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关于将聚对二甲苯 C 聚合物用作周围神经电极基底的应用。

On the use of Parylene C polymer as substrate for peripheral nerve electrodes.

机构信息

Institute of Neurosciences, Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, and Centro de Investigación Biomédica en Red en Enfermedades Neurodegenerativas (CIBERNED), Bellaterra, Spain.

Laboratory for Biomedical Microtechnology, Department of Microsystems Engineering-IMTEK, Albert-Ludwig-University Freiburg, Freiburg, Germany.

出版信息

Sci Rep. 2018 Apr 13;8(1):5965. doi: 10.1038/s41598-018-24502-z.

Abstract

Parylene C is a highly flexible polymer used in several biomedical implants. Since previous studies have reported valuable biocompatible and manufacturing characteristics for brain and intraneural implants, we tested its suitability as a substrate for peripheral nerve electrodes. We evaluated 1-year-aged in vitro samples, where no chemical differences were observed and only a slight deviation on Young's modulus was found. The foreign body reaction (FBR) to longitudinal Parylene C devices implanted in the rat sciatic nerve for 8 months was characterized. After 2 weeks, a capsule was formed around the device, which continued increasing up to 16 and 32 weeks. Histological analyses revealed two cell types implicated in the FBR: macrophages, in contact with the device, and fibroblasts, localized in the outermost zone after 8 weeks. Molecular analysis of implanted nerves comparing Parylene C and polyimide devices revealed a peak of inflammatory cytokines after 1 day of implant, returning to low levels thereafter. Only an increase of CCL2 and CCL3 was found at chronic time-points for both materials. Although no molecular differences in the FBR to both polymers were found, the thick tissue capsule formed around Parylene C puts some concern on its use as a scaffold for intraneural electrodes.

摘要

对灵长类动物的研究发现,注射神经毒素会导致长期的运动功能障碍,这是由于内源性神经保护机制的丧失,从而加剧了神经元的进行性变性。在这项研究中,我们使用了慢性坐骨神经挤压(CCI)模型,这是一种经典的、可重现的、在啮齿动物中模拟慢性周围神经损伤的模型。CCI 导致轴突进行性丧失,导致脱髓鞘,以及初级感觉神经元和背根神经节(DRG)的死亡。这些变化与人类慢性周围神经病相似,包括糖尿病性神经病和化疗诱导的神经病。CCI 后,运动神经元和运动轴突丧失,导致运动单位减少,从而导致肌肉萎缩和力量下降。CCI 后,运动单位的丧失导致肌肉萎缩和力量下降,这是通过肌电图(EMG)和生物力学测试来评估的。我们使用 EMG 来评估肌肉的电活动,以及生物力学测试来评估肌肉的力量和耐力。这些测试可以帮助我们了解 CCI 对运动神经元和运动轴突的影响,以及这些影响如何导致肌肉萎缩和力量下降。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e85/5899141/5c58d4b6f6b3/41598_2018_24502_Fig1_HTML.jpg

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