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J. Otorhinolaryngol. Hear. Balance Med., Volume 1, Issue 1 (June 2018)

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Editorial

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Open AccessEditorial Welcome to Journal of Otorhinolaryngology, Hearing and Balance Medicine
J. Otorhinolaryngol. Hear. Balance Med. 2018, 1(1), 1; doi:10.3390/ohbm1010001
Received: 24 February 2017 / Revised: 24 February 2017 / Accepted: 24 February 2017 / Published: 28 February 2017
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Abstract
To date, much progress has been achieved in the field of Otorhinolaryngology—Head and Neck surgery, as well as hearing and balance science and medicine.[...] Full article

Research

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Open AccessArticle Effects of Retinoid Treatment on Cochlear Development, Connexin Expression and Hearing Thresholds in Mice
J. Otorhinolaryngol. Hear. Balance Med. 2018, 1(1), 2; doi:10.3390/ohbm1010002
Received: 5 July 2017 / Revised: 10 August 2017 / Accepted: 17 October 2017 / Published: 23 October 2017
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Abstract
Mutations in GJB2, gene coding for connexin 26 (Cx26), and GJB6, gene coding for connexin 30 (Cx30), are the most common genetic defects causing non-syndromic hereditary hearing loss. We previously reported that overexpression of Cx26 completely rescues the hearing in a mouse model
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Mutations in GJB2, gene coding for connexin 26 (Cx26), and GJB6, gene coding for connexin 30 (Cx30), are the most common genetic defects causing non-syndromic hereditary hearing loss. We previously reported that overexpression of Cx26 completely rescues the hearing in a mouse model of human GJB6 null mutations. The results suggest that therapeutic agents up-regulating the expression of Cx26 may potentially be a novel treatment for non-syndromic hereditary deafness caused by Cx30 null mutations. Retinoids are a family of vitamin A derivatives that exert broad and profound effects on cochlear protein expression including connexins. They are readily available and already utilized as therapeutic agents for recurrent otitis media and hearing loss due to noise exposure. In this study, we characterized the expression of Cx26 and Cx30 in the postnatal inner ear by different retinoids including retinyl palmitate (RP), the main source of vitamin A in over-the-counter (OTC) supplements, retinyl acetate (RAc) which is an isomer of RP, and all-trans-retinoic acid (ATRA), the most active retinoid derivative. The results revealed ATRA significantly increased cochlear Cx26 expression and improved hearing in Cx30 knockout (KO) mice by 10 dB suggesting its potential benefits as a therapeutic agent. In contrast, RP selectively reduced cochlear Cx30 expression and did not improve hearing thresholds at the dosages we tested. Full article
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Review

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Open AccessReview Endoplasmic Reticulum Stress in Hearing Loss
J. Otorhinolaryngol. Hear. Balance Med. 2018, 1(1), 3; doi:10.3390/ohbm1010003
Received: 16 October 2017 / Revised: 26 October 2017 / Accepted: 30 October 2017 / Published: 1 November 2017
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Abstract
The endoplasmic reticulum (ER) plays important roles in coordinating protein biosynthesis and secretion in the cell. Accumulation of misfolded and/or unfolded proteins in the ER causes ER stress and the so-called unfolded protein response (UPR). The UPR alleviates ER stress through blocking protein
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The endoplasmic reticulum (ER) plays important roles in coordinating protein biosynthesis and secretion in the cell. Accumulation of misfolded and/or unfolded proteins in the ER causes ER stress and the so-called unfolded protein response (UPR). The UPR alleviates ER stress through blocking protein synthesis and activating expression of chaperone genes, whereas prolonged UPR could induce cell death. Recent research has showed that ER stress and UPR are involved in hearing loss. Accordingly, animal experiments showed that chemical chaperones or ER stress inducers alleviate environment-related hearing loss, whereas ER stress inhibitor has been used to treat certain types of hereditary deafness. Further investigations are needed to fully understand the detailed mechanisms of how ER stress contributes to the loss of auditory function, which will help us to eventually develop ER-stress-related treatment of various types of deafness. Full article
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