Noise-induced Sensorineural Hearing Loss Research Articles

Sound elicits stereotyped facial movements that provide a sensitive index of hearing abilities in mice

Sound elicits rapid movements of muscles in the face, ears, and eyes that protect the body from injury and trigger brain-wide internal state changes. Here, we performed quantitative facial videography from mice resting atop a piezoelectric force plate and observed that broadband sounds elicited rapid and stereotyped facial twitches. Facial motion energy (FME) adjacent to the whisker array was 30 dB more sensitive than the acoustic startle reflex and offered greater inter-trial and inter-animal reliability than sound-evoked pupil dilations or movement of other facial and body regions. FME tracked the low-frequency envelope of broadband sounds, providing a means to study behavioral discrimination of complex auditory stimuli, such as speech phonemes in noise. Approximately 25% of layer 5-6 units in the auditory cortex (ACtx) exhibited firing rate changes during facial movements. However, FME facilitation during ACtx photoinhibition indicated that sound-evoked facial movements were mediated by a midbrain pathway and modulated by descending corticofugal input. FME and auditory brainstem response (ABR) thresholds were closely aligned after noise-induced sensorineural hearing loss, yet FME growth slopes were disproportionately steep at spared frequencies, reflecting a central plasticity that matched commensurate changes in ABR wave 4. Sound-evoked facial movements were also hypersensitive in Ptchd1 knockout mice, highlighting the use of FME for identifying sensory hyper-reactivity phenotypes after adult-onset hyperacusis and inherited deficiencies in autism risk genes. These findings present a sensitive and integrative measure of hearing while also highlighting that even low-intensity broadband sounds can elicit a complex mixture of auditory, motor, and reafferent somatosensory neural activity.

The role of molecular-biological characteristics of the organism in the development of professional sensorineural hearing loss

The researchers have analyzed the data available in domestic and foreign literature sources on the modern representation and the role of molecular biological features of the body in the development of professional sensorineural hearing loss is carried out. Genetically determined sensorineural hearing loss occurs twice as often in developed countries as in underdeveloped ones. Hearing impairment affects up to 30% of the global community, and 70 million people are deaf. Modern scientists devote their research to the study of the contribution of genetic factors in the formation of phenotypic features of the development and course of a number of occupational diseases. The analysis of genetic markers associations with occupational diseases makes it possible to identify groups of people with an increased risk of developing certain diseases among workers and to develop timely preventive measures. The results of the literature analysis made it possible to systematize the data on the study of the influence of molecular biological characteristics of the body on the formation of sensorineural hearing loss. The researchers presented the data on the studied candidate genes of predisposition to noise-induced sensorineural hearing loss. An in-depth analysis of the results of recent studies shows that the main targets in the analysis of genetic factors of predisposition to professional sensorineural hearing loss are genes encoding proteins of the systems of activation and regulation of the heat shock factor, neutralization of reactive oxygen species and transmission of signals of the immune system. Ethics. The authors have conducted the study in compliance with the ethical principles of conducting medical research with the participation of a person as a subject; personal responsibility of the authors for the conclusions and results obtained in the study; confidentiality, non-proliferation of information; scientific validity of the research methods and techniques used; objectivity in the interpretation of results, conclusions; professional competence (self-respect and self-restraint).

NADPH Oxidase 3 Deficiency Protects From Noise-Induced Sensorineural Hearing Loss.

The reactive oxygen species (ROS)-generating NADPH oxidase NOX3 isoform is highly and specifically expressed in the inner ear. NOX3 is needed for normal vestibular development but NOX-derived ROS have also been implicated in the pathophysiology of sensorineural hearing loss. The role of NOX-derived ROS in noise-induced hearing loss, however, remains unclear and was addressed with the present study. Two different mouse strains, deficient in NOX3 or its critical subunit p22phox, were subjected to a single noise exposure of 2 h using an 8–16 kHz band noise at an intensity of 116–120 decibel sound pressure level. In the hours following noise exposure, there was a significant increase in cochlear mRNA expression of NOX3 in wild type animals. By using RNAscope in situ hybridization, NOX3 expression was primarily found in the Rosenthal canal area, colocalizing with auditory neurons. One day after the noise trauma, we observed a high frequency hearing loss in both knock-out mice, as well as their wild type littermates. At day seven after noise trauma however, NOX3 and p22phox knockout mice showed a significantly improved hearing recovery and a marked preservation of neurosensory cochlear structures compared to their wild type littermates. Based on these findings, an active role of NOX3 in the pathophysiology of noise-induced hearing loss can be demonstrated, in line with recent evidence obtained in other forms of acquired hearing loss. The present data demonstrates that the absence of functional NOX3 enhances the hearing recovery phase following noise trauma. This opens an interesting clinical window for pharmacological or molecular intervention aiming at post prevention of noise-induced hearing loss.

MiR-153/KCNQ4 axis contributes to noise-induced hearing loss in a mouse model

Damage to the cochlear sensory epithelium is a key contributor to noise-induced sensorineural hearing loss (SNHL). KCNQ4 plays an important role in the cochlear potassium circulation and outer hair cells survival. As miR-153 can target and regulate KCNQ4, we sought to study the role of miR-153 in SNHL. 12-week-old male CBA/J mice were exposed to 2–20 kHz broadband noise at 96 dB SPL to induce temporary threshold shifts and 101 dB SPL to induce permanent threshold shifts. Hearing loss was determined by auditory brainstem responses (ABR). Relative expression of miR-153 and KCNQ4 in mice cochlea were determined by Real-Time quantitative PCR. miR-153 mimics were co-transfected with wild type or mutated KCNQ4 into HEK293 cells. Luciferase reporter assay was used to validate the binding between miR-153 and KCNQ4. AAV-sp-153 was constructed and administrated intra-peritoneally 24- and 2-h prior and immediately after noise exposure to knockdown miR-153. The KCNQ4 is mainly expressed in outer hair cells (OHCs). We showed that the expression of KCNQ4 in mice cochlea was reduced and miR-153 expression was significantly increased after noise exposure compared to control. miR-153 bound to 3′UTR of KNCQ4, and the knockdown of miR-153 with the AAV-sp-153 administration restored KCNQ4 mRNA and protein expression. In addition, the knockdown of miR-153 reduced ABR threshold shifts at 8, 16, and 32 kHz after permanent threshold shifts (PTS) noise exposure. Correspondingly, OHC losses were attenuated with inhibition of miR-153. This study demonstrates that miR-153 inhibition significantly restores KNCQ4 in cochlea after noise exposure, which attenuates SNHL. Our study provides a new potential therapeutic target in the prevention and treatment of SNHL.

Hearing loss and tinnitus: association studies for complex-hearing disorders in mouse and man.

Genome-wide association studies (GWAS) provide an unbiased first look at genetic loci involved in aging and noise-induced sensorineural hearing loss and tinnitus. The hearing phenotype, whether audiogram-based or self-report, is regressed against genotyped information at representative single nucleotide polymorphisms (SNPs) across the genome. Findings include the fact that both hearing loss and tinnitus are polygenic disorders, with up to thousands of genes, each of effect size of < 0.02. Smaller human GWAS' were able to use objective measures and identified a few loci; however, hundreds of thousands of participants have been required for the statistical power to identify significant variants, and GWAS is unable to assess rare variants with mean allele frequency < 1%. Animal studies are required as well because of inability to access the human cochlea. Mouse GWAS builds on linkage techniques and the known phenotypic differences in auditory function between inbred strains. With the advantage that the laboratory environment can be controlled for noise and aging, the Hybrid Mouse Diversity Panel (HDMP) combines 100 strains sequenced at high resolution. Lift-over regions between mice and humans have identified over 17,000 homologous genes. Since most significant SNPs are either intergenic or in introns, and binding sites between species are poorly preserved between species, expression quantitative trait locus information is required to bring humans and mice into agreement. Transcriptome-wide analysis studies (TWAS) can prioritize putative causal genes and tissues. Diverse species, each making a distinct contribution, carry a synergistic advantage in the quest for treatment and ultimate cure of sensorineural hearing difficulties.

Protective Effects of Curcumin and N-Acetyl Cysteine Against Noise-Induced Sensorineural Hearing Loss: An Experimental Study.

We investigated the effectiveness of N-acetyl cysteine (NAC) and curcumin, which have known antioxidant and anti-inflammatory effects, in reducing acoustic trauma. We randomly divided 40 adult male rats into four groups: a control group (group 1), a curcumin group (group 2), a NAC group (group 3), and an ethyl alcohol group (group 4). The rats were exposed to 110dB sound at a frequency of 4kHz for 2h to simulate acoustic trauma. Group 1, group 2, group 3, and group 4received 1ml saline, 200mg/kg curcumin, 350mg/kg NAC, or 1ml ethyl alcohol, respectively, intraperitoneally 30min before and 24 and 48h after acoustic trauma. Distortion product otoacoustic emissions (DPOAEs) were recorded before and after the acoustic trauma, and 72h after drug administration. In group 2, signal-to-noise ratio (SNR) values in frequencies of 1000Hz, 1500Hz, and 4000Hz decreased in the second measurements when compared to the first, and showed improvements in the third measurements in comparison to the second ones. In group 3, SNR values decreased in the second measurements, but only the values at 6000Hz were found to be statistically significant (p = 0.007). The values in the third measurements were statistically significant when compared to the second ones. There was a statistically significant difference in the third measurements in both groups 2 and 3, possibly due to curcumin and NAC treatment. This study showed that curcumin and NAC may be effective against noise-induced hearing loss.

Prevalencia de hipoacusia neurosensorial inducida por ruido en empresas del sector madera de la ciudad de Cartagena. 2015

Determinar prevalencia de hipoacusia neurosensorial inducida por ruido en los trabajadores expuestos a ruido en cuatro empresas dedicadas al procesamiento de madera en la ciudad de Cartage­na. Métodos. Sé realizó un estudio descriptivo de corte transversal en cuatro empresas de aserríos del sector madera de la ciudad de Cartagena, dedicadas a la transformación de la troza de madera en tablas y listones a través de operaciones de corte, cepillado y canteado de la madera. La población objeto de estudio fue de veinte trabajadores del área de maquinado expuestos a ruido. Se hizo una evaluación preliminar para conocer en forma detallada el ambiente de trabajo y las circunstancias bajo las cuales se exponen los trabajadores al ruido, las características del ruido y sus fuentes. Resultados. La prevalencia de hipoacusia neurosensorial inducida por ruido fue del 20%. Se encontró en el grupo objeto de es­tudio un 5 % con hipoacusia entre trabajadores de 41 a 45 años de edad y un 15% en trabajadores de más de 46 años de edad. En cuanto al tiempo de servicio en las distintas empresas, los trabajadores de 1 a 30 años presentaron el 20% de hipoacusia neurosensorial inducida por el ruido. En la medición de la exposición al ruido basada por puesto de trabajo en las distintas empresas seleccionadas se determinó el nivel continuo equivalente que oscila entre 95,7 dB(A) a 101,9 dB(A) el cual sobrepasa los valores límites permisibles de acuerdo a los criterios de ACGIH de USA. El nivel de riesgo es alto en una de las empresas mientras se encontró un nivel de riesgo medio en las otras empresas seleccionadas.

Complex-Tone Pitch Discrimination in Listeners With Sensorineural Hearing Loss.

Physiological studies have shown that noise-induced sensorineural hearing loss (SNHL) enhances the amplitude of envelope coding in auditory-nerve fibers. As pitch coding of unresolved complex tones is assumed to rely on temporal envelope coding mechanisms, this study investigated pitch-discrimination performance in listeners with SNHL. Pitch-discrimination thresholds were obtained for 14 normal-hearing (NH) and 10 hearing-impaired (HI) listeners for sine-phase (SP) and random-phase (RP) complex tones. When all harmonics were unresolved, the HI listeners performed, on average, worse than NH listeners in the RP condition but similarly to NH listeners in the SP condition. The increase in pitch-discrimination performance for the SP relative to the RP condition (F0DL ratio) was significantly larger in the HI as compared with the NH listeners. Cochlear compression and auditory-filter bandwidths were estimated in the same listeners. The estimated reduction of cochlear compression was significantly correlated with the increase in the F0DL ratio, while no correlation was found with filter bandwidth. The effects of degraded frequency selectivity and loss of compression were considered in a simplified peripheral model as potential factors in envelope enhancement. The model revealed that reducing cochlear compression significantly enhanced the envelope of an unresolved SP complex tone, while not affecting the envelope of a RP complex tone. This envelope enhancement in the SP condition was significantly correlated with the increased pitch-discrimination performance for the SP relative to the RP condition in the HI listeners.

Relation between temporal envelope coding, pitch discrimination, and compression estimates in listeners with sensorineural hearing loss

Recent physiological studies in animals showed that noise-induced sensorineural hearing loss (SNHL) increased the amplitude of envelope coding in single auditory-nerve fibers. The present study investigated whether SNHL in human listeners was associated with enhanced temporal envelope coding, whether this enhancement affected pitch discrimination performance, and whether loss of compression following SNHL was a potential factor in envelope coding enhancement. Envelope processing was assessed in normal-hearing (NH) and hearing-impaired (HI) listeners in a behavioral amplitude-modulation detection task. Fundamental frequency difference limens (F0DLs) were obtained in the same listeners for complex tones with varying harmonic resolvability. Basilar-membrane input/output functions were measured to assess individual compression ratios. For NH listeners, F0DLs decreased with increasing harmonic resolvability. For the unresolved conditions, all five HI listeners performed as good as or better than NH listeners with matching musical experience. Two HI listeners showed lower amplitude-modulation detection thresholds than NH listeners for low modulation rates, and one of these listeners also showed a loss of cochlear compression. Overall, these findings suggest that some HI listeners may benefit from an enhancement of temporal envelope coding in pitch discrimination of unresolved complex tones, and that this enhancement may be also ascribed to a reduction of cochlear compression following SNHL.

The effects of hearing loss on neural processing and plasticity.

The effects of hearing loss on neural processing and plasticity.

Noise-induced hearing loss increases the temporal precision of complex envelope coding by auditory-nerve fibers

While changes in cochlear frequency tuning are thought to play an important role in the perceptual difficulties of people with sensorineural hearing loss (SNHL), the possible role of temporal processing deficits remains less clear. Our knowledge of temporal envelope coding in the impaired cochlea is limited to two studies that examined auditory-nerve fiber responses to narrowband amplitude modulated stimuli. In the present study, we used Wiener-kernel analyses of auditory-nerve fiber responses to broadband Gaussian noise in anesthetized chinchillas to quantify changes in temporal envelope coding with noise-induced SNHL. Temporal modulation transfer functions (TMTFs) and temporal windows of sensitivity to acoustic stimulation were computed from 2nd-order Wiener kernels and analyzed to estimate the temporal precision, amplitude, and latency of envelope coding. Noise overexposure was associated with slower (less negative) TMTF roll-off with increasing modulation frequency and reduced temporal window duration. The results show that at equal stimulus sensation level, SNHL increases the temporal precision of envelope coding by 20–30%. Furthermore, SNHL increased the amplitude of envelope coding by 50% in fibers with CFs from 1–2 kHz and decreased mean response latency by 0.4 ms. While a previous study of envelope coding demonstrated a similar increase in response amplitude, the present study is the first to show enhanced temporal precision. This new finding may relate to the use of a more complex stimulus with broad frequency bandwidth and a dynamic temporal envelope. Exaggerated neural coding of fast envelope modulations may contribute to perceptual difficulties in people with SNHL by acting as a distraction from more relevant acoustic cues, especially in fluctuating background noise. Finally, the results underscore the value of studying sensory systems with more natural, real-world stimuli.

Eye Color as a Risk Factor for Acquired Sensorineural Hearing Loss: A Systematic Review

Objectives: There is controversy as to whether eye color has an effect on acquired sensorineural hearing loss. The objectives of this review were to analyze the literature evaluating the association between eye color and acquired causes of sensorineural hearing loss and to propose the potential mechanisms of this association. Methods: Six databases were searched to identify clinical studies relating eye color and acquired causes of sensorineural hearing loss such as noise, cisplatin ototoxicity, radiation, and presbycusis. Included articles were independently assessed for quality by two authors using the Downs and Black rating scale. Results: Seventeen articles were eligible for review. Eye color was not found to have an effect in the non-exposed population or in presbycusis. In noise-induced sensorineural hearing loss, light-eyed patients had more significant loss following noise exposure, although the variability reported due to eye color was modest (r2 = 1-14%). Two out of three studies reported that dark eye color is associated with cisplatin ototoxicity. In one study, green-eyed patients were found to be at higher risk of radiation-induced hearing loss. Conclusions: Eye color does not appear to play a role in hearing loss in non-exposed individuals or presbycusis. It is possible that dark-eyed individuals, with greater inner ear melanin content, are better protected against noise-induced hearing loss. Evidence suggests that melanin can be protective against radiation-induced sensorineural hearing loss, but that it may predispose individuals to cisplatin ototoxicity. Future studies are required to support these conclusions.

The Effect of Noise Exposure on the Cervical Vestibular Evoked Myogenic Potential

The purpose of this study was to investigate the effects of noise exposure on the cervical vestibular evoked myogenic potential (cVEMP) in individuals with asymmetric noise-induced sensorineural hearing loss (NIHL). A cross-sectional observational study was used to compare cVEMP characteristics in 43 individuals with a history of noise exposure greater in one ear (e.g., the left ear of a right-handed rifle shooter) and asymmetric sensorineural hearing loss consistent with the history of noise exposure and in 14 age-matched controls. The characteristics of hearing loss were examined further for the noise-exposed participants with abnormal cVEMPs and the noise-exposed participants with normal cVEMPs. Thirty-three percent of the noise-exposed participants had abnormal cVEMPs, whereas cVEMPs were present and symmetrical in 100% of the age-matched controls, and cVEMP threshold was greater in the noise-exposed group than in the control group. Abnormal cVEMPs occurred most often in the ears with poorer hearing (or greater NIHL), and the noise-exposed participants who had abnormal cVEMPs had poorer high-frequency pure-tone thresholds (greater NIHL) and greater interaural high-frequency pure-tone threshold differences than the noise-exposed participants with normal cVEMPs. These findings are consistent with previous studies that suggest that the sacculocollic pathway may be susceptible to noise-related damage. There is emerging evidence that the severity of NIHL is associated with the presence or absence of cVEMPs.

Noise levels in a neonatal intensive care unit in the Cape metropole

Introduction. Continuous noise exposure is potentially harmful to infants\' auditory systems and wellbeing. Although the effects of noise on infants in a neonatal intensive care unit (NICU) have been well researched overseas, limited studies have been conducted in South Africa. Aim. To conduct a detailed noise assessment in a state hospital NICU in the Cape metropole. Study design and setting. Non-experimental descriptive design involving measurement, analysis and description of the noise levels and events in the NICU, Tygerberg Children\'s Hospital, Western Cape. Method. Noise levels were measured over two 12-hour periods in both NICU rooms, during which observations were made to identify the sources and frequency of occurrence of NICU noises. Measurements of sound decay were made to determine whether the noise levels were a result of direct noise or reverberant noise from room reinforcements. Results. Noise levels ranged from 62.3 to 66.7 dBA (LAeq), which exceeds American and British NICU standards (50 - 60 dBA). Staff conversations were the largest single contributor to the number of noise events. The largest single non-human contributor was monitor alarm noise. The NICU was found to be an extremely reverberant environment, suggesting that high noise levels were largely a result of reverberant room reinforcements. Conclusion. Results highlight the need for noise reduction, which is vital to optimise newborn care, reduce acoustic trauma risks and enhance the infants\' wellbeing and physiological stability in the NICU. Moreover, it is especially important to limit NICU noise levels in developing countries as premature infants in the NICU are often at increased risk for developing noiseinduced sensorineural hearing loss as a result of NICU noise exposure and/or treatment with ototoxic medication and are often not routinely screened for hearing loss. Recommendations. Practical suggestions for noise reduction in the NICU are made. South African Journal of Child Health Vol. 2 (2) 2008: pp. 50-54

0928 Nervous system impairments of the patients with radiation-induced, vascular and noise-induced sensorineural hearing loss

0928 Nervous system impairments of the patients with radiation-induced, vascular and noise-induced sensorineural hearing loss

소음성 난청에서의 Mitochondrial DNA A3243G, A1555G, A7445G 돌연변이

본 연구는 소음성 감각신경성난청 환자의 유전적 관련요인을 파악하고자 관련성이 의심되는 mitochondrial DNA의 돌연변이와 소음성 감각신경성난청과의 관련성을 조사하였다. 말초혈액 백혈구로부터 DNA를 추출한 후, mtDNA 3243, 1555, 7445부위의 <TEX>$A{\rightarrow}G$</TEX> 돌연변이 유무를 관찰하기 위하여 mtDNA 3243, 1555, 7445부위 가 포함된 mtDNA fragment를 중합효소 연쇄반응으로 증폭하고 유전자 제한효소로 소화하여 전기영동하고 ethidium bromide 용액으로 염색하여 UV transilluminator에서 관찰하였다. 그리고, PCR 산물을 이용하여 DNA 염기서열을 분석하여 mtDNA 3243, 1555, 7445부 위에서의 염기서열 분석을 실시하여 mtDNA 3243, 1555, 7445부위 의 <TEX>$A{\rightarrow}G$</TEX> 돌연변이를 관찰하였다 MtDNA A3243G, A1555G, A7445G의 돌연변이를 관찰한 결과 돌연변이 부위가 포함된 fragment가 소음성 감각신경성난청 환자군, 감각신경성난청 환자군, 대조군 모두에서 증폭됨을 관찰하였다. 또한 PCR 산물을 제한효소로 처 리 한 결과에서도 mtDNA에서 3243, 1555, 7445부위의 <TEX>$A{\rightarrow}G$</TEX> 돌연변이가 일어나지 않았음을 알 수 있었다. PCR산물을 이용하여 DNA 염기서열을 분석하여 mtDNA 3243, 1555, 7445부위에서의 염기서열을 확인한 결과 이미 밝혀진 사람의 mtDNA 3243, 1555, 7445부 위의 염기서열과 동일한 염기서열임이 확인되었으므로 mtDNA 3243, 1555, 7445부위의 <TEX>$A{\rightarrow}G$</TEX> 돌연변이가 일어나지 않았음을 확인하였다. 소음성 감각신경성난청과 mtDNA 3243, 1555, 7445부위의 <TEX>$A{\rightarrow}G$</TEX> 돌연변이와는 관련이 없는 것으로 관찰되었다. Mitochondrial DNA mutations have been reported in recent years in association with sensorineural hering loss. The purpose of this study is to identify the association between the noise-induced sensorineural hearing loss and the A to G mutation at nucleotide 3243, 1555, 7445 of mitochondrial DNA. Study subjects were established by history and chart review, and audiological and clinical data were obtained. Blood was sampled from 214 normal controls, 102 noise-induced hearing loss, and 28 sensorineural hearing loss. The DNA of these individuals were extracted, and mitochondrial DNA fragments were analyzed by polymerase chain reaction. Subsequently, the coding sequence of mitochondrial DNA 3243, 1555, 7445 were sequenced, and compared to the normal sequence, and all sequence variations were analyzed by restriction enzymes. Mitochondrial DNA mutations <TEX>$(3243A{\rightarrow}G,\;1555A{\rightarrow}4G,\;7445A{\rightarrow}G)$</TEX> were not detected by polymerase chain reactions in any patients with noise-induced hearing loss, sensorineural hearing loss, and normal controls. The DNA sequencing of PCR products did not revealed an A to G substitution at nucleotide 3243, 1555, 7445 of mitochondrial DNA. The noise-induced sensorineural hearing loss was not associated with mitochondrial DNA mutation <TEX>$(3243A{\rightarrow}G,\;1555A{\rightarrow}4G,\;7445A{\rightarrow}G)$</TEX>.

Noise-induced hearing loss: the effect of melanin in the stria vascularis

Conflicting investigations regarding the potential protective effect of melanin against noise-induced sensorineural hearing loss have suggested that eumelanin and pheomelanin may have differing effects within the stria vascularis. Three strains of C57BL/ 6J mice, (+/+, a/ a) wild-types (dark coats/black eyes), ( c2j/ c2j, a/ a), albinos (white coats/pink eyes), and (+/+, Ay/ Ay) yellow mice (yellow coats/black eyes), were subjected to five consecutive days of broad band noise exposure at 112 dB(A) SPL for 3 h/day. Cochlear function was evaluated with auditory brainstem response audiometry to pure tones immediately pre-exposure, 5–6 h post-exposure, and 14 days post-exposure. No significant difference in the degree of sensorineural hearing loss induced in the three strains of mice was identified. The eumelanin and pheomelanin content of each stria vascularis and amount of protein per stria for both mouse and guinea pig ( 2/ NCR) were determined via high performance liquid chromatography. No pheomelanin was found in the stria of yellow mice, suggesting that coat color is not an accurate predictor of strial melanin content. The melanin content per mg of strial protein was higher in mice than in guinea pigs. A species-specific difference in melanin content does not explain the absence of a protective effect in mice.

The influence of stochastic behavior on the human threshold of hearing

The inner hair cells in the cochlea perform the crucial task of transforming mechanical sound signals into electrical activity. The cochlear nerve fibers code this information and convey it to the brain for further processing. This study investigates the performance of the system inner hair cell – primary auditory afferent nerve fibers at the physical limit of the mechano-electrical transduction for the human auditory frequency range. The Brownian motion of the hair cell’s receptive organelle, the hair bundle, does not blunt the sensitivity, but in fact enlarges – especially in frequency regions which are most important for the perception of music and speech – via the mechanism of nonlinear stochastic resonance (SR) the dynamical range of the mechano-electrical transduction by at least one order of magnitude. The coding efficiency of small sinusoidal hair bundle deflections shows basic properties of the human hearing threshold curve for pure tones and corresponds to experimental results of noise-induced tuning curves in mechano-receptors in the rat foot. Furthermore, the model explains how altered coding efficiency contributes to pathological changes in the spiking pattern which arise from morphological changes in the hair bundle structure (e.g., in noise-induced sensorineural hearing loss of cochlear origin).

Mitochondrial DNA A3243G mutation in noise-induced sensorineural hearing loss

Mitochondrial DNA A3243G mutation in noise-induced sensorineural hearing loss

Hazardous Sound Levels Produced by Extracorporeal Shock Wave Lithotripsy

Sound emitted from the Dornier system GmbH lithotriptor was found to be of sufficient intensity to warrant concern about noise-induced sensorineural hearing loss. The patients were exposed to impulses of 112 dB. peak sound pressure level. Operating room personnel were exposed to sounds of less intensity, although the number of impulses they were exposed to was much greater, thereby increasing the risk of hearing loss. Hearing protection is recommended for patients and operating room personnel.