Measurement of impact force for triboluminescent-enhanced composites by modified impulse method

Barely visible impact damage in composites can result in hidden damage such as delamination and cracking. Triboluminescence is currently being looked at as a way of inundating composites with a sensory level mechanism for impact events. ZnS:Mn doped resin sensing plates are embedded within glass fiber-reinforced composites and are impacted at low velocities (3.45-3.51 m/s). The damage created by the impact can be seen under black light analysis and allows for quick visual inspection of the composite. The striker during impact registers a bounce which can be used to determine final impact velocity, which in turn defines the force at impact. By measuring the amount of time between consecutive impacts, an indirect estimation of impact force was made using the temporal occurrence of triboluminescence. Triboluminescent emissions occurred for impacts greater than 300 N. The measured impact energy averaged 36.79 J (±0.48). The calculated impact force and impact energy corresponded to the amount of damage area found on the composite, showing that triboluminescent crystal inclusion into composites can provide damage sensing capability to woven fiber composites

Cortico-Basal Ganglia Reward Network: Microcircuitry

Many of the brain's reward systems converge on the nucleus accumbens, a region richly innervated by excitatory, inhibitory, and modulatory afferents representing the circuitry necessary for selecting adaptive motivated behaviors. The ventral subiculum of the hippocampus provides contextual and spatial information, the basolateral amygdala conveys affective influence, and the prefrontal cortex provides an integrative impact on goal-directed behavior. The balance of these afferents is under the modulatory influence of dopamine neurons in the ventral tegmental area. This midbrain region receives its own complex mix of excitatory and inhibitory inputs, some of which have only recently been identified. Such afferent regulation positions the dopamine system to bias goal-directed behavior based on internal drives and environmental contingencies. Conditions that result in reward promote phasic dopamine release, which serves to maintain ongoing behavior by selectively potentiating ventral subicular drive to the accumbens. Behaviors that fail to produce an expected reward decrease dopamine transmission, which favors prefrontal cortical-driven switching to new behavioral strategies. As such, the limbic reward system is designed to optimize action plans for maximizing reward outcomes. This system can be commandeered by drugs of abuse or psychiatric disorders, resulting in inappropriate behaviors that sustain failed reward strategies. A fuller appreciation of the circuitry interconnecting the nucleus accumbens and ventral tegmental area should serve to advance discovery of new treatment options for these conditions