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Hearing protection devices (HPDs) remain the first line of defense against hazardous noise exposure and noise-induced hearing loss (NIHL). Despite the increased awareness of NIHL as a major occupational health hazard, implementation of effective hearing protection interventions remains challenging in at-risk occupational groups including those in public safety that provide fire, emergency medical, or law enforcement services. A reduction of situational awareness has been reported as a primary barrier to including HPDs as routine personal protective equipment. This study examined the effects of hearing protection and simulated NIHL on spatial awareness in ten normal hearing subjects. In a sound-attenuating booth and using a head-orientation tracker, speech intelligibility and localization accuracy were collected from these subjects under multiple listening conditions. Results demonstrate that the use of HPDs disrupts spatial hearing as expected, specifically localization performance and monitoring of speech signals. There was a significant interaction between hemifield and signal-to-noise ratio (SNR), with speech intelligibility significantly affected when signals were presented from behind at reduced SNR. Results also suggest greater spatial hearing disruption using over-the-ear HPDs when compared to the removal of high frequency cues typically associated with NIHL through low-pass filtering. These results are consistent with reduced situational awareness as a self-reported barrier to routine HPD use, and was evidenced in our study by decreased ability to make accurate decisions about source location in a controlled dual-task localization experiment.

Despite the high prevalence of noise-induced hearing loss (NIHL), no effective treatments exist currently. Underlying mechanisms behind NIHL include elevated reactive oxygen species and inflammation, all which ultimately lead to cellular apoptosis. Z-VAD-FMK, an apoptosis inhibitor, has demonstrated protective effects against cochlear hair cells exposed to ototoxic agents; however, its potential for treating NIHL remains unexplored. This study assessed the efficacy of Z-VAD-FMK as a therapeutic for noise-induced cochlear injury in a rodent model. Rodents were assigned to one of four groups: (1) unexposed, (2) noise-exposed, (3) noise + vehicle, and (4) noise + Z-VAD-FMK. Noise delivery consisted of 1 h of 110 dB continuous white-noise, with Z-VAD-FMK administered intraperitoneally 6 h afterward. Auditory brainstem responses (ABRs), cochlear hair cell density, and protein levels were evaluated post-interventions. Noise exposure caused a permanent threshold shift across all frequencies, with minimal recovery by day 28. However, post-exposure treatment with Z-VAD-FMK significantly mitigated ABR threshold, amplitudes, and latencies shifts particularly at low and mid frequencies. Treatment rescued outer hair cells across middle and basal cochlear turns and reduced caspase-9 and IL-1β levels, as indicated by protein analysis. Our findings indicate that a single intraperitoneal injection of Z-VAD-FMK can partially mitigate cochlear dysfunction induced by acoustic overexposure in a rodent model, highlighting its potential as a therapeutic intervention for NIHL.

Infrared neural stimulation (INS) has been proposed as a novel method for neural stimulation. In order for INS to translate to clinical use, which would involve the use of implanted devices over years or decades, the efficacy and safety of chronic INS needs to be determined. We examined a population of cats that were chronically implanted with an optical fiber to stimulate the cochlea with infrared radiation, the first known chronic application of INS. Through behavioral responses, the cats demonstrate that stimulation occurs and a perceptual event results. Long-term stimulation did not result in a change in the electrophysiological responses, either optically-evoked or acoustically-evoked. Spiral ganglion neuron counts and post implantation tissue growth, which was localized at the optical fiber, were similar in chronically stimulated and sham implanted cochleae. Results from chronic INS experiments in the cat cochlea support future work toward INS-based neuroprostheses for humans.

Exposure to occupational or recreational loud noise activates multiple biological regulatory circuits and damages the cochlea, causing permanent changes in hearing sensitivity. Currently, no effective clinical therapy is available for the treatment or mitigation of noise-induced hearing loss (NIHL). Here, we describe an application of localized and non-invasive therapeutic hypothermia and targeted temperature management of the inner ear to prevent NIHL. We developed a custom-designed cooling neck collar to reduce the temperature of the inner ear by 3-4°C post-injury to deliver mild therapeutic hypothermia. This localized and non-invasive therapeutic hypothermia successfully mitigated NIHL in rats. Our results show that mild hypothermia can be applied quickly and safely to the inner ear following noise exposure. We show that localized hypothermia after NIHL preserves residual hearing and rescues noise-induced synaptopathy over a period of months. This study establishes a minimally-invasive therapeutic paradigm with a high potential for rapid translation to the clinic for long-term preservation of hearing health.

Cervical vestibular evoked myogenic potentials (cVEMPs) provide an objective measure of the integrity of the sacculo-collic pathway leading to their widespread use as a clinical tool in the diagnostic vestibular test battery. Though the application of cVEMPs in preclinical models to assess vestibular function, as performed in relevant clinical populations, remains limited. The present study aimed to establish a rodent model of cVEMP with standardized methods and protocols, examine the neural basis of the responses, and characterize and validate important features for interpretation and assessment of vestibular function. We compared air-conducted sound (ACS)-evoked VEMPs from the sternocleidomastoid muscles in naïve Brown Norway rats. A custom setup facilitated repeatable and reliable measurements which were carried out at multiple intensities with ACS between 1 and 16 kHz and over 7 days. The myogenic potentials were identified by the presence of a positive (P1)-negative (N1) waveform at 3-5 ms from the stimulus onset. Threshold, amplitude, and latency were compared with intensity- and frequency-matched responses within and between animals. cVEMP responses were repeatedly evoked with stimulus intensities between 50-100 dB SPL with excellent test-retest reliability and across multiple measurements over 7 days for all frequencies tested. Suprathreshold, cVEMP responses at 90 dB SPL for 6-10 kHz stimuli demonstrated significantly larger amplitudes ( < 0.01) and shorter latencies ( < 0.001) compared to cVEMP responses for 1-4 kHz stimuli. Latency of cVEMP showed sex-dependent variability, but no significant differences in threshold or amplitude between males and females was observed. The results provide a replicable and reliable setup, test protocol, and comprehensive characterization of cVEMP responses in a preclinical model which can be used in future studies to elucidate pathophysiological characteristics of vestibular dysfunctions or test efficacy of therapeutics.

Prevention or treatment for acoustic injury has been met with many translational challenges, resulting in the absence of FDA-approved interventions. Localized hypothermia following noise exposure mitigates acute cochlear injury and may serve as a potential avenue for therapeutic approaches. However, the mechanisms by which hypothermia results in therapeutic improvements are poorly understood. This study performs the transcriptomic analysis of cochleae from juvenile rats that experienced noise-induced hearing loss (NIHL) followed by hypothermia or control normothermia treatment. Differential gene expression results from RNA sequencing at 24 h post-exposure to noise suggest that NIHL alone results in increased inflammatory and immune defense responses, involving complement activation and cytokine-mediated signaling. Hypothermia treatment post-noise, in turn, may mitigate the acute inflammatory response. This study provides a framework for future research to optimize hypothermic intervention for ameliorating hearing loss and suggests additional pathways that could be targeted for NIHL therapeutic intervention.

A key barrier to translation of biomedical research discoveries is a lack of understanding among scientists regarding the complexity and process of implementation. To address this challenge, the National Science Foundation's Innovation Corps™ (I-Corps™) program trains researchers in entrepreneurship. We report results from the implementation of an I-Corps™ training program aimed at biomedical scientists from institutions funded by the National Center for Advancing Translational Sciences (NCATS). National/regional instructors delivered 5-week I-Corps@NCATS short courses to 62 teams (150 individuals) across six institutions. Content included customer discovery, value proposition, and validating needs. Teams interviewed real-life customers and presented the value of innovations for specific end-users weekly, culminating in a \"Finale\" featuring their refined business thesis and business model canvas. Methodology was developed to evaluate the newly adapted program. National mixed-methods evaluation assessed program implementation, reach, effectiveness using observations of training delivery and surveys at Finale ( = 55 teams), and 3-12 months post-training ( = 34 teams). Innovations related to medical devices (33%), drugs/biologics (20%), software applications (16%), and diagnostics (8%). An average of 24 interviews was conducted. Teams reported increased readiness for commercialization over time (83%, 9 months; 14%, 3 months). Thirty-nine percent met with institutional technology transfer to pursue licensing/patents and 24% pursued venture capital/investor funding following the short courses. I-Corps@NCATS training provided the NCATS teams a rigorous and repeatable process to aid development of a business model based on customer needs. Outcomes of this pilot program support the expansion of I-Corps™ training to biomedical scientists for accelerating research translation.

Exposures to hazardous noise causes irreversible injury to the structures of the inner ear, leading to changes in hearing and balance function with strong links to age-related cognitive impairment. While the role of noise-induced hearing loss in long-term health consequences, such as progression or development of Alzheimer's Disease (AD) has been suggested, the underlying mechanisms and behavioral and cognitive outcomes or therapeutic solutions to mitigate these changes remain understudied. This study aimed to characterize the association between blast exposure, hearing loss, and the progression of AD pathology, and determine the underlying mechanisms. We employed a well-accepted preclinical mouse model (3xTg) with a predisposition to AD pathology. Wild type (WT) and 3xTg (AD) mice were exposed to blasts in an ecologically valid oxyacetylene gas tube at 4 months of age. We compared functional outcomes (auditory brainstem responses and vestibular evoked myogenic potentials), cognitive deficits (novel object recognition, water maze), affective deficits (open field) and anxiety between WT and AD sham and blast-exposed mice over 3 months. We also carried out immunohistochemical and Western Blot analysis for amyloid beta (Ab) amyloid fibrils, Tau, and Gasdermin-D of the peripheral auditory system and multiple brain regions including auditory cortex and brainstem. Auditory and vestibular analyses revealed a combination of temporary and permanent functional loss post-blast combined with hair cell loss and synaptopathy. We assessed changes in cognitive function and anxiety after the induction of hearing loss in WT and AD mice. The AD, WT-blast and AD-blast animals had challenges with the novel object recognition. AD mice post-blast exhibited significant increases in fecal boli present when compared to WT mice. In open field, there was a decrease in overall mean speed and total distance traveled in AD mice. Finally, there was significant elevation of Ab, Tau and Gasdermin in the cochlea as well as brainstem and cortex suggesting that pyroptosis related mechanisms play a significant role in the pathology of AD. These results suggest that strong association between early hearing loss and progression of AD pathology. Our novel results may inform potential biomarkers and therapeutic strategies.

Light at infrared wavelengths has been demonstrated to modulate the pattern of neural signals transmitted from the angular motion sensing semicircular canals of the vestibular system to the brain. In the present study, we have characterized physiological eye movements evoked by focused, pulsed infrared radiation (IR) stimuli directed at an individual semicircular canal in a mammalian model. Pulsed IR (1863 nm) trains were directed at the posterior semicircular canal in a rat using 200–400 µm optical fibers. Evoked bilateral eye movements were measured using a custom-modified video-oculography system. The activation of vestibulo–ocular motor pathways by frequency modulated pulsed IR directed at single posterior semicircular canals evoked significant, characteristic bilateral eye movements. In this case, the resulting eye movements were disconjugate with ipsilateral eye moving upwards with a rotation towards the stimulated ear and the contralateral eye moving downwards. The eye movements were stable through several hours of repeated stimulation and could be maintained with 30 + minutes of continuous, frequency-modulated IR stimulation. Following the measurements, the distance of the fiber from target structures and orientation of the beam relative to vestibular structures were determined using micro-computed tomography. Results highlight the spatial selectivity of optical stimulation. Our results demonstrate a novel strategy for direct optical stimulation of the vestibular pathway in rodents and lays the groundwork for future applications of optical neural stimulation in inner ear research and therapeutic applications.

Firefighters are exposed to extensive hazardous noise while on the job, both during routine tasks at the station and when responding to calls. However, little is known about firefighters’ occupational noise hazards. This study employed mixed methods, including focus groups, a survey, and audiometric testing, to identify sources of noise in the firefighters’ work environment, determine hearing protective strategies, discern firefighters’ perceptions of occupational noise exposure and impacts to their health, and quantify the prevalence of hearing loss among South Florida firefighters. A total of 6 senior officers served in an expert panel, 12 participated in focus groups, 300 completed the survey, and 214 received audiometric tests. Most firefighters were unaware of the risk and their departments’ policies, and did not participate in hearing protection practices and avoided using hearing protection devices, which they believed impede team communication and situational awareness. Nearly 30% of participating firefighters showed mild to profound hearing loss, a prevalence that is considerably worse than expected by normal aging alone. Educating firefighters about noise-induced hearing loss early in their careers may have significant health implications for their future. These findings provide insights for developing technologies and programs to mitigate the effects of noise exposure in the firefighting population.