The supporting-cell antigen: a receptor-like protein tyrosine phosphatase expressed in the sensory epithelia of the avian inner ear.
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After noise- or drug-induced hair-cell loss, the sensory epithelia of the avian inner ear can regenerate new hair cells. Few molecular markers are available for the supporting-cell precursors of the hair cells that regenerate, and little is known about the signaling mechanisms underlying this regenerative response. Hybridoma methodology was used to obtain a monoclonal antibody (mAb) that stains the apical surface of supporting cells in the sensory epithelia of the inner ear. The mAb recognizes the supporting-cell antigen (SCA), a protein that is also found on the apical surfaces of retinal Muller cells, renal tubule cells, and intestinal brush border cells. Expression screening and molecular cloning reveal that the SCA is a novel receptor-like protein tyrosine phosphatase (RPTP), sharing similarity with human density-enhanced phosphatase, an RPTP thought to have a role in the density-dependent arrest of cell growth. In response to hair-cell damage induced by noise in vivo or hair-cell loss caused by ototoxic drug treatment in vitro, some supporting cells show a dramatic decrease in SCA expression levels on their apical surface. This decrease occurs before supporting cells are known to first enter S-phase after trauma, indicating that it may be a primary rather than a secondary response to injury. These results indicate that the SCA is a signaling molecule that may influence the potential of nonsensory supporting cells to either proliferate or differentiate into hair cells. (+info)
Inner ear damage in guinea pigs exposed to stable and impulse noise.
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OBJECTIVE: To investigate the inner ear damage after exposure to stable noise, impulse noise and stable plus impulse noise in guinea pigs. METHODS: Ninety-six healthy guinea pigs were divided into 3 equal groups. (1) Stable noise group: exposed to 110 dBA stable noise for 3 days, 4 hours per day. (2) Impulse noise group: exposed to 165 dBA simulated cannon fire impulse noise 10 times successively at an interval of 10 seconds. (3) stable plus impulse noise group: exposed to the same stable noise as that in the first group, then after a 2-hour rest, the animals were followed with impulse noise exposures as that in the second group. After those exposure, each of the 3 groups was further divided into 4 subgroups according to the time after the noise exposure, namely, the right after, 7 d, 14 d and 30 d groups. The evoked cortical potential responses to click and tone burst stimulation sound were examined. The surface preparation and celloidine embedded serial section of the cochlea were observed under a light microscope. RESULTS: Both the stable and impulse noise could increase the hearing threshold and damage the inner ear hair cells. The damage in the first group was relatively slight, whereas in group 3 the damage was more severe than that in the other 2 groups. CONCLUSION: For seamen who are working in heavy noise environment, corresponding measures should be taken to protect their ears from noise which induces hearing loss. (+info)
Heat stress and protection from permanent acoustic injury in mice.
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The inner ear can be permanently damaged by overexposure to high-level noise; however, damage can be decreased by previous exposure to moderate level, nontraumatic noise (). The mechanism of this "protective" effect is unclear, but a role for heat shock proteins has been suggested. The aim of the present study was to directly test protective effects of heat stress in the ear. For physiological experiments, CBA/CaJ mice were exposed to an intense octave band of noise (8-16 kHz) at 100 dB SPL for 2 hr, either with or without previous whole-body heat stress (rectal temperature to 41. 5 degrees C for 15 min). The interval between heat stress and sound exposure varied in different groups from 6 to 96 hr. One week later, inner ear function was assessed in each animal via comparison of compound action potential thresholds to mean values from unexposed controls. Permanent threshold shifts (PTSs) were approximately 40 dB in the group sound-exposed without previous heat stress. Heat-stressed animals were protected from acoustic injury: mean PTS in the group with 6 hr heat-stress-trauma interval was reduced to approximately 10 dB. This heat stress protection disappeared when the treatment-trauma interval surpassed 24 hr. A parallel set of quantitative PCR experiments measured heat-shock protein mRNA in the cochlea and showed 100- to 200-fold increase over control 30 min after heat treatment, with levels returning to baseline at 6 hr after treatment. Results are consistent with the idea that upregulation of heat shock proteins protects the ear from acoustic injury. (+info)
Rescue of hearing, auditory hair cells, and neurons by CEP-1347/KT7515, an inhibitor of c-Jun N-terminal kinase activation.
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We have studied the mechanisms of auditory hair cell death after insults in vitro and in vivo. We show DNA fragmentation of hair cell nuclei after ototoxic drug and intense noise trauma. By using phospho-specific c-Jun-N-terminal kinase (JNK) and c-Jun antibodies in immunohistochemistry, we show that the JNK pathway, associated with stress, injury, and apoptosis, is activated in hair cells after trauma. CEP-1347, a derivative of the indolocarbazole K252a, is a small molecule that has been shown to attenuate neurodegeneration by blocking the activation of JNK (). Subcutaneously delivered CEP-1347 attenuated noise-induced hearing loss. The protective effect was demonstrated by functional tests, which showed less hearing threshold shift in CEP-1347-treated than in nontreated guinea pigs, and by morphometric methods showing less hair cell death in CEP-1347-treated cochleas. In organotypic cochlear cultures, CEP-1347 prevented neomycin-induced hair cell death. In addition to hair cells, CEP-1347 promoted survival of dissociated cochlear neurons. These results suggest that therapeutic intervention in the JNK signaling cascade, possibly by using CEP-1347, may offer opportunities to treat inner ear injuries. (+info)
Strategy for prevention and control of the risks due to noise.
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OBJECTIVES: To propose a strategy for progressively controlling the exposure to noise in industry as much as possible. To propose a method that could, in the first stage, be used by the workers and management themselves to control exposures to noise as much as possible, and then, in later stages, when necessary, progressively call in the assistance of specialists and experts to identify more complex solutions and organise personal protection and medical surveillance. METHODS: The strategy includes three stages. Stage 1 is observation, simple and easy to use by the workers to recognise the problems, identify straightforward solutions, and call for assistance when needed. Stage 2 is analysis, more complex but more costly, performed with the assistance of occupational health specialists to identify more technical control measures and set up a programme to conserve hearing. Stage 3 is expertise, performed with the assistance of acoustic experts for special measurements and control measures. CONCLUSIONS: The proposed strategy enriches the assessment procedure that is usually recommended, by providing for one preliminary stage used by the people directly concerned. It explicitly recognises (a) the competence of the workers and management about their working conditions and (b) that knowledge and measurements of acoustics are not an absolute prerequisite for solving-at least partly-noise problems. It attempts to organise in sequence and optimise the cooperation between the workers, the occupational health specialists, and the experts in acoustics. (+info)
Noise-induced hearing loss.
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Hearing loss caused by exposure to recreational and occupational noise results in devastating disability that is virtually 100 percent preventable. Noise-induced hearing loss is the second most common form of sensorineural hearing deficit, after presbycusis (age-related hearing loss). Shearing forces caused by any sound have an impact on the stereocilia of the hair cells of the basilar membrane of the cochlea; when excessive, these forces can cause cell death. Avoiding noise exposure stops further progression of the damage. Noise-induced hearing loss can be prevented by avoiding excessive noise and using hearing protection such as earplugs and earmuffs. Patients who have been exposed to excessive noise should be screened. When hearing loss is suspected, a thorough history, physical examination and audiometry should be performed. If these examinations disclose evidence of hearing loss, referral for full audiologic evaluation is recommended. (+info)
Predicting vulnerability to acoustic injury with a noninvasive assay of olivocochlear reflex strength.
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Permanent noise-induced damage to the inner ear is a major cause of hearing impairment, arising from exposures occurring during both work- and pleasure-related activities. Vulnerability to noise-induced hearing loss is highly variable: some have tough, whereas others have tender ears. This report documents, in an animal model, the efficacy of a simple nontraumatic assay of normal ear function in predicting vulnerability to acoustic injury. The assay measures the strength of a sound-evoked neuronal feedback pathway to the inner ear, the olivocochlear efferents, by examining otoacoustic emissions created by the normal ear, which can be measured with a microphone in the external ear. Reflex strength was inversely correlated with the degree of hearing loss after subsequent noise exposure. These data suggest that one function of the olivocochlear efferent system is to protect the ear from acoustic injury. This assay, or a simple modification of it, could be applied to human populations to screen for individuals most at risk in noisy environments. (+info)
Predicting exposure conditions that facilitate the potentiation of noise-induced hearing loss by carbon monoxide.
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Hearing loss is the most common occupational disease in the United States, with noise serving as the presumed causative agent in most instances. This investigation characterizes the exposure conditions that facilitate the potentiation of noise-induced hearing loss (NIHL) by carbon monoxide (CO). Auditory function was compared in rats exposed 4 weeks earlier to noise alone, CO alone, combined exposure, and air in the exposure chamber. This interval between exposure and auditory threshold assessment was selected to permit recovery of temporary threshold shifts. The compound action potential (CAP) threshold evoked by pure tone stimuli was used as a measure of auditory sensitivity. The no adverse effect level (NOAEL) with respect to potentiation of NIHL was found to be 300 ppm CO. Potentiation of NIHL by CO increases linearly as CO concentration increases between 500 -1500 ppm. Benchmark dose software (version 1. 1B) published by the U.S. EPA National Center for Environmental Assessment was employed to determine a benchmark concentration of CO that produced either a 5-dB potentiation of NIHL or an increase in auditory threshold equivalent to 10% of the effect of noise alone. The lower bound for these benchmark concentrations were 320 and 194 ppm CO, respectively. Unlike CO dose, the relationship between noise severity and potentiation of NIHL by CO shows a nonlinear relationship. The greatest potentiation was observed at moderate noise exposures (100 dB, 2-h, octave band-limited noise, or OBN) that produce limited permanent threshold shifts. Repeated exposures to 95-dB noise for 2-h periods in combination with 1200 ppm CO also yielded potentiation of NIHL, though such effects were not observed following a single combined exposure. These results underscore the potential risk of hearing loss from combined exposure to noise and CO, and the risks associated with repeated exposure. (+info)