polymer film that contains horseradish peroxidase. Prior work with these sensors has established that they are both sensitive and selective toward hydrogen peroxide. When implanted in the striatal region of the rat brain, a biphasic response is observed upon electrical stimulation of the dopaminergic pathway that innervates the striatal tissue. No response is observed at sensors lacking HRP, which are not sensitive to peroxide, suggesting that the biphasic response is due to the production of hydrogen peroxide by two separate mechanisms. Additional measurements of dopamine and oxygen, and the administration of two drugs with well-known effects on the biochemical kinetics of the dopamine neurons, are used to identify those mechanisms. One appears to be the production of peroxide upon the oxidation of dopamine by molecular oxygen. This occurs during the electrical stimulation itself, which elevates both dopamine and oxygen levels in the extracellular space. The other appears to be the production of peroxide as a byproduct in the oxidative metabolic conversion of dopamine to DOPAC by the mitochondrial enzyme, monoamine oxidase. The production of peroxide due to dopamine metabolism is also observed after rats receive a dose of L-DOPA, a drug used in the treatment of Parkinson's disease.     

Intracarotid transplantation of autologous adipose-derived mesenchymal stem cells significantly improves neurological deficits in rats after MCAo

We aimed to evaluate whether adipose-derived mesenchymal stem cells (ADMSCs) that were transplanted via internal carotid can improve the neurological function after acute ischemic stroke and explore the underlying mechanisms. Total 40 adult Sprague–Dawley rats were subjected to transient (1.5 h) middle cerebral artery occlusion (MCAo) to induce ischemia/reperfusion injury. These rats were randomly divided into two groups with 20 ones in each group, which were intracarotid-injected with autologous ADMSCs (2.0 × 10⁶) and saline (control) at day 3 after MCAo, respectively. Behavioral tests (adhesive-removal and modified neurological severity score) were performed before and after MCAo. Histology was used to evaluate the ischemia lesion volume and pathological changes. The apoptosis and astroglial reactivity were determined by TUNEL and glial fibrillary acidic protein (GFAP) staining, respectively. Besides, we applied immunofluorescence to identify the distribution of ADMSCs and the neural makers (NeuN and GFAP) expressed by them under confocal microscope. Significant improvement of neurological deficits was observed in rats transplanted with ADMSCs when compared to controls. But there was no obvious difference on ischemia lesion volume between these two groups. The injected ADMSCs migrated to the brain infarct region and mainly localized in the ischemic core and boundary zone of the lesion, which can express NeuN and GFAP in the brain. In addition, autologous transplantation of ADMSCs significantly attenuated astroglial reactivity, inhibited cellular apoptosis and promoted cellular proliferation. Our data indicated that intracarotid transplantation of autologous ADMSCs had the potential therapeutic application for ischemic stroke.     

Spatiotemporally controlled and multifactor involved assay of neuronal compartment regeneration after chemical injury in an integrated microfluidics

Studies on the degeneration and regeneration of neurons as individual compartments of axons or somata can provide critical information for the clinical therapy of nervous system diseases. A controllable in vitro platform for multiple purposes is key to such studies. In the present study, we describe an integrated microfluidic device designed for achieving localized stimulation to neuronal axons or somata. We observed neuronal compartment degeneration after localized chemical stimulation and regeneration under the accessorial function of an interesting compound treatment or coculture with desired cells in controllable chambers. In a spatiotemporally controlled manner, this device was used to investigate hippocampal neuronal soma and axon degeneration after acrylamide stimulation, as well as subsequent regeneration after treatment with the monosialoganglioside GM1 or with cocultured glial cells (astrocytes or Schwann cells). To gain insight into the molecular mechanisms that mediate neuronal injury and regeneration, as well as to investigate whether acrylamide stimulation to neurons induces changes in Ca(2+) concentrations, the related neuronal genes and real-time Ca(2+) signal in neurons were also analyzed. The results showed that neuronal axons were more resistant to acrylamide injury than neuronal somata. Under localized stimulation, axons had self-destruct programs different from somata, and somatic injury caused the secondary response of axon collapse. This study provides a foundation for future in-depth analyses of spatiotemporally controlled and multifactor neuronal compartment regeneration after various injuries. The microfluidic device is also useful in evaluating potential therapeutic strategies to treat chemical injuries involving the central nervous system.     

Electrochemical activation and inhibition of neuromuscular systems through modulation of ion concentrations with ion-selective membranes

Conventional functional electrical stimulation aims to restore functional motor activity of patients with disabilities resulting from spinal cord injury or neurological disorders. However, intervention with functional electrical stimulation in neurological diseases lacks an effective implantable method that suppresses unwanted nerve signals. We have developed an electrochemical method to activate and inhibit a nerve by electrically modulating ion concentrations in situ along the nerve. Using ion-selective membranes to achieve different excitability states of the nerve, we observe either a reduction of the electrical threshold for stimulation by up to approximately 40%, or voluntary, reversible inhibition of nerve signal propagation. This low-threshold electrochemical stimulation method is applicable in current implantable neuroprosthetic devices, whereas the on-demand nerve-blocking mechanism could offer effective clinical intervention in disease states caused by uncontrolled nerve activation, such as epilepsy and chronic pain syndromes.     

铝掺杂对氧化锌压敏陶瓷电性能的影响

研究了微量铝(Al)掺杂对氧化锌(ZnO)压敏陶瓷显微结构、电性能和本征点缺陷浓度等方面的影响及其作用机理。研究结果表明, 介电损耗峰值能够在一定程度上反映ZnO压敏陶瓷本征点缺陷浓度, 微量Al掺杂能够引起ZnO压敏陶瓷本征点缺陷浓度的显著降低。氧空位缺陷对应的损耗峰峰值从88.82下降到1.74, 锌填隙缺陷对应的损耗峰峰值从133.38下降到8.14。随着Al掺杂量的增加, ZnO压敏陶瓷平均晶粒尺寸从9.15 μm逐渐下降到6.24 μm, 而压敏电压从235 V/mm逐渐提高到292 V/mm。可见Al掺杂抑制了ZnO压敏陶瓷中本征点缺陷的形成, 而本征缺陷浓度的降低导致材料显微结构和电性能发生明显变化。本文阐述了Al掺杂对ZnO压敏陶瓷本征缺陷的影响机理, 建立了ZnO压敏陶瓷显微形貌、电性能、介电性能和本征点缺陷之间的联系。