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Every year, thousands of Americans suffer from pathological and traumatic events that result in loss of dexterity and strength of the hand. Although many supportive devices have been designed to restore functional hand movement, most are very complex and expensive. The goal of this project was to design and implement a cost-effective, electrically powered exoskeleton for the human hand that could improve grasping strength. A 3-D printed thermoplastic exoskeleton that allowed independent and enhanced movement of the index, middle and ring fingers was constructed. In addition, a 3-D printed structure was designed to house three linear actuators, an Arduino-based control system, and a power supply. A single force sensing resistor was located on the lower inner-surface of the index fingertip which was used to proportionally activate the three motors, one motor per finger, as a function of finger force applied to the sensor. The device was tested on 4 normal human subjects. Results showed that the activation of the motor control system significantly reduced the muscle effort needed to maintain a sub-maximal grasp effort.

The hypothesis that upper airway (UA) pressure and flow modulate respiratory muscle activity in a respiratory phase-specific fashion was assessed in anesthetized, tracheotomized, spontaneously breathing piglets. We generated negative pressure and inspiratory flow in phase with tracheal inspiration or positive pressure and expiratory flow in phase with tracheal expiration in the isolated UA. Stimulation of UA negative pressure receptors with body temperature air resulted in a 10--15% enhancement of phasic moving-time-averaged posterior cricoarytenoid electromyographic (EMG) activity above tonic levels obtained without pressure and flow in the UA (baseline). Stimulation of UA positive pressure receptors increased phasic moving-time-averaged thyroarytenoid EMG activity above tonic levels by 45% from baseline. The same enhancement of posterior cricoarytenoid or thyroarytenoid EMG activity was observed with the addition of flow receptor stimulation with room temperature air. Tidal volume and diaphragmatic and abdominal muscle activity were unaffected by UA flow and/or pressure, whereas respiratory timing was minimally affected. We conclude that laryngeal afferents, mainly from pressure receptors, are important in modulating the respiratory activity of laryngeal muscles.

The quantification of respiratory variability may provide insight into the integrative control of breathing. To test the hypothesis that sleep and/or increased chemical drive modifies respiratory variability, six male adult Sprague-Dawley rats were instrumented with diaphragm electromyographic (EMG) electrodes and exposed to 0, 2.5, and 5.0% CO2 with a balance of room air during wakefulness and behaviorally determined sleep. Respiratory interval (Ttot), peak diaphragm EMG, and ventilation index (peak diaphragm EMG/Ttot) were calculated for 1,024 sequential breaths. The variability of breathing was quantified with a measurement of signal complexity, the approximate entropy, and two autocorrelation measurements, the autoregressive power spectrum slope and the detrended fluctuation analysis slope. Elevated chemical drive and/or sleep significantly modulated the variability of ventilation index and Ttot. There were also significant interactions between state and CO2 drive in all respiratory parameters. We conclude that state (sleep or wakefulness) and increased chemical drive affect respiratory variability differentially.

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