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Welle, C. G.

Publications and source records attributed to Welle, C. G..

2 recordsLinked to original sources

Automated Reactive Accelerated Aging for Rapid In Vitro Evaluation of Neural Implants Performance

ObjectiveNovel therapeutic applications for neural implants require miniaturized devices. Pilot clinical studies suggest that rapid failure of the miniaturized neural implants in the body presents a major challenge for this type of technology. Miniaturization imposes stricter requirements for reliability of materials and designs. Evaluation of neural implant performance over clinically relevant timescales presents time-and cost-prohibitive challenges for animal models.\n\nApproachIn vitro reactive accelerated aging (RAA) was developed to expedite durability testing of these devices. RAA simulates an aggressive physiological environment associated with an immune response and implicated in device failure. It uses hydrogen peroxide, which mimics reactive oxygen species (ROS), and high temperature to accelerate chemical reactions that lead to device degradation. RAA accurately simulates the degradation pattern of neural implants observed in vivo, but requires daily maintenance and is prone to variability in performance.\n\nMain resultsThis work introduces automated reactive accelerated aging (aRAA) that is compatible with multiplexing. The core of aRAA is electrochemical detection for feedback control of hydrogen peroxide concentration, implemented with simple off-the shelf components.\n\nSignificanceaRAA allows multiple parallel experiments for a high-throughput optimization of reactive aging conditions to more quickly and more rigorously simulate the in vivo environment. aRAA is a cost-effective tool for rapid in vitro evaluation of durability of neural implants, ultimately expediting the development of a new generation of miniaturized devices with long functional lifespans.

bioengineering

Alterations in neurovascular coupling following acute traumatic brain injury

Traumatic brain injury (TBI) is a leading cause of mortality and disability worldwide. A challenge for diagnosing and assessing the severity of TBI, however, is that quantitative biomarkers are lacking. We explored potential functional indicators for TBI by noninvasively monitoring sensory-evoked electrical and hemodynamic activity using a novel hybrid optical and electrophysiological measurement approach. By combining diffuse correlation spectroscopy with co-localized electrophysiological measurements in a mouse model of TBI, we observed concomitant alterations in somatosensory-evoked cerebral blood flow and electrical potentials following controlled cortical impact. Injury acutely reduced the amplitude of stimulus-evoked responses, which mostly recovered to baseline values within 30 min; intertrial variability for these parameters was also acutely altered. The kinetics of recovery, however, varied among specific components of the evoked waveforms, and we observed strong correlations between the two measurement modalities for only a select subset of waveform parameters. Overall, our results identify a novel set of potential biomarkers for TBI and demonstrate the utility of combined, noninvasive optical and electrophysiological measurements for detecting injury-induced abnormalities in neurovascular reactivity.

neuroscience