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Biomaterials. Electronic dura mater for long-term multimodal neural interfaces (2015)

I. R. Minev ; P. Musienko ; A. Hirsch ; [weitere]

American Association for the Advancement of Science (AAAS)

In: Science. 347(6218): 159-63. doi: 10.1126/science.1260318.

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Publikationsdatum: 2015-01-13

Beschreibung: The mechanical mismatch between soft neural tissues and stiff neural implants hinders the long-term performance of implantable neuroprostheses. Here, we designed and fabricated soft neural implants with the shape and elasticity of dura mater, the protective membrane of the brain and spinal cord. The electronic dura mater, which we call e-dura, embeds interconnects, electrodes, and chemotrodes that sustain millions of mechanical stretch cycles, electrical stimulation pulses, and chemical injections. These integrated modalities enable multiple neuroprosthetic applications. The soft implants extracted cortical states in freely behaving animals for brain-machine interface and delivered electrochemical spinal neuromodulation that restored locomotion after paralyzing spinal cord injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Minev, Ivan R -- Musienko, Pavel -- Hirsch, Arthur -- Barraud, Quentin -- Wenger, Nikolaus -- Moraud, Eduardo Martin -- Gandar, Jerome -- Capogrosso, Marco -- Milekovic, Tomislav -- Asboth, Leonie -- Torres, Rafael Fajardo -- Vachicouras, Nicolas -- Liu, Qihan -- Pavlova, Natalia -- Duis, Simone -- Larmagnac, Alexandre -- Voros, Janos -- Micera, Silvestro -- Suo, Zhigang -- Courtine, Gregoire -- Lacour, Stephanie P -- New York, N.Y. -- Science. 2015 Jan 9;347(6218):159-63. doi: 10.1126/science.1260318.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bertarelli Foundation Chair in Neuroprosthetic Technology, Laboratory for Soft Bioelectronic Interfaces, Centre for Neuroprosthetics, Institute of Microengineering and Institute of Bioengineering, Ecole Polytechnique Federale de Lausanne (EPFL), Switzerland. ; International Paraplegic Foundation Chair in Spinal Cord Repair, Centre for Neuroprosthetics and Brain Mind Institute, EPFL, Switzerland. Pavlov Institute of Physiology, St. Petersburg, Russia. ; International Paraplegic Foundation Chair in Spinal Cord Repair, Centre for Neuroprosthetics and Brain Mind Institute, EPFL, Switzerland. ; Translational Neural Engineering Laboratory, Center for Neuroprosthetics and Institute of Bioengineering, EPFL, Lausanne, Switzerland. ; Bertarelli Foundation Chair in Neuroprosthetic Technology, Laboratory for Soft Bioelectronic Interfaces, Centre for Neuroprosthetics, Institute of Microengineering and Institute of Bioengineering, Ecole Polytechnique Federale de Lausanne (EPFL), Switzerland. International Paraplegic Foundation Chair in Spinal Cord Repair, Centre for Neuroprosthetics and Brain Mind Institute, EPFL, Switzerland. ; School of Engineering and Applied Sciences, Kavli Institute for Bionano Science and Technology, Harvard University, Cambridge, MA, USA. ; Laboratory for Biosensors and Bioelectronics, Institute for Biomedical Engineering, University and ETH Zurich, Switzerland. ; Translational Neural Engineering Laboratory, Center for Neuroprosthetics and Institute of Bioengineering, EPFL, Lausanne, Switzerland. The BioRobotics Institute, Scuola Superiore Sant'Anna, Pisa 56025, Italy. ; International Paraplegic Foundation Chair in Spinal Cord Repair, Centre for Neuroprosthetics and Brain Mind Institute, EPFL, Switzerland. gregoire.courtine@epfl.ch stephanie.lacour@epfl.ch. ; Bertarelli Foundation Chair in Neuroprosthetic Technology, Laboratory for Soft Bioelectronic Interfaces, Centre for Neuroprosthetics, Institute of Microengineering and Institute of Bioengineering, Ecole Polytechnique Federale de Lausanne (EPFL), Switzerland. gregoire.courtine@epfl.ch stephanie.lacour@epfl.ch.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25574019" target="_blank"〉PubMed〈/a〉

Schlagwort(e): Animals ; Biocompatible Materials/therapeutic use ; Brain-Computer Interfaces ; Drug Delivery Systems/*methods ; *Dura Mater ; Elasticity ; Electric Stimulation/*methods ; Electrochemotherapy/*methods ; *Electrodes, Implanted ; Locomotion ; Mice ; Mice, Inbred Strains ; Motor Cortex/physiopathology ; Multimodal Imaging ; Neurons/physiology ; Paralysis/etiology/physiopathology/*therapy ; Platinum ; *Prostheses and Implants ; Silicon ; Spinal Cord/physiopathology ; Spinal Cord Injuries/complications/physiopathology/*therapy

Print ISSN: 0036-8075

Digitale ISSN: 1095-9203

Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik

Publiziert von American Association for the Advancement of Science (AAAS)

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{gamma}HV68 prevents development of murine lupus [Immunology] (2012)

Larson, J. D., Thurman, J. M., Rubtsov, A. V., Claypool, D., Marrack, P., van Dyk, L. F., Torres, R. M., Pelanda, R.

National Academy of Sciences

In: PNAS - Proceedings of the National Academy of Sciences

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Publikationsdatum: 2012-05-02

Beschreibung: Gammaherpesvirus infections, such as those caused by EBV, have been suggested to promote the development of autoimmunity. To test this idea, we infected healthy WT and lupus-prone B6.Sle123 mice with an EBV-related and rodent-specific gammaherpesvirus, γHV68. Although acute γHV68 infection increased autoantibody levels for 4 to 6 wk, latent infection inhibited these responses for 1 y. The inhibition of autoantibody expression was only observed in B6.Sle123 females and not in males, which already displayed lower autoantibody titers. Contrary to the initial hypothesis, infection of young B6.Sle123 mice, both male and female, resulted in suppression of lymphoid activation and expansion and of glomerular inflammation and sclerosis, preserving kidney function. Moreover, γHV68 infection led to reduced autoantibody titers, lymphoid activation, and glomerular inflammation whether lupus-prone females were infected before or during disease manifestation. Finally, γHV68 infection also inhibited autoantibody production in the genetically distinct MRL/lpr lupus-prone mice. Our findings indicate that γHV68 infection strongly inhibits the development and progression of lupus-like disease in mice that spontaneously develop this condition mediating its beneficial effects at the humoral, cellular, and organ levels. The mechanisms by which the virus exerts this down-modulatory action are not yet clear, but appear to operate via reduced activation of dendritic cells, T cells, and B cells. Gammaherpesviruses coevolved with the vertebrate immune systems, establishing lifelong infections in humans and other mammals. Our findings that γHV68 infection prevents rather than exacerbates autoimmunity in mice suggest that infection with gammaherpesviruses may be protective rather than pathological in most individuals.

Print ISSN: 0027-8424

Digitale ISSN: 1091-6490

Thema: Biologie , Medizin , Allgemeine Naturwissenschaft