Taurine, Coenzyme Q10, and Hydrogen Water Prevents Germanium Dioxide-Induced Mitochondrial Dysfunction and Associated Sensorineural Hearing Loss in mouse.

Mitochondrial dysfunction has been implicated in numerous common diseases as well as aging and plays an important role in the pathogenesis of sensorineural hearing loss (SNHL). In the current study, we showed that supplementation with germanium dioxide (GeO2) in CBA/J mice resulted in SNHL due to the degeneration of the stria vascularis and spiral ganglion, which were associated with down-regulation of mitochondrial respiratory chain associated genes and up-regulation in apoptosis associated genes in the cochlea. Supplementation with taurine, coenzyme Q10, or hydrogen-rich water, attenuated the cochlear degeneration and associated SNHL induced by GeO2. These results suggest that daily supplements or consumption of antioxidants, such as taurine, coenzyme Q10, and hydrogen-rich water, may be a promising intervention to slow SNHL associated with mitochondrial dysfunction.

Prevalence of Sensorineural Hearing Loss in Pediatric Patients with Sickle Cell Disease: A Meta-analysis.

OBJECTIVES: To determine the prevalence of Sensorineural Hearing Loss (SNHL) attributable to Sickle Cell Disease (SCD) in the global pediatric population and to identify factors contributing to its severity. STUDY DESIGN: Meta-analysis. METHODS: We performed a comprehensive literature search for scientific articles in PubMed, Scopus, CINAHL, Web of Science, and the Cochrane Library that reported the incidence of hearing loss in populations under 18 years of age with excluding studies analyzing patients on iron chelation therapy, adults, or those without objective audiological analysis. RESULTS: We identified 138 initial studies with 17 selected for analysis after applying the exclusion criteria. A total of 1,282 SCD patients and 553 controls were included in the meta-analysis. There was a statistically significant increase in the prevalence of SNHL in children with SCD compared to the general population with a cumulative risk ratio of 3.33. CONCLUSION: This is the first systematic investigation of the relationship between SCD and SNHL in pediatric patients across the globe. The increased prevalence of SNHL in the pediatric SCD population warrants future research into the predictors of SNHL severity and merits routine audiometric monitoring of SCD patients to reduce the social and developmental morbidity of hearing loss at a young age. PROSPERO Registration #: CRD42019132601. Laryngoscope, 131:1147-1156, 2021.

An update on drug design strategies to prevent acquired sensorineural hearing loss.

INTRODUCTION: Acute sensorineural hearing loss is a dramatic event for the patient. Different pathologies might result in acute sensorineural hearing loss, such as sudden hearing loss, exposure to medications/drugs or loud sound. Current therapeutic approaches include steroids and hyperbaric oxygen in addition to other methods. Research activities of the past have shed light on the molecular mechanisms involved in damage to hair cells, the synapses at the hair cell spiral ganglion junction and the stria vascularis. Molecular events and signaling pathways which underlie damage to these structures have been discovered. Areas covered: This paper summarizes current research efforts involved in investigating the molecular mechanisms involved in acute sensorineural hearing loss. Expert opinion: While progress has been made in unraveling basic mechanisms involved in acute sensorineural hearing loss, it is difficult to translate basic concepts to the clinic. There are often conflicting data in animal and human studies on the effect of a given intervention. There is also a lack of high quality clinical trials (double blind, placebo controlled and high powered). However, this author is confident that research efforts will pay out and that some of these efforts will translate into new therapeutic options for patients with acute hearing loss.

Preventive effect of curcumin and its highly bioavailable preparation on hearing loss induced by single or repeated exposure to noise: A comparative and mechanistic study.

We sought to determine the preventive effects of curcumin and its highly bioavailable preparation on noise-induced hearing loss in a novel murine model of permanent hearing loss developed by repeated exposure to noise. Upon exposure to noise (8-kHz octave band noise, 90 dB sound pressure level, 1 h), hearing ability was impaired in a temporary and reversible manner. During repeated noise exposure (1-h exposure per day, 5 days), there was a progressive increase in the auditory threshold shift at 12 and 20 kHz. The threshold shift persisted for at least 6 days after noise exposure. Oral administration of curcumin for 3 days before and each day during noise exposure significantly alleviated the hearing loss induced by repeated noise exposure. Curcumin abolished intranuclear translocation of nuclear factor-κB-p65 and generation of 4-hydroxynonenal-adducted proteins found in the cochlea after noise exposure. Theracurmin®, a highly absorbable and bioavailable preparation of curcumin, had strong preventive effects on hearing loss induced by repeated noise exposure. Together, these data suggest that curcumin exerts a preventive effect on noise-induced hearing loss and is therefore a good therapeutic candidate for preventing sensorineural hearing loss.

Protective Effect of Selenium Against Cisplatin-Induced Ototoxicity in an Experimental Design.

Cisplatin is an effective chemotherapeutic agent in the treatment of several types of malignant solid tumors but its clinical use is associated with ototoxicity. In the present study, we investigated the effect of selenium administration on lipid peroxidation (malondialdehyde [MDA]) and cisplatin-induced ototoxicity in rats. Healthy wistar albino rats (n = 21) were randomly divided into 3 groups: control (C), cisplatin (Cis), cisplatin and selenium (Cis+Se). Cisplatin was administered for 3 days to Cis and Cis+Se groups. Cis+Se group received selenium 5 days before cisplatin injection and continued for 11 consecutive days. Hearing thresholds and lipid peroxidation (MDA) levels of the rats were recorded before injections and at the end of experimental protocol. The cochleas of animals were harvested for histologic and immunuhistochemical examinations. In biochemichal analyses, pretreatment with selenium prevented the elevation of MDA levels in Cis+Se group rats. Moreover, animals in Cis+Se group had better hearing threshold levels than animals in cis group. Samples obtained from the animals in Cis group revealed extensive loss of the normal microarchitecture of the organ of Corti. On the other hand, animals in Cis+Se group exhibited a preservation of the morphology of the organ of Corti and outer hair cells. In the immunohistochemical examinations of cochlear tissues stained with anti-caspase-3, a higher degree of immunopositivity was found in the Cis group. When Cis+Se group and Cis group were compared, significantly less immunopositivity occurred in the Cis+Se group (P < 0.05). Thus, it appears that pretreatment with selenium may reduce cisplatin-induced ototoxicity in rats.

Dietary LC-PUFA in iron-deficient anaemic pregnant and lactating guinea pigs induce minor defects in the offsprings' auditory brainstem responses.

OBJECTIVES: We previously demonstrated that a mild pre-natal/early post-natal iron-deficient anaemic (IDA) diet devoid of long-chain polyunsaturated fatty acids (LC-PUFA) affected development, neurophysiology, and cerebral lipid biochemistry of the guinea pigs' progeny. Impacts of dietary LC-PUFA on altered cerebral development resulting from pre-natal IDA are unknown. To address this health issue, impacts of mild gestational IDA in the presence of dietary LC-PUFA on the offsprings' neural maturation were studied in guinea pigs using auditory brainstem responses (ABRs) and assessments of brain fatty acids (FAs). METHODS: Female guinea pigs (n = 10/group) were fed an iron sufficient (IS) or IDA diet (146 and 12.7 mg iron/kg, respectively) with physiological amounts of LC-PUFA, during the gestation and lactation periods. From post-natal day (PNd) 9 onwards, the IS + PUFA diet was given to both groups of weaned offspring. Cerebral tissue and offsprings' ABR were collected on PNd24. RESULTS: There was no difference in peripheral and brainstem transmission times (BTTs) between IS + PUFA and IDA + PUFA siblings (n = 10/group); the neural synchrony was also similar in both groups. Despite the absence of differences in auditory thresholds, IDA + PUFA siblings demonstrated a sensorineural hearing loss in the extreme range of frequencies (32, 4, and 2 kHz), as well as modified brain FA profiles compared to the IS + PUFA siblings. DISCUSSION: The present study reveals that siblings born from dams exposed to a moderate IDA diet including balanced physiological LC-PUFA levels during pregnancy and lactation demonstrate minor impairments of ABR compared to the control siblings, particularly on the auditory acuity, but not on neural synchrony, auditory nerve velocity and BTT.

Designer aminoglycosides prevent cochlear hair cell loss and hearing loss.

Bacterial infections represent a rapidly growing challenge to human health. Aminoglycosides are widely used broad-spectrum antibiotics, but they inflict permanent hearing loss in up to ~50% of patients by causing selective sensory hair cell loss. Here, we hypothesized that reducing aminoglycoside entry into hair cells via mechanotransducer channels would reduce ototoxicity, and therefore we synthesized 9 aminoglycosides with modifications based on biophysical properties of the hair cell mechanotransducer channel and interactions between aminoglycosides and the bacterial ribosome. Compared with the parent aminoglycoside sisomicin, all 9 derivatives displayed no or reduced ototoxicity, with the lead compound N1MS 17 times less ototoxic and with reduced penetration of hair cell mechanotransducer channels in rat cochlear cultures. Both N1MS and sisomicin suppressed growth of E. coli and K. pneumoniae, with N1MS exhibiting superior activity against extended spectrum ß lactamase producers, despite diminished activity against P. aeruginosa and S. aureus. Moreover, systemic sisomicin treatment of mice resulted in 75% to 85% hair cell loss and profound hearing loss, whereas N1MS treatment preserved both hair cells and hearing. Finally, in mice with E. coli-infected bladders, systemic N1MS treatment eliminated bacteria from urinary tract tissues and serially collected urine samples, without compromising auditory and kidney functions. Together, our findings establish N1MS as a nonototoxic aminoglycoside and support targeted modification as a promising approach to generating nonototoxic antibiotics.

Investigation of protective role of curcumin against paclitaxel-induced inner ear damage in rats.

OBJECTIVES/HYPOTHESIS: The aim of this study was to investigate the potential protective effect of curcumin on paclitaxel-induced ototoxicity in rats by means of immunohistochemical and histopathological analysis and distortion product otoacoustic emissions (DPOAEs). STUDY DESIGN: Animal study. METHODS: Forty Sprague-Dawley rats were randomized into five groups. Group 1 was administered no paclitaxel and curcumin during the study. Groups 2, 3, 4 and 5 were administered 5 mg/kg paclitaxel; 200 mg/kg curcumin; 5 mg/kg paclitaxel, followed by 200 mg/kg curcumin; 200 mg/kg curcumin and a day later 5 mg/kg paclitaxel followed intraperitoneally by 200 mg/kg curcumin once a week for 4 consecutive weeks, respectively. After the final DPOAEs test, the animals were sacrificed and their cochlea were prepared for hematoxylin and eosin and caspase-3 staining. RESULTS: The DPOAEs thresholds and histopathological and immunohistochemical findings were substantially correlated in all groups. The histopathologic findings in the cochlea of the paclitaxel-treated animals showed not only changes in the organ of Corti, but also damage to the stria vascularis and spiral limbus, including nuclear degeneration, cytoplasmic vacuolization, and atrophy of intermediate cells. Additionally, cochlear changes in group 2, such as intense apoptosis, were confirmed by caspase-3 immunohistochemical staining. In group 4, coreceiving curcumin could not sufficiently prevent paclitaxel-induced ototoxicity, and the results in group 5 were similar to the control group. CONCLUSIONS: In our study, we have concluded that pre- and coreceiving curcumin can significantly protect the cochlear morphology and functions on paclitaxel-induced ototoxicity in rats. Curcumin might be considered as a potential natural product that, used as a dietary supplement, could be easily given to patients undergoing paclitaxel chemotherapy. LEVEL OF EVIDENCE: NA

Societal-level Risk Factors Associated with Pediatric Hearing Loss: A Systematic Review.

OBJECTIVE: To determine if the current body of evidence describes specific threshold values of concern for modifiable societal-level risk factors for pediatric hearing loss, with the overarching goal of providing actionable guidance for the prevention and screening of audiological deficits in children. DATA SOURCES: Three related systematic reviews were performed. Computerized PubMed, Embase, and Cochrane Library searches were performed from inception through October 2013 and were supplemented with manual searches. REVIEW METHODS: Inclusion/exclusion criteria were designed to determine specific threshold values of societal-level risk factors on hearing loss in the pediatric population. Searches and data extraction were performed by independent reviewers. RESULTS: There were 20 criterion-meeting studies with 29,128 participants. Infants less than 2 standard deviations below standardized weight, length, or body mass index were at increased risk. Specific nutritional deficiencies related to iodine and thiamine may also increase risk, although data are limited and threshold values of concern have not been quantified. Blood lead levels above 10 µg/dL were significantly associated with pediatric sensorineural loss, and mixed findings were noted for other heavy metals. Hearing loss was also more prevalent among children of socioeconomically disadvantaged families, as measured by a poverty income ratio less than 0.3 to 1, higher deprivation category status, and head of household employment as a manual laborer. CONCLUSIONS: Increasing our understanding of specific thresholds of risk associated with causative factors forms the foundation for preventive and targeted screening programs as well as future research endeavors.

Pomegranate extract: a potential protector against aminoglycoside ototoxicity.

OBJECTIVE: To investigate the effectiveness of pomegranate extract as protection against aminoglycoside ototoxicity. DESIGN: Prospective, randomised, controlled, experimental study. SUBJECTS: Eighteen Wistar albino rats were randomly allocated to 5 days of either: saline injections; gentamicin injections; or pomegranate extract (100 µl/day via gavage) plus gentamicin injections. Distortion product otoacoustic emissions were tested before treatment and on day 3. After treatment, reactive oxygen species levels were measured in each rat's right cochlea and right kidney via chemiluminescence. RESULTS: Baseline emission amplitudes were similar. Post-treatment emissions differed significantly in the two treatment groups (p < 0.001). Cochlear reactive oxygen species levels were significantly higher in the gentamicin group (mean ± standard deviation, 316.6 ± 36.5 relative light units per mg) than the gentamicin plus pomegranate extract group (240 ± 24.6 relative light units per mg) (p = 0.004); control group levels were 119.1 ± 10.3 relative light units per mg. Renal reactive oxygen species levels were similar for the control and gentamicin plus pomegranate extract groups (p = 0.59) but much higher in the gentamicin group (p = 0.004). CONCLUSION: Concurrent systemic pomegranate extract administration reduced reactive oxygen species level increases and otoacoustic emission changes, following aminoglycoside injection.

Gestational vitamin A deficiency: a novel cause of sensorineural hearing loss in the developing world?

Hearing loss is a substantial public health problem with profound social and economic consequences in the developing world. The World Health Organization (WHO) estimates that there are 360 million people living with disabling hearing loss globally, and 80% of these individuals are from low- and middle-income countries. The epidemiology of hearing impairment remains poorly defined in most impoverished societies. Middle ear infections in childhood are a key determinant; however, congenital anomalies may also comprise an important etiology and may arise from gestational malnutrition. While evidence exists that preventable vitamin A deficiency exacerbates the severity of ear infections and, consequently, hearing loss, antenatal vitamin A deficiency during sensitive periods of fetal development may represent an etiologically distinct and virtually unexplored causal pathway. Evidence from multiple animal systems clearly shows that fetal inner ear development requires adequate vitamin A nutriture to proceed normally. Inner ear malformations occur in experimentally imposed maternal vitamin A deficiency in multiple species in a dose-response manner. These anomalies are likely due to the loss of retinoic acid-dependent regulation of both hindbrain development and otic morphogenic processes. Based on in vivo evidence in experimental animals, we hypothesize that preventable gestational vitamin A deficiency, especially during early stages of fetal development, may predispose offspring to inner ear malformations and sensorineural hearing loss. As vitamin A deficiency affects an estimated 20 million pregnant women globally, we hypothesize that, in undernourished settings, routine provision of supplemental vitamin A at the recommended allowance throughout pregnancy may promote normal inner ear development and reduce risk of an as yet unknown fraction of sensorineural hearing loss. If our hypothesis proves correct, gestational vitamin A deficiency would represent a potentially preventable etiology of sensorineural hearing loss of substantial public health significance.

Novel treatment strategy for Japanese newborns with high serum unbound bilirubin.

BACKGROUND: Serum unbound bilirubin (UB) is a measure of bilirubin not bound to albumin, and has been reported to be better than total bilirubin level at identifying infants at risk of developing bilirubin-induced neurotoxicity, including auditory abnormalities. A detailed treatment strategy for newborns with high serum UB has not been established. The aim of this study was to assess auditory outcomes in newborns with serum UB ≥1.00 µg/dL who were treated according to a novel treatment protocol. METHODS: A prospective clinical study was conducted in newborns weighing >1500 g with serum UB ≥1.00 µg/dL who were admitted to Kobe University Hospital and Kakogawa Municipal Hospital, Japan from 2006 to 2011. Enrolled newborns were treated as follows: (i) if serum UB was 1.00-1.50 µg/dL, phototherapy and infusion were given with or without albumin or immunoglobulin therapy; and (ii) if serum UB was >1.50 µg/dL, exchange transfusion was performed immediately. Auditory brainstem responses were evaluated at the time of discharge. RESULTS: A total of 89 Japanese newborns with UB ≥1.00 µg/dL were enrolled at a median age of 4 days. Of these, 85 had UB 1.00-1.50 µg/dL and four had UB >1.50 µg/dL. After being treated according to the protocol, no newborns were diagnosed with auditory brainstem response abnormalities. CONCLUSIONS: The present treatment protocol for Japanese newborns with serum UB ≥1.00 µg/dL may be useful for the prevention of bilirubin-induced auditory abnormalities.

Astragalosides reduce cisplatin ototoxicity in guinea pigs.

Cisplatin is known to cause high-frequency neurosensory hearing loss. While reactive oxygen species have been shown to play a role, reactive nitrogen species have been implicated, but not proven to be involved, in cisplatin ototoxicity. The purpose of the present study was to investigate the role of nitric oxide (NO) in cisplatin ototoxicity by administering astragalosides, a natural antioxidant, in conjunction with cisplatin. Guinea pigs were injected with cisplatin, astragalosides or both. Auditory brainstem-evoked responses (ABRs) were measured before and 3 days after cisplatin administration. The cochlear tissue was then assayed for NO and malondialdehyde (MDA), and cochleae were also examined by scanning electron microscopy. Cisplatin alone caused significant ABR threshold shifts at all stimuli tested, whereas astragalosides alone caused no shifts. There was a significant reduction in threshold shift for clicks, 8-kHz and 16-kHz tone bursts (but not 32 kHz) when astragalosides was given with cisplatin. Both the MDA concentration and the NO concentration in the astragalosides/cisplatin group were significantly lower than those of the cisplatin group. Correspondingly, the loss of outer hair cells in the astragalosides/cisplatin group was much less than that in the cisplatin group. This suggests that astragalosides reduces cisplatin ototoxicity by its antioxidant property.

Does early treatment prevent deafness in thiamine-responsive megaloblastic anaemia syndrome?

Thiamine-responsive megaloblastic anaemia (TRMA; OMIM 249270) syndrome is an autosomal recessive disorder characterized by diabetes mellitus, megaloblastic anaemia, and sensorineural deafness. Progressive hearing loss is one of the cardinal findings of the syndrome and is known to be irreversible. Whether the deafness in TRMA syndrome can be prevented is not yet known. Here, we report a four-month-old female infant diagnosed with TRMA syndrome at an early age. There was no hearing loss at the time of diagnosis. The patient's initial auditory evoked brainstem response measurements were normal. Although she was given thiamine supplementation regularly following the diagnosis, the patient developed moderate sensorineural hearing loss at 20 months of age, indicating that early diagnosis and treatment with oral thiamine (100 mg/day) could not prevent deafness in TRMA syndrome. It would be premature to draw general conclusions from one case, but we believe that further patient-based observations can shed light on the pathophysiology of this rare syndrome as well as prediction of its prognosis.

Protective effects of Salvia miltiorrhiza against cisplatin-induced ototoxicity in guinea pigs.

OBJECTIVE: The aim of the study was to investigate the protective effects of Salvia miltiorrhiza (SM) against cisplatin-induced ototoxicity in guinea pigs. METHODS: Thirty-nine guinea pigs were randomly divided into 3 groups. The first group (control group) received physiologic saline by intraperitoneal (i.p.) injection for 5 days. The second group (cisplatin group) was treated with cisplatin (2 mg/kg per day, i.p. injection) for 5 days. The third group (SM group) was given SM (8 g/kg per day, i.p. injection) for 2 days and then was given SM (8 g/kg per day, i.p. injection) and cisplatin (2 mg/kg per day, i.p. injection) for 5 days. Auditory brain stem response (ABR) and cochlea blood flow measurement were used to evaluate cochlea function. The structures of cochlea were observed by light microscope, scanning electron microscope, transmission electron microscope (TEM), and immunohistochemical examination. RESULTS: Cisplatin could cause severe acoustic damages including significant elevation of ABR threshold, substantial losses of outer hair cells and inner hair cells, and severe damage on the stria vascularis and spiral ganglion cells (SGCs). Although in SM group, the increased tendency of threshold was milder than that in cisplatin group. The damages in cochlea and stria vascularis were also less severe than those in cisplatin group. The expression of induced nitric oxide synthase in the cochlea and SGC in SM group was lower than that in cisplatin group. CONCLUSIONS: Salvia miltiorrhiza can significantly reduce the cisplatin-induced side effects.

Protective effect of Korean red ginseng extract on cisplatin ototoxicity in HEI-OC1 auditory cells.

Ginseng extract is known to have many beneficial effects, including the reversal of pathological and physiological changes induced by ischemia, stress, and aging. Cisplatin, an effective antineoplastic drug, can cause irreversible sensorineural hearing loss and serious tinnitus in humans; thus cisplatin-induced ototoxicity is a useful experimental model for ototoxicity. This study investigated the protective effects of Korean red ginseng extract on cisplatin-induced ototoxicity in auditory cells. Pretreatment with 2.5 mg/mL of ginseng extract prior to application of 20 microM of cisplatin significantly increased cell viability after 48 h of incubation in auditory cells. Pretreatment with ginseng extract significantly attenuated the cisplatin-induced increase in reactive oxygen species (ROS). Ginseng extract also inhibited the expression of caspase-3 and poly-ADP-ribose polymerase related to cisplatin-induced apoptosis because a major mechanism of cisplatin-induced toxicity involves ROS production. Thus, Korean red ginseng extract can play both an anti-apoptotic and anti-oxidative role on cisplatin-induced ototoxicity in an auditory cell line.

Geldanamycin induces production of heat shock protein 70 and partially attenuates ototoxicity caused by gentamicin in the organ of Corti explants.

BACKGROUND: Heat shock protein 70 (HSP70) protects inner ear cells from damage and death induced by e.g. heat or toxins. Benzoquinone ansamycin antibiotic geldanamycin (GA) was demonstrated to induce the expression of HSP70 in various animal cell types. The aim of our study was to investigate whether GA induces HSP70 in the organ of Corti (OC), which contains the auditory sensory cells, and whether GA can protect these cells from toxicity caused by a common aminoglycoside antibiotic gentamicin. METHODS: To address these questions, we used the OC explants isolated from p3-p5 rats. As a read-out, we used RT-PCR, ELISA and immunofluorescence. RESULTS: We found that GA at the concentration of 2 microM efficiently induced HSP70 expression on mRNA and protein level in the OC explants. Confocal microscopy revealed that HSP70 induced by GA is expressed by hair cells and interdental cells of spiral limbus. Preincubation of explants with 2 muM GA prior to adding gentamicin (500 microM) significantly reduced the loss of outer but not inner hair cells, suggesting different mechanisms of otoprotection needed for these two cell types. CONCLUSION: GA induced HSP70 in the auditory sensory cells and partially protected them from toxicity of gentamicin. Understanding the molecular mechanisms of GA otoprotection may provide insights for preventative therapy of the hearing loss caused by aminoglycoside antibiotics.

[iNOS and AChE expression on guinea pigs cochlea spiral ganglion induced by streptomycin and attenuation by Salvia miltiorrhiza injection].

AIM: To study the expression of iNOS and AChE on ginea pigs cochlea spiral ganglion induced by streptomycin (SM) and attenuation by salvia miltiorrhiza injection (Chinese Traditional medicine-dansen DS). METHODS: 32 guinea pigs were divided into 4 groups randomly (n=8): control group, SM group, DS + SM group, DS group. SABC immunohistochemical staining and image quantitative analysis technique were used to observe the expression of iNOS and AChE, as well as grey value analysis, and ABR measurements were used to observe ototoxicity. RESULTS: After 10 days with drugs, the ABR threshold value of SM increased more significantly than that of the control (P < 0.01), while the ABR threshold value of DS+ SM co-treatment increased than the control group, but lower than that of SM group (P < 0.01). The results of immunohistochemical staining implied the expression of iNOS and AChE in SG of SM group were higher than that of control group, and had positive correlate. CONCLUSION: The ABR threshold value increases and the expression of iNOS and AChE strengthen on SM ototoxicity, and has some correlation. DS can attenuate the ototoxicity induced by SM, and has protective function.

[Diagnosis, expert examination and prevention of occupational neurosensory deafness in workers of oil producing and petrochemical industries].

The authors designed a complex of informative criteria for diagnosis and medical examination of occupational neurosensory deafness, in order to objectively form risk groups of ear diseases. The article deals with justified adequate therapeutic and prophylactic recommendations on primary and secondary prevention, that enable better quality of preliminary and periodic medical examinations of workers exposed to occupational noise.

Sendai virus vector-mediated transgene expression in the cochlea in vivo.

We injected a recombinant Sendai virus (SeV) vector into the guinea pig cochlea using two different approaches--the scala media and scala tympani--and investigated which cell types took up the vector. The hearing threshold shift and distribution of transfected cells in animals using the scala media approach were different compared to those using the scala tympani approach. SeV can transfect very different types of cells, including stria vascularis, spiral ganglion neurons, and sensory epithelia of the organ of Corti, and fibrocytes of the scala tympani. Because SeV vectors can potentially deliver stimuli to the cochlea to induce hair cell regeneration, it may be a powerful tool for repairing the organ of Corti.