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Introduction: myo7aa, the homolog of the human Usher 1B syndrome pathogenic gene, myo7A, plays an important role in stereociliary development and maintenance, therefore, is critical for hearing and balance. However, the molecular mechanisms that myo7aa regulate hearing and balance still need to be studied. Methods: In this study, we generated two independent zebrafish myo7aa knockout lines using CRISPR/Cas9 technology. To investigate the effects of myo7aa on hearing, YO-PRO-1 staining and startle response assay were used. To gain insight into the specific molecular mechanisms by which myo7aa affects hearing, transcriptome sequencing and bioinformatics analysis were employed. Results: Our study showed that hair cells of myo7aa-/- zebrafish can not take up YO-PRO-1 fluorescent dye and are insensitive to acoustic stimulation in myo7aa-/- zebrafish compared to wild type. Genes related to the Rho GTPase signaling pathway, such as arhgap33, dab2ip, and arghef40, are significantly down-regulated in myo7aa-/- zebrafish embryos at 3 dpf. GTP and ATP compensation can partially rescue the hair cell defects in myo7aa knockout zebrafish. Discussion: Our findings suggest that zebrafish myo7aa affects congenital hearing by regulating Rho GTPase signaling, and loss of myo7aa leads to abnormal Rho GTPase signaling and impairs hair cell function. myo7aa, myo7A, arhgap33, dab2ip, arghef40 and myo7aa-/- fonts in the abstract are italicized. -/- is a superscript format.

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Background: According to observational research, migraine may increase the risk of Meniere's disease (MD). The two have not, however, been proven to be causally related. Methods: Using Mendelian random (MR) analysis, we aimed to evaluate any potential causal relationship between migraine and MD. We extracted single-nucleotide polymorphisms (SNPs) from large-scale genome-wide association studies (GWAS) involving European individuals, focusing on migraine and MD. The main technique used to evaluate effect estimates was inverse-variance weighting (IVW). To assess heterogeneity and pleiotropy, sensitivity analyses were carried out using weighted median, MR-Egger, simple mode, weighted mode, and MR-PRESSO. Results: There was no discernible causative link between genetic vulnerability to MD and migraine. The migraine dose not increase the prevalence of MD in the random-effects IVW method (OR = 0.551, P = 0.825). The extra weighted median analysis (OR = 0.674, P = 0.909), MR-Egger (OR = 0.068, P = 0.806), Simple mode (OR = 0.170, P = 0.737), and Weighted mode (OR = 0.219, P= 0.760) all showed largely consistent results. The MD dose not increase the prevalence of migraine in the random-effects IVW method (OR = 0.999, P = 0.020). The extra weighted median analysis (OR = 0.999, P = 0.909), MR-Egger (OR = 0.999, P = 0.806), Simple mode (OR = 0.999, P = 0.737), and Weighted mode (OR = 1.000, P = 0.760). Conclusion and significance: This Mendelian randomization study provides casual evidence that migraine is not a risk factor for MD and MD is also not a risk factor for migraine.

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Background: Wave In, which refers to the negativity between waves I and II in auditory brainstem response (ABR), is an electrophysiological phenomenon observed in previous studies. The term "high jugular bulb" (HJB) describes a jugular bulb that is located in a high position in the posterior aspect of the internal acoustic canal. The present study aimed to explore the correlation between wave In and the possibility of a HJB. Methods: This retrospective study included a cohort of pediatric patients diagnosed with profound hearing loss who were enrolled in a government-sponsored cochlear implantation program at an academic medical center between January 2019 and December 2022. The analysis involved examining the results obtained from the ABR test and high-resolution computed tomography (HRCT) of the temporal bone in the patients. The position of the jugular bulb was classified according to the Manjila and Semaan classification. Results: A total of 221 pediatric patients were included in the study. Twenty-four patients, with a median age of 3 years and a range of 1-7 years, showed significant bilateral (n = 21) or unilateral (n = 3) wave In (mean latency: right ear, 2.16 ms ± 0.22 ms; left ear, 2.20 ms ± 0.22 ms). The remaining 197 patients showed an absence of ABR. The HRCT images revealed that 18 of the 24 patients (75%) had HJB, but only 41 of the 197 patients who lacked ABR (20.8%) showed signs of HJB. The ratio difference was considered statistically significant based on the chi-squared test (χ2 = 32.10, p < 0.01). More than 50% of the HJBs were categorized as type 4 jugular bulbs, which are located above the inferior margin of the internal auditory canal. Conclusion: ABR wave In in pediatric patients with profound hearing loss suggests a high possibility of HJB. The physiological mechanism underlying this correlation needs further investigation.

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Introduction: The pathogenic gene CDH23 plays a pivotal role in tip links, which is indispensable for mechanoelectrical transduction in the hair cells. However, the underlying molecular mechanism and signal regulatory networks that influence deafness is still largely unknown. Methods: In this study, a congenital deafness family, whole exome sequencing revealed a new mutation in the pathogenic gene CDH23, subsequently; the mutation has been validated using Sanger sequencing method. Then CRISPR/Cas9 technology was employed to knockout zebrafish cdh23 gene. Startle response experiment was used to compare with wide-type, the response to sound stimulation between wide-type and cdh23-/-. To further illustrate the molecular mechanisms underlying congenital deafness, comparative transcriptomic profiling and multiple bioinformatics analyses were performed. Results: The YO-PRO-1 assay result showed that in cdh23 deficient embryos, the YO-PRO-1 signal in inner ear and lateral line neuromast hair cells were completely lost. Startle response experiment showed that compared with wide-type, the response to sound stimulation decreased significantly in cdh23 mutant larvae. Comparative transcriptomic showed that the candidate genes such as atp1b2b and myof could affect hearing by regulating ATP production and purine metabolism in a synergetic way with cdh23. RT-qPCR results further confirmed the transcriptomics results. Further compensatory experiment showed that ATP treated cdh23-/- embryos can partially recover the mutant phenotype. Conclusion: In conclusion, our study may shed light on deciphering the principal mechanism and provide a potential therapeutic method for congenital hearing loss under the condition of CDH23 mutation.

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Introduction: Noise-induced calcium overload in sensory hair cells has been well documented as an early step in the pathogenesis of noise-induced hearing loss (NIHL). Alterations in cellular calcium homeostasis mediate a series of cellular events, including activation of calcium-dependent protein kinases and phosphatases. Using cell-membrane- and blood-brain-barrier-permeable calpain-1 (µ-calpain) and calpain-2 (m-calpain) inhibitor MDL-28170, we tested the involvement of calpains, a family of calcium-dependent cysteine proteases, and the potential of MDL-28170 in preventing NIHL. Methods: CBA/J mice at the age of 12 weeks were exposed to broadband noise with a frequency spectrum from 2-20 kHz for 2 h at 101 dB sound pressure level to induce permanent hearing loss as measured by auditory brainstem response and distortion product otoacoustic emissions. Morphological damage was assessed by quantification of remaining sensory hair cells and inner hair cell synapses 2 weeks after the exposure. Results: MDL-28170 treatment by intraperitoneal injection significantly attenuated noise-induced functional deficits and cochlear pathologies. MDL-28170 treatment also prevented noise-induced cleavage of alpha-fodrin, a substrate for calpain-1. Furthermore, MDL-28170 treatment prevented reduction of PI3K/Akt signaling after exposure to noise and upregulated p85α and p-Akt (S473) in outer hair cells. Discussion: These results indicate that noise-induced calpain activation negatively regulates PI3K/Akt downstream signaling, and that prevention of NIHL by treatment with MDL-28170 is associated with upregulation of PI3K/Akt survival signaling pathways.

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OBJECTIVES: The main purpose of cochlear implantation for prelingual deafness is to restore the deaf children's auditory function, obtain normal speech development, learning and social ability, and improve the quality of life. Previous studies mostly focused on the improvement of simple hearing or speech ability. This study aims to evaluate the changes of hearing and speech ability and family life quality of patients after cochlear implantation, and to explore the effect of cochlear implantation on hearing and speech rehabilitation of patients. METHODS: In February 2021, using the convenient sampling method, 171 patients who have completed cochlear implantation were selected from the database of cochlear implantation follow-up center of a class III Tertiary hospital in Hunan Province. Questionnaires were used to investigate the patients' parents, which were Categories of Auditory Performance (CAP), Speech/Spatial and Qualities of Hearing Scale-Parents' Version (SSQ-P), and Children using Hearing Implants Quality of Life (CuHI-QoL). T-test and analysis of variance were used to explore the postoperative auditory and speech ability of patients at different ages in different periods (<2.5-year group, 2.5-4.5-year group and >4.5-year group), and Pearson correlation analysis was used to explore the correlation. Multiple linear regression was used to explore the relationship between the dimension of patients' quality of life and the scores of scale for evaluating auditory ability (CAP, speech perception, spatial hearing, and other hearing characteristics). RESULTS: The values of CAP and SSQ-P in the <2.5-year group were lower than those in the 2.5-4.5-year and >4.5-year groups (all P<0.05). Pearson correlation analysis showed that postoperative years and CuHI-QoL scores (parental expectations and patients' quality of life) were positively correlated with score of CAP, SSQ-P and its dimension, respectively (all P<0.05). The results of multiple linear regression analysis showed the CAP scores and speech perception were the influencing factors for the quality of life (R2=0.170, P<0.01). CONCLUSIONS: Two and a half years after operation is the rapid growth period of patients' hearing and language ability, and the growth rate becomes slow after stabilization. With the extension of postoperative years, the patients' hearing and speech ability becomes stronger, and the quality of life is better.

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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.

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Objective:The purpose of this study is to review the difficulties that can occur during cochlear implant surgery in patients with inner ear abnormalities and the management. Method:A retrospective analysis was made on 186 cases of cochlear implant with inner ear malformation, the types of inner ear malformations included 6 cases（3.23%） of isolated semicircular dysplasia, 137 cases（73.66%） of isolated large vestibular aqueducts, 26 cases（13.98%） of Mondini malformations, 6 cases（3.23%） of incomplete septal type Ⅲ, 3 cases（1.61%） of internal auditory stenosis, 7 cases（3.76%） of cochlear dysplasia and 1 case（0.54%） of incomplete septal typeⅠ. Two hundred patients with normal inner ear structures were randomly selected as the control group. The data collected included the types of inner ear abnormalities, intraoperative manifestations, clinical management strategies, and postoperative speech rehabilitation, and the literature was reviewed. Result:148 patients（77.49%） with inner ear malformation underwent successful surgery, electrode insertion was incomplete in 6 patients（3.14%）, and cerebrospinal fluid blowout occurred in 29 patients（15.18%）, it was difficult to locate the window because of the abnormal structure of the window in 8 cases（4.19%）. In 191 patients, the facial recess approach was adopted intraoperatively, and 17.8% of the patients had significant structural abnormalities of the facial nerve, significantly more than the group with normal inner ear structure. Only 1 patient showed delayed facial nerve paralysis 1 week after surgery, and recovered well after treatment. 6.81% of the patients adopted the expanded round window approach, which was significantly lower than that of the group with normal inner ear structure（28%）. There was no significant difference between patients with inner ear malformation and patients with extremely severe deafness with normal inner ear structure who received cochlear implant in speech rehabilitation. Conclusion:Cochlear implant is safe, feasible and effective for patients with inner ear malformation. For patients with inner ear malformation, special attention should be paid to the preoperative imaging reading to predict the possible risks during the operation. The safest surgical plan, including the type of electrode and the manner in which the window is opened, must be prepared before the operation, and the operation must be performed or directed by an experienced surgeon who can adjust the optimal surgical plan according to what is seen during the operation.

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Gentamicin-induced cochlear hair cell ototoxicity, such as oxidative stress and apoptosis, could be attenuated by mouse inner ear stem cells (IESCs). However, it is still unclear whether such protective effects could be mediated by exosomes derived from IESCs (IESCs-ex). In the present study, HEI-OC1 cells were exposed to gentamicin (2 mM) to establish an ototoxicity model and further treated with exosomes isolated from miR-182-5p transferred or non-transferred IESCs. IESCs-ex improved HEI-OC1 cell viability, as assayed by the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyltetrazolium bromide method, and alleviated the oxidative stress response induced by the gentamicin treatment, as confirmed by measuring the malondialdehyde, superoxide dismutase, catalase, and glutathione peroxidase levels. IESCs-ex increased relative miR-182-5p expression and decreased FOXO3 expression in the gentamicin-exposed HEI-OC1 cells. Furthermore, exosomes derived from miR-182-5p mimics that were pre-treated with IESCs could increase miR-182-5p and Bcl-2 expressions and decrease FOXO3 and Bax expressions in gentamicin-exposed HEI-OC1 cells. All of these results indicate that IESCs-ex could attenuate gentamicin-induced HEI-OC1 cell apoptosis and oxidative stress through the miR-182-5p/FOXO3 axis.

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Posttranslational modification of histones alters their interaction with DNA and nuclear proteins, influencing gene expression and cell fate. In this study, we investigated the effect of G9a (KMT1C, EHMT2), a major histone lysine methyltransferase encoded by the human EHMT2 gene and responsible for histone H3 lysine 9 dimethylation (H3K9me2) on noise-induced permanent hearing loss (NIHL) in adult CBA/J mice. The conditions of noise exposure used in this study led to losses of cochlear synapses and outer hair cells (OHCs) and permanent auditory threshold shifts. Inhibition of G9a with its specific inhibitor BIX 01294 or with siRNA significantly attenuated these pathological features. Treatment with BIX 01294 also prevented the noise-induced decrease of KCNQ4 immunolabeling in OHCs. Additionally, G9a was increased in cochlear cells, including both outer and inner sensory hair cells, some spiral ganglion neurons (SGNs), and marginal cells, 1 h after the completion of the noise exposure. Also subsequent to noise exposure, immunoreactivity for H3K9me2 appeared in some nuclei of OHCs following a high-to-low frequency gradient with more labeled OHCs in the 45-kHz than the 32-kHz region, as well as in the marginal cells and in some SGNs of the basal turn. These findings suggest that epigenetic modifications of H3K9me2 are involved in NIHL and that pharmacological targeting of G9a may offer a strategy for protection against cochlear synaptopathy and NIHL.

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Mitochondria modulate cellular calcium homeostasis by the combined action of the mitochondrial calcium uniporter (MCU), a selective calcium entry channel, and the sodium calcium exchanger (NCLX), which extrudes calcium from mitochondria. In this study, we investigated MCU and NCLX in noise-induced hearing loss (NIHL) using adult CBA/J mice and noise-induced alterations of inner hair cell (IHC) synapses in MCU knockout mice. Following noise exposure, immunoreactivity of MCU increased in cochlear sensory hair cells of the basal turn, while immunoreactivity of NCLX decreased in a time- and exposure-dependent manner. Inhibition of MCU activity via MCU siRNA pretreatment or the specific pharmacological inhibitor Ru360 attenuated noise-induced loss of sensory hair cells and synaptic ribbons, wave I amplitudes, and NIHL in CBA/J mice. This protection was afforded, at least in part, through reduced cleavage of caspase 9 (CC9). Furthermore, MCU knockout mice on a hybrid genetic CD1 and C57/B6 background showed resistance to noise-induced seizures compared to wild-type littermates. Owing to the CD1 background, MCU knockouts and littermates suffer genetic high frequency hearing loss, but their IHCs remain intact. Noise-induced loss of IHC synaptic connections and reduction of auditory brainstem response (ABR) wave I amplitude were recovered in MCU knockout mice. These results suggest that cellular calcium influx during noise exposure leads to mitochondrial calcium overload via MCU and NCLX. Mitochondrial calcium overload, in turn, initiates cell death pathways and subsequent loss of hair cells and synaptic connections, resulting in NIHL.

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Studies have suggested that gentamicin may induce hair cell apoptosis through the Hsp90/Akt signaling pathway. Nevertheless, the exact mechanisms remain unclear. The following study investigated Hsp90 expression in gentamicin-treated cochleae (in vitro and in vivo) and explored whether the Hsp90/Akt signaling pathway has a role in gentamicin ototoxicity. For in vitro experiments, organotypic cultures from post-natal organ of Corti, collected from post-natal day 2 or 3 (p2-3) CBA/J explants were treated with 0.2 mM gentamicin for 24 h; for the in vivo experiments, 6-week-old male CBA/J mice were injected with gentamicin (150 mg/kg) to induce hearing loss. P-Akt and AKT proteins expression and the levels of Hsp90-Akt complex were examined using immunochemistry and western blot. Our data suggested that Hsp90 expression decreased in the hair ear cells after treatment. In addition, the pAkt and Hsp90/AKT levels significantly decreased in treated mice compared to the control group. To conclude, these results support the idea that the Hsp90/Akt signaling pathway may have an important role in the ototoxic effects of gentamicin.

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The TPRN gene encodes taperin, which is prominently present at the taper region of hair cell stereocilia. Mutations in TPRN have been reported to cause autosomal recessive nonsyndromic deafness 79(DFNB 79). To investigate the role of taperin in pathogenesis of hearing loss, we generated TPRN knockout mice using TALEN technique. Sanger sequencing confirmed an 11 bp deletion at nucleotide 177-187 in exon 1 of TPRN, which results in a truncated form of taperin protein. Heterozygous TPRN+/- mice showed apparently normal auditory phenotypes to their wide-type (WT) littermates. Homozygous TPRN-/- mice exhibited progressive sensorineural hearing loss as reflected by auditory brainstem response to both click and tone burst stimuli at postnatal days 15 (P15), 30 (P30), and 60 (P60). Alex Fluor-594 phalloidin labeling showed no obvious difference in hair cell numbers in the cochlea between TPRN-/- mice and WT mice under light microscope. However, scanning electronic microscopy revealed progressive degeneration of inner hair cell stereocilia, from apparently normal at postnatal days 3 (P3) to scattered absence at P15 and further to substantial loss at P30. The outer hair cell stereocilia also showed progressive degeneration, though much less severe, Collectively, we conclude that taperin plays an important role in maintenance of hair cell stereocilia. Establishment of TPRN knockout mice enables further investigation into the function of this gene.

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This study aimed to investigate the p19 expression in cisplatin-treated rats and the role of p19 in the degeneration of inner ear cells. It also searched for p19 gene alterations in patients with profound sensorineural deafness. P19ink4d is essential for the postmitotic maintenance of hair cells. It is presumed that a mutation in the functional homolog of p19 or a disturbance in its regulated expression can be the underlying cause of hearing loss. Experiments were conducted on male and female Sprague-Dawley rats (aged 6-7 weeks, 280-320 g) with thresholds of auditory brainstem responses <30 dB in the sound pressure level, and signs of middle ear infection were used for the experiment. For clinical evaluation, 400 children (age less than 13 years) from unrelated families with severe or profound sensorineural hearing loss (SNHL) were recruited at the second Xiangya Hospital of Central South University between 2005 and 2013, and genomic DNA for deafness gene analysis was obtained from peripheral blood samples of the patients and their lineal relatives. It was found that the p19 expression increased over time in the inner ear cells after cisplatin administration, but the p19 mRNA and protein levels significantly decreased in rats with manifested hearing loss induced by cisplatin. However, no mutation existed within the coding exons of p19 in the patients with profound sensorineural deafness. To conclude, the results support the concept that p19 may play an important role in the ototoxic effects of cisplatin and is probably involved in the pathogenesis of hearing loss.

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AIM: To study the distribution characteristics of common mutations in the GJB2, SLC26A4, and mtDNA genes in children with severe or profound sensorineural hearing loss (SNHL) in southwestern China. MATERIALS AND METHODS: A total of 1,164 individuals were recruited to screen for the common GJB2, SLC26A4, and mtDNA mutations by microarrays. Subsequencing for the coding region of the GJB2 gene in the samples without the GJB2 hotspot mutations as well as subsequencing for the exon 1 of the TRMU gene in those samples with the mtDNA hotspot mutations was performed by Sanger sequencing. All mutations were analyzed in association with medical imaging. RESULTS: In this study, 28.43% of all subjects carried mutations. The mutation frequencies in the GJB2, SLC26A4, and mtDNA genes were 17.27%, 7.04%, and 4.12%, respectively. No TRMU mutation was found in the study. The frequency of the mtDNA mutations in the multiethnic minorities was six times that in the Han (11.23% vs. 1.91%; p approaches 0.000) and in the urban group was one-third of that in the suburban group(1.49% vs. 4.47%; p=0.047). The frequency of the GJB2 mutations in urban and suburban groups was 23.38% and 15.99%, respectively (p=0.012). The enlarged vestibular aqueduct (EVA) was the most common inner ear malformation and ∼79.10% of EVA cases were associated with the SLC26A4 mutations. CONCLUSIONS: More than one-fourth of children with severe or profound SNHL carried the common deafness mutations. The proportions of ethnic minorities and urban subjects could impact the frequency of the GJB2 and mtDNA mutations. The SLC26A4 hotspot mutations are prevalent and correlate strongly with EVA.

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OBJECTIVE: To screen and identify the frequency and characteristic of mutation in stereocilium-related gene Taperin of Chinese prelingual nonsyndromic hearing impairment with DNA microarray combined with PCR. METHOD: One hundred and thirty-four patients of prelingual nonsyndromic deafness and one hundred health individuals in China were investigated in this study. Genomic DNA was extracted from the patients and was subjected to DNA microarray to screen mutations in 4 most common genes. The samples that carried none of the common mutant alleles were subjected to PCR and sequenced to detect mutations in Taperin gene. RESULT: Ninteen out of one hundred and thirty-four patients of prelingual nonsyndromic deafness were detected carring common deafness gene with DNA microarray. Taperin gene were detected in one hundred and fifteen patients with PCR. A187S was detected in Taperin as hetrozygous state in 2 patients and their unaffected members of their family. It occurred at the evolutionary conservation of the amino acids of taperin according to alignment analysis. Two polymorphism, 157C>T and 318C>T, were found in the patients and the control group. CONCLUSION: A novel Taperin mutation, A187S was detected in Chinese patients with prelingual nonsyndromic hearing loss, which may be relevant to hearing loss. Two polymorphism, 157C>T and 318C>T, were found in Chinese in our research. The carrier frequency for Taperin mutation is about 1.74% of prelingual nonsyndromic deafness in Chinese patients.

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OBJECTIVE: To review the clinical manifestations and management of nasal sinus mucoceles with visual loss. METHOD: Medical records for 23 patients of paranasal sinus mucoceles with visual impairment were re viewed retrospectively during 8-year period (from 2002 to 2010). Ten mucoceles were found in the frontal or fronto-ethmoidal sinuses, 6 in the ethmoidal sinuses, 7 in the sphenoidal or spheno-ethmoidal sinuses. Because the majority of early chief complaints were problems related to vision, patients were often seen by ophthalmologists first. Poor vision was more common in patients with sphenoid or spheno-ethmoidal sinus mucoceles because of their proximity to the optic nerve. CT and MRI were important tools for diagnosing nasal sinus mucocele. The patients received endoscopic surgery to remove mucocele and to decompress the optic nerve. Steroid therapy was given postoperatively and routine examination with endoscopy were carried out during follow-up. RESULT: Postoperatively, the majority of symptoms, such as exophthalmos, epiphora, diplopia and headache, disappeared in all patients. However, vision recovery was observed only in some patients. Recovery of vision depended on the timing of surgery and severity of initial visual loss. Delay in treatment can seriously compromise recovery of vision impairment. Moreover, patients without light perception before surgery had poor visual recovery even if optic nerve decompressions were performed. CONCLUSION: Endoscopic surgery is effective to nasal sinus mucocele with visual loss. Because visual recovery depends on prompt diagnosis and surgical intervention, a good understanding of the disease and prompt imaging studies are important.

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