The communicative interchanges of a congenitally deaf child who received a cochlear implant at 24 months of age were videotaped in fifteen hourly sessions over a nine month period while she participated in auditory-verbal therapy prior to and following implantation. The present study examined selected early communicative behaviors. Using Tait's (1993) protocol for charting communicative adult-child interaction, gestures, eye-gaze, and sound uttered either by the child or an adult during communicative interchanges were transcribed from the videotapes. Results corresponded with Tait's, revealing growth in the child's communicative interaction across sessions. In less than three months following implantation phonemic measures rose dramatically. Almost all phonemic measure correlations were significant, high, and positive.

In translational research, disease models in preclinical studies are used as media for discovery of drugs or novel therapeutics. Development of in vitro models for various neurological diseases that enable efficient pharmacological or toxicological screening has been ongoing but challenging. Recognizing the potential benefit of in vitro disease models, dysfunctions in the cortical neuronal networks were induced to mimic the functional pathology of neurological symptoms using microelectrode arrays. Two different disease states – tinnitusand excitotoxicity – were investigated and discussed. In this model, pentylenetetrazol-induced increase in spontaneous firing rate and synchrony in the auditory cortical networks was used as correlate of tinnitus. Potential tinnitus treatment drugs from several different classes – including the novel class of potassium channel openers – were screened and quantified. The potentialtherapeutic values of these drugs were also discussed as the basis for drug repurposing. Functional excitotoxicity was induced by cisplatin (a cancer drug that causes neurological sideeffects) and glutamate (the major excitatory neurotransmitter). As proof-of-principle that the model may contribute to expediting the development of therapeutics, cisplatin excitotoxicity wasprevented by the antioxidant D-methionine, while glutamate excitotoxicity was prevented by ceftriaxone (a modulator of a glutamate reuptake transporter). In the latter part of the study, with …