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This article introduces a methodology to increase the integration density of functional electronic features on fibers/threads/wires through additive deposition of functional materials via printed electronics. It opens the possibility to create a multifunctional intelligent system on a single fiber/thread/wire while combining the advantages of existing approaches, i.e., the scalability of coating techniques and the microfeatures of semiconductor-based fabrication. By directly printing on threads (of diameters ranging from 90 to 1000 μm), micropatterned electronic devices and multifunctional electronic systems could be formed. Contact and noncontact printing methods were utilized to create various shapes from serpentines and meanders to planar coils and interdigitated electrodes, as well as complex multilayer structures for thermal and light actuators, humidity, and temperature sensors. We demonstrate the practicality of the method by integrating a multifunctional thread into a FFP mask for breath monitoring. Printing technologies provide virtually unrestricted choices for the types of threads, materials, and devices used. They are scalable via roll-to-roll processes and offer a resource-efficient way to democratize electronics across textile products.

Unlabelled: After traumatic brain injury (TBI), neurons surviving the initial insult can undergo chronic (secondary) degeneration via poorly understood mechanisms, resulting in long-term cognitive impairment. Although a neuroinflammatory response is promptly activated after TBI, it is unknown whether it has a significant role in chronic phases of TBI (>1 year after injury). Using a closed-head injury model of TBI in mice, we showed by MRI scans that TBI caused substantial degeneration at the lesion site within a few weeks and these did not expand significantly thereafter. However, chronic alterations in neurons were observed, with reduced dendritic spine density lasting >1 year after injury. In parallel, we found a long-lasting inflammatory response throughout the entire brain. Deletion of one allele of CX3CR1, a chemokine receptor, limited infiltration of peripheral immune cells and largely prevented the chronic degeneration of the injured brain and provided a better functional recovery in female, but not male, mice. Therefore, targeting persistent neuroinflammation presents a new therapeutic option to reduce chronic neurodegeneration., Significance Statement: Traumatic brain injury (TBI) often causes chronic neurological problems including epilepsy, neuropsychiatric disorders, and dementia through unknown mechanisms. Our study demonstrates that inflammatory cells invading the brain lead to secondary brain damage. Sex-specific amelioration of chronic neuroinflammation rescues the brain degeneration and results in improved motor functions. Therefore, this study pinpoints an effective therapeutic approach to preventing secondary complications after TBI., (Copyright © 2016 the authors 0270-6474/16/369962-14$15.00/0.)