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Neuroimmunol Neuroinflammation 2019;6:15  I  http://dx.doi.org/10.20517/2347-8659.2019.019                               Page 15 of 24

               20. Tissue-engineered electrodes for brain-machine interfaces

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               Ulises Aregueta Robles , Aaron Gilmour , Josef Goding , Nigel Lovell , Penny Martens , Laura
                                                                    1,2
               Poole-Warren , Rylie Green 1,2
                            1
               1 Graduate School of Biomedical Engineering, University of New South Wales, Sydney, Australia
               2 Department of Bioengineering, Imperial College London, London, UK
               State-of-the-art neural interfaces rely on conventional metallic electrodes. Ideally, bionic devices should
               safely operate for a lifetime; However, the fibrotic tissue encapsulation leads to inefficient stimulation and
               formation of toxic by-products, ultimately compromising the electrical and biological performance of
               these bionic interfaces. This limitation further challenges the development of smaller and more densely
               packed electrodes aiming for a more specific neuronal stimulation. Conductive hydrogel (CH) coatings,
               based on poly (vinyl alcohol) polymers modified with conductive polymers, can provide enhanced
               electrical properties, superior to those of traditional platinum (Pt) electrodes. These coating materials
               can be further modified to include an overlaying layer of neural progenitors encapsulated within a 3D
               biosynthetic hydrogel. This study tested the hypothesis that a CH coated electrode decorated with a loaded
               cell coating provides a more physiological interface able to integrate electrodes with the neural tissue
               without significantly reducing the charge transfer properties. The aim of this study was to develop and
               assess a tissue-engineered, living electrode (LE) coating for brain-machine interfaces. LEs were fabricated
               by first coating intra-cortical Pt electrodes with CH followed by an overlaying degradable bio-synthetic
               hydrogel coat loaded with primary neural progenitor cells. The electrical performance of LEs was compared
               with conventional Pt electrodes in vitro and in vivo. in vitro studies confirmed that overlaying a neural
               cell-loaded coat on the CH did not significantly impacted the electrode impedance and charge storage
               capacity. These results suggest that the electrical performance of LEs was comparable to standalone CH
               coated electrodes and significantly superior to Pt electrodes. In vivo studies showed that implanted LEs and
               uncoated Pt electrodes in a rat brain model did not cause any adverse events over 8 weeks. LEs presented
               a significantly higher signal to noise ratio than Pt electrodes. On-going research is assessing the tissue
               response to implanted LEs. These results demonstrate the potential for LEs to support the development of
               more robust neural interfaces.





               21. Golgi fragmentation induced by cyclin-dependent kinase 5 overactivation is associated
               with isoflurane-induced cognitive decline

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               Long Fan , Fang-Fang Miao , Tian-Long Wang , Zhongcong Xie
               1 Department of Anesthesiology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China
               2 Anesthesiology department of Mass general hospital of Harvard Medical School, USA

               Isoflurane is a widely used anesthetic. Isoflurane exposure induces cognitive decline, especially in elderly
               patients, while the underlying mechanism remains to be elucidated. In the present study, we explored
               whether Golgi fragmentation is relevant to isoflurane-induced cognitive decline and the underlying
               molecular mechanism in aged mice. Sixteen-month-old C57BL/6J mice inhaled 1.4% isoflurane for 2 h daily
               for three consecutive days. To inhibit aberrant cyclin-dependent kinase 5 (Cdk5), 10 mg/kg roscovitine
               was given 30 min before isoflurane treatment. The Golgi structure, Cdk5 activity, and level of p25/p35
               were assessed 2 h after isoflurane exposure. Spatial learning and memory ability of mice were evaluated
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