nce fatigability during gait could be a target for rehabilitation for pwCMT. Perceived fatigue did not correlate to gait fatigue, underscoring the differentiation between perceived fatigue and performance fatigability. Several articular, muscular and neurological diseases generate mobility loss in the shoulder and pelvis girdles. Joint mobilization contributes to improving shoulder-pelvis girdles dissociation, but current mobilization techniques are not always successful and standardized. A robotic medical device, DPA Med®, by inducing trunk mobilization through lower limb oscillation has been developed for producing such a shoulder-pelvis girdles dissociation and is already used worldwide in rehabilitation hospitals. To determine the optimal lower limb oscillation frequency that generated the best shoulder-pelvis girdles dissociation using the DPA Med® device. Thirty healthy adult volunteers (mean age 38.6 [SD 15.2] years, mean height 174 [SD 11.9] cm, mean body mass 70.3 [SD 14.7] kg) participated in this prospective study. A kinematic analysis quantified pelvic and shoulder girdle mobility (rotation and lateral tilt) at different DPA Med® frequencies, from 0.5 Hz to 1 Hz. A visual analysis of the lower limb movemenissociation similar to that of normal gait and allowed to establish the existence of an optimal DPA Med® oscillation frequency for lower limb mobility at 0.808 Hz. Further studies are required to evaluate its potentially benefits on gait disorders.In this paper, we aimed to test whether we could predict sport type (badminton or running) and marathon proficiency from the valence, form, and content of the athletes' self-reported inner speech. RP-6306 Additionally, we wanted to assess the difference between self-talk during high intensity and low intensity exercise. The present study corroborated existing research - we were able to predict both sport type in Study 1 and intensity level as well as marathon proficiency in Study 2 from questionnaire data using machine learning models. In Study 1, we found that badminton players engage more in worry and anxiety-control while runners are more prone to task disengagement. Interestingly, it seemed in Study 2 that the more participants engaged in condensed, positive, and repetitive self-talk when not pushing themselves, the slower their fastest marathons and half marathons were. We discuss potential explanations for these findings and make suggestions for future research.Various methods have been tested and deployed clinically to identify and minimize cisplatin ototoxicity. Upon early identification of hearing loss, one of the possible approaches to reducing future ototoxicity is to increase the gaps or breaks between cycles or doses of cisplatin. However, recent findings about the retention of cisplatin in the cochlea and the potential for its long-term ototoxic effects call into question whether such an approach is effective in reducing hearing loss. The current study was undertaken to determine whether increasing the rest intervals between cycles of cisplatin altered the resulting ototoxicity. CBA/CaJ mice were exposed to a cumulative dose of 48 mg/kg cisplatin delivered in three cycles of 16 mg/kg (4 mg/kg per day for 4 consecutive days). The cycles were separated by either 10, 17, or 87 days to determine if the inter-cycle rest intervals affected resulting ototoxicity. Ototoxicity was measured using auditory brainstem response threshold shifts and hair cell losses. Results indicated that longer intervals between cycles of cisplatin led to lower threshold shifts and outer hair cell lesions. The results support the principle that 'slowing down' cisplatin dosing by increasing rest intervals between doses can reduce the ototoxic side effect. Further testing is needed to optimize the timing and to determine the impact of longer inter-cycle intervals on cisplatin's anti-tumor efficacy.Electrode array insertion into the inner ear is a critical step in cochlear implantation, and artificial scala tympani models can be a valuable tool for studying the dynamics of this process. This technical note describes the fabrication of electrode array dummies and scala tympani models that address shortcomings of previously published cochlear models. In particular, we improve the reproduction of frictional properties with an easy-to-apply polymer brush coating that creates hydrophilic surfaces, and produce geometries with accurate macro-anatomy based on microtomographic scans. The presented methods rely only on commonly available materials and tools and are based on publicly available data. Our validation shows very good agreement of insertion forces both in terms of linear insertion depth and insertion speed compared to previously published measurements of insertions in cadaveric temporal bones.Long-term exposure to moderate intensity noise that does not cause measureable hearing loss can cause striking changes in sound-evoked neural activity in auditory cortex. It is unclear if these changes originate in the cortex or result from functional deficits in the neural output of the cochlea. To explore this issue, rats were exposed for 6-weeks to 18-24 kHz noise at 45, 65 or 85 dB SPL and then compared the noise-induced changes in the cochlear compound action potential (CAP) with the neurophysiological alterations in the anterior auditory field (AAF) of auditory cortex. The 45-dB exposure, which had no effect on the cochlear CAP also had no effect on the AAF. In contrast, the 85-dB exposure greatly reduced CAP amplitudes at high frequencies, but had little or no effect on low frequencies. Despite the large reduction in high-frequency CAP neural responses, high frequency AAF neural responses (spike rate and local field potential amplitude) remained largely within normal limits, evidence of central gain compensation. AAF responses were also enhanced at the low frequencies even though CAP responses were normal; this AAF hyperactivity only occurred at low-moderate intensities (level-dependent enhanced central gain). The 65-dB exposure also caused a moderate reduction in high-frequency CAP amplitudes. Notwithstanding this cochlear loss, AAF responses were boosted into the normal range, evidence of homeostatic gain compensation. Our results suggest that the noise-induced neuroplastic changes in the auditory cortex from so-called "non-traumatic" exposures are triggered from functional deficits in the neural output of the cochlea.