OtoRhinoLaryngology by Sfakianakis G.Alexandros Sfakianakis G.Alexandros,Anapafseos 5 Agios Nikolaos 72100 Crete Greece,tel : 00302841026182,00306932607174
Τετάρτη 18 Απριλίου 2018
Beyond the audiogram: application of models of auditory fitness for duty to assess communication in the real world
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Evidence-based occupational hearing screening II: validation of a screening methodology using measures of functional hearing ability
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Examining Acoustic and Kinematic Measures of Articulatory Working Space: Effects of Speech Intensity
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Children's Acoustic and Linguistic Adaptations to Peers With Hearing Impairment
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The Prevalence of Speech and Language Disorders in French-Speaking Preschool Children From Yaoundé (Cameroon)
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A Systematic Review of Semantic Feature Analysis Therapy Studies for Aphasia
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The Role of Language in Nonlinguistic Stimuli: Comparing Inhibition in Children With Language Impairment
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Auditory–Perceptual Assessment of Fluency in Typical and Neurologically Disordered Speech
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Gaze Toward Naturalistic Social Scenes by Individuals With Intellectual and Developmental Disabilities: Implications for Augmentative and Alternative Communication Designs
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Examining Acoustic and Kinematic Measures of Articulatory Working Space: Effects of Speech Intensity
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Children's Acoustic and Linguistic Adaptations to Peers With Hearing Impairment
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The Prevalence of Speech and Language Disorders in French-Speaking Preschool Children From Yaoundé (Cameroon)
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A Systematic Review of Semantic Feature Analysis Therapy Studies for Aphasia
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The Role of Language in Nonlinguistic Stimuli: Comparing Inhibition in Children With Language Impairment
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Auditory–Perceptual Assessment of Fluency in Typical and Neurologically Disordered Speech
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Gaze Toward Naturalistic Social Scenes by Individuals With Intellectual and Developmental Disabilities: Implications for Augmentative and Alternative Communication Designs
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Examining Acoustic and Kinematic Measures of Articulatory Working Space: Effects of Speech Intensity
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Children's Acoustic and Linguistic Adaptations to Peers With Hearing Impairment
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The Prevalence of Speech and Language Disorders in French-Speaking Preschool Children From Yaoundé (Cameroon)
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A Systematic Review of Semantic Feature Analysis Therapy Studies for Aphasia
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The Role of Language in Nonlinguistic Stimuli: Comparing Inhibition in Children With Language Impairment
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Auditory–Perceptual Assessment of Fluency in Typical and Neurologically Disordered Speech
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Gaze Toward Naturalistic Social Scenes by Individuals With Intellectual and Developmental Disabilities: Implications for Augmentative and Alternative Communication Designs
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Vestibular Manifestations in Subjects With Enlarged Vestibular Aqueduct.
Vestibular Manifestations in Subjects With Enlarged Vestibular Aqueduct.
Otol Neurotol. 2018 Apr 16;:
Authors: Song JJ, Hong SK, Lee SY, Park SJ, Kang SI, An YH, Jang JH, Kim JS, Koo JW
Abstract
OBJECTIVE: To describe the results of a thorough evaluation in a large series of patients with an enlarged vestibular aqueduct (EVA), focusing on vestibular manifestations with etiological considerations.
STUDY DESIGN: Retrospective chart review of patients with EVA.
SETTING: Tertiary referral center.
PATIENTS: A total of 22 EVA patients with a median age of 8 years (6 mo-35 yr) who underwent both audiovestibular and radiologic examinations.
MAIN OUTCOME MEASURES: Patient demographics, radiologic findings, audiologic results, vestibular symptoms, findings of neurotologic examinations, and laboratory evaluations were collected and analyzed. Standard descriptive statistics were used to summarize patient characteristics. Subjects who had a history of vertigo attack were categorized as "vestibulopathy group," while subjects without any history of vertigo as "non-vestibulopathy group."
RESULTS: Of the 41 ears included, 37 (90.2%) had hearing loss on initial audiometric evaluations. Among the 22 patients, 14 (63.6%) complained of dizziness. Of the 14 vertiginous patients, seven had recurrent episodes, five had a history of single attack, and two presented with postural imbalances. There were no significant differences between vestibulopathy and non-vestibulopathy groups with regard to the relationship between the development of vestibular symptoms and aqueductal size, hearing threshold, or age at first visit. Four of the 22 (18.2%) patients developed secondary benign paroxysmal positional vertigo (BPPV) and all patients complained of simultaneous decreases in hearing.
CONCLUSIONS: Our results demonstrate that patients may develop vestibular symptoms during their clinical course, and all patients with an enlarged vestibular aqueduct should be cautioned regarding the potential development of vestibular pathology. Moreover, the non-negligible incidence of secondary BPPV mandates positional tests when evaluating EVA patients with vertigo.
PMID: 29664869 [PubMed - as supplied by publisher]
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A Novel GJB2 compound heterozygous mutation c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) causes sensorineural hearing loss in a Chinese family.
A Novel GJB2 compound heterozygous mutation c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) causes sensorineural hearing loss in a Chinese family.
J Clin Lab Anal. 2018 Apr 17;:e22444
Authors: Shi X, Zhang Y, Qiu S, Zhuang W, Yuan N, Sun T, Gao J, Qiao Y, Liu K
Abstract
OBJECTIVE: To investigate whether a novel compound heterozygous mutations c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) in GJB2 result in hearing loss.
METHODS: Allele-specific PCR-based universal array (ASPUA) screening and sequence analysis were applied to identify these mutations. 3D model was built to perform molecular dynamics (MD) simulation to verify the susceptibility of the mutations. Furthermore, WT- and Mut-GJB2 DNA fragments, containing the mutation of c.257C>G and c.176del16 were respectively cloned and transfected into HEK293 and spiral ganglion neuron cell (SGNs) by lenti-virus delivery system to indicate the subcellular localization of the WT- and Mut-CX26 protein.
RESULTS: A novel compound heterozygous mutation c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) in GJB2 was identified in a Chinese family, in which 4 siblings with profound hearing loss, but the fifth child is normal. By ASPUA screening and sequencing, a compound heterozygote mutations in GJB2 c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) were identified in these four deaf children, each of the mutated GJB2 gene were inherited from their parents. There is no mutation of GJB2 gene identified in the normal child. Besides, the compound heterozygous mutation GJB2 c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) could lead to the alterations of the subcellular localization of each corresponding mutated CX26 protein and could cause the hearing loss, which has been predicted by MD simulation and verified in both 293T and SGNs cell line.
CONCLUSION: The c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) compound mutations in GJB2 detected in this study are novel, and which may be associated with hearing loss in this Chinese family.
PMID: 29665173 [PubMed - as supplied by publisher]
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The Plasma Membrane Calcium ATPases in Calcium Signaling Network.
The Plasma Membrane Calcium ATPases in Calcium Signaling Network.
Curr Protein Pept Sci. 2018 Apr 16;:
Authors: Wu X, Weng L, Zhang J, Liu X, Huang J
Abstract
The plasma membrane Ca2+ ATPases (PMCAs) are responsible for the clearance of Ca2+ out of cells after intracellular Ca2+ transients. Cooperating with Na+/Ca2+ exchangers (NCXs) and Ca2+ buffering proteins, PMCAs play an essential role in maintaining the long-term cellular Ca2+ homeostasis. The plasma membrane Ca2+ ATPase was first discovered in red blood cell membrane about 50 years ago, and then other PMCA isoforms and alternatively spliced variants had been identified from different tissues and different developmental stages, revealing a surprising complexity of the PMCA family. In mammals, there are four PMCA isoforms encoded by four distinct genes. Isoform 1 and 4 are found in virtually all tissues, whereas isoform 2 and 3 are primarily expressed in excitable cells such as neurons and myocytes. Perturbation of PMCAs function has been implicated in a variety of diseases and disorders, including hearing loss, ataxia, paraplegia, and infertility. Here, we would like to review the recent progresses in the study of the PMCAs and related disorders, in particular how these pathological conditions help us to gain an in-depth insight into the function of PMCAs and their contribution in the regulation of Ca2+ signaling network.
PMID: 29663880 [PubMed - as supplied by publisher]
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Identification of variants in the mitochondrial lysine-tRNA (MT-TK) gene in myoclonic epilepsy-pathogenicity evaluation and structural characterization by in silico approach.
Related Articles |
Identification of variants in the mitochondrial lysine-tRNA (MT-TK) gene in myoclonic epilepsy-pathogenicity evaluation and structural characterization by in silico approach.
J Cell Biochem. 2018 Apr 16;:
Authors: Nadeem MS, Ahmad H, Mohammed K, Muhammad K, Ullah I, Baothman OAS, Ali N, Anwar F, Zamzami MA, Shakoori AR
Abstract
Variations in mitochondrial genes have an established link with myoclonic epilepsy. In the present study we evaluated the nucleotide sequence of MT-TK gene of 52 individuals from 12 unrelated families and reported three variations in 2 of the 13 epileptic patients. The DNA sequences coding for MT-TK gene were sequenced and mutations were detected in all participants. The mutations were further analyzed by the in silico analysis and their structural and pathogenic effects were determined. All the investigated patients had symptoms of myoclonus, 61.5% were positive for ataxia, 23.07% were suffering from hearing loss, 15.38% were having mild to severe dementia, 69.23% were males, and 61.53% had cousin marriage in their family history. DNA extracted from saliva was used for the PCR amplification of a 440 bp DNA fragment encompassing complete MT-TK gene. The nucleotide sequence analysis revealed three mutations, m.8306T>C, m.8313G>C, and m.8362T>G that are divergent from available reports. The identified mutations designate the heteroplasmic condition. Furthermore, pathogenicity of the identified variants was predicted by in silico tools viz., PON-mt-tRNA and MitoTIP. Secondary structure of altered MT-TK was predicted by RNAStructure web server. Studies by MitoTIP and PON-mt-tRNA tools have provided strong evidences of pathogenic effects of these mutations. Single nucleotide variations resulted in disruptive secondary structure of mutant MT-TK models, as predicted by RNAStructure. In vivo confirmation of structural and pathogenic effects of identified mutations in the animal models can be prolonged on the basis of these findings.
PMID: 29663531 [PubMed - as supplied by publisher]
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Effects of Hearing Loss and Fast-Acting Compression on Amplitude Modulation Perception and Speech Intelligibility
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Effects of Hearing Loss and Fast-Acting Compression on Amplitude Modulation Perception and Speech Intelligibility
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Effects of Hearing Loss and Fast-Acting Compression on Amplitude Modulation Perception and Speech Intelligibility
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A Novel GJB2 compound heterozygous mutation c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) causes sensorineural hearing loss in a Chinese family.
A Novel GJB2 compound heterozygous mutation c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) causes sensorineural hearing loss in a Chinese family.
J Clin Lab Anal. 2018 Apr 17;:e22444
Authors: Shi X, Zhang Y, Qiu S, Zhuang W, Yuan N, Sun T, Gao J, Qiao Y, Liu K
Abstract
OBJECTIVE: To investigate whether a novel compound heterozygous mutations c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) in GJB2 result in hearing loss.
METHODS: Allele-specific PCR-based universal array (ASPUA) screening and sequence analysis were applied to identify these mutations. 3D model was built to perform molecular dynamics (MD) simulation to verify the susceptibility of the mutations. Furthermore, WT- and Mut-GJB2 DNA fragments, containing the mutation of c.257C>G and c.176del16 were respectively cloned and transfected into HEK293 and spiral ganglion neuron cell (SGNs) by lenti-virus delivery system to indicate the subcellular localization of the WT- and Mut-CX26 protein.
RESULTS: A novel compound heterozygous mutation c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) in GJB2 was identified in a Chinese family, in which 4 siblings with profound hearing loss, but the fifth child is normal. By ASPUA screening and sequencing, a compound heterozygote mutations in GJB2 c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) were identified in these four deaf children, each of the mutated GJB2 gene were inherited from their parents. There is no mutation of GJB2 gene identified in the normal child. Besides, the compound heterozygous mutation GJB2 c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) could lead to the alterations of the subcellular localization of each corresponding mutated CX26 protein and could cause the hearing loss, which has been predicted by MD simulation and verified in both 293T and SGNs cell line.
CONCLUSION: The c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) compound mutations in GJB2 detected in this study are novel, and which may be associated with hearing loss in this Chinese family.
PMID: 29665173 [PubMed - as supplied by publisher]
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Characterization of Hair Cell-Like Cells Converted From Supporting Cells After Notch Inhibition in Cultures of the Organ of Corti From Neonatal Gerbils.
Related Articles |
Characterization of Hair Cell-Like Cells Converted From Supporting Cells After Notch Inhibition in Cultures of the Organ of Corti From Neonatal Gerbils.
Front Cell Neurosci. 2018;12:73
Authors: Li Y, Jia S, Liu H, Tateya T, Guo W, Yang S, Beisel KW, He DZZ
Abstract
The senses of hearing and balance depend upon hair cells, the sensory receptors of the inner ear. Hair cells transduce mechanical stimuli into electrical activity. Loss of hair cells as a result of aging or exposure to noise and ototoxic drugs is the major cause of noncongenital hearing and balance deficits. In the ear of non-mammals, lost hair cells can spontaneously be replaced by production of new hair cells from conversion of supporting cells. Although supporting cells in adult mammals have lost that capability, neonatal supporting cells are able to convert to hair cells after inhibition of Notch signaling. We questioned whether Notch inhibition is sufficient to convert supporting cells to functional hair cells using electrophysiology and electron microscopy. We showed that pharmacological inhibition of the canonical Notch pathway in the cultured organ of Corti prepared from neonatal gerbils induced stereocilia formation in supporting cells (defined as hair cell-like cells or HCLCs) and supernumerary stereocilia in hair cells. The newly emerged stereocilia bundles of HCLCs were functional, i.e., able to respond to mechanical stimulation with mechanotransduction (MET) current. Transmission electron microscopy (TEM) showed that HCLCs converted from pillar cells maintained the pillar cell shape and that subsurface cisternae, normally observed underneath the cytoskeleton in outer hair cells (OHCs), was not present in Deiters' cells-derived HCLCs. Voltage-clamp recordings showed that whole-cell currents from Deiters' cells-derived HCLCs retained the same kinetics and magnitude seen in normal Deiters' cells and that nonlinear capacitance (NLC), an electrical hallmark of OHC electromotility, was not detected from any HCLCs measured. Taken together, these results suggest that while Notch inhibition is sufficient for promoting stereocilia bundle formation, it is insufficient to convert neonatal supporting cells to mature hair cells. The fact that Notch inhibition led to stereocilia formation in supporting cells and supernumerary stereocilia in existing hair cells appears to suggest that Notch signaling may regulate stereocilia formation and stability during development.
PMID: 29662441 [PubMed]
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Hearing, self-motion perception, mobility, and aging.
Related Articles |
Hearing, self-motion perception, mobility, and aging.
Hear Res. 2018 Mar 31;:
Authors: Campos J, Ramkhalawansingh R, Pichora-Fuller MK
Abstract
Hearing helps us know where we are relative to important events and objects in our environment and it allows us to track our changing position dynamically over space and time. Auditory cues are used in combination with other sensory inputs (visual, vestibular, proprioceptive) to help us perceive our own movements through space, known as self-motion perception. Whether we are maintaining standing balance, walking, or driving, audition can provide unique and important information to help optimize self-motion perception, and consequently to support safe mobility. Recent epidemiological and experimental studies have provided evidence that hearing loss is associated with greater walking difficulties, poorer overall physical functioning, and a significantly increased risk of falling in older adults. Importantly, the mechanisms underlying the associations between hearing status and mobility are poorly understood. It is also critical to consider that age-related hearing loss is often concomitant with declines in other sensory, motor, and cognitive functions and that these declines may interact, particularly during realistic, everyday tasks. Overall, exploring the role of auditory cues and the effects of hearing loss on self-motion perception specifically, and mobility more generally, are important to both building fundamental knowledge about the perceptual processes underlying the ability to perceive our movements through space, as well as to optimizing mobility-related interventions for those with hearing loss so that they can function better when confronted by everyday, real-world, sensory-motor challenges. The goal of this paper is to explore the role of hearing in self-motion perception across a range of mobility-related behaviors. First, we briefly review the ways in which auditory cues are used to perceive self-motion and how sound inputs affect behaviors such as standing balance, walking, and driving. Next, we consider age-related changes in auditory self-motion perception and the potential consequences to performance on mobility-related tasks. We then describe how hearing loss is associated with declines in mobility-related abilities and increased adverse outcomes such as falls. We describe age-related changes to other sensory and cognitive functions and how these may interact with hearing loss in ways that affect mobility. Finally, we briefly consider the implications of the hearing-mobility associations with respect to applied domains such as screening for mobility problems and falls risk in those with hearing loss and developing interventions and training approaches targeting safe and independent mobility throughout the lifespan.
PMID: 29661612 [PubMed - as supplied by publisher]
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A Novel GJB2 compound heterozygous mutation c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) causes sensorineural hearing loss in a Chinese family.
A Novel GJB2 compound heterozygous mutation c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) causes sensorineural hearing loss in a Chinese family.
J Clin Lab Anal. 2018 Apr 17;:e22444
Authors: Shi X, Zhang Y, Qiu S, Zhuang W, Yuan N, Sun T, Gao J, Qiao Y, Liu K
Abstract
OBJECTIVE: To investigate whether a novel compound heterozygous mutations c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) in GJB2 result in hearing loss.
METHODS: Allele-specific PCR-based universal array (ASPUA) screening and sequence analysis were applied to identify these mutations. 3D model was built to perform molecular dynamics (MD) simulation to verify the susceptibility of the mutations. Furthermore, WT- and Mut-GJB2 DNA fragments, containing the mutation of c.257C>G and c.176del16 were respectively cloned and transfected into HEK293 and spiral ganglion neuron cell (SGNs) by lenti-virus delivery system to indicate the subcellular localization of the WT- and Mut-CX26 protein.
RESULTS: A novel compound heterozygous mutation c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) in GJB2 was identified in a Chinese family, in which 4 siblings with profound hearing loss, but the fifth child is normal. By ASPUA screening and sequencing, a compound heterozygote mutations in GJB2 c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) were identified in these four deaf children, each of the mutated GJB2 gene were inherited from their parents. There is no mutation of GJB2 gene identified in the normal child. Besides, the compound heterozygous mutation GJB2 c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) could lead to the alterations of the subcellular localization of each corresponding mutated CX26 protein and could cause the hearing loss, which has been predicted by MD simulation and verified in both 293T and SGNs cell line.
CONCLUSION: The c.257C>G (p.T86R)/c.176del16 (p.G59A fs*18) compound mutations in GJB2 detected in this study are novel, and which may be associated with hearing loss in this Chinese family.
PMID: 29665173 [PubMed - as supplied by publisher]
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Characterization of Hair Cell-Like Cells Converted From Supporting Cells After Notch Inhibition in Cultures of the Organ of Corti From Neonatal Gerbils.
Related Articles |
Characterization of Hair Cell-Like Cells Converted From Supporting Cells After Notch Inhibition in Cultures of the Organ of Corti From Neonatal Gerbils.
Front Cell Neurosci. 2018;12:73
Authors: Li Y, Jia S, Liu H, Tateya T, Guo W, Yang S, Beisel KW, He DZZ
Abstract
The senses of hearing and balance depend upon hair cells, the sensory receptors of the inner ear. Hair cells transduce mechanical stimuli into electrical activity. Loss of hair cells as a result of aging or exposure to noise and ototoxic drugs is the major cause of noncongenital hearing and balance deficits. In the ear of non-mammals, lost hair cells can spontaneously be replaced by production of new hair cells from conversion of supporting cells. Although supporting cells in adult mammals have lost that capability, neonatal supporting cells are able to convert to hair cells after inhibition of Notch signaling. We questioned whether Notch inhibition is sufficient to convert supporting cells to functional hair cells using electrophysiology and electron microscopy. We showed that pharmacological inhibition of the canonical Notch pathway in the cultured organ of Corti prepared from neonatal gerbils induced stereocilia formation in supporting cells (defined as hair cell-like cells or HCLCs) and supernumerary stereocilia in hair cells. The newly emerged stereocilia bundles of HCLCs were functional, i.e., able to respond to mechanical stimulation with mechanotransduction (MET) current. Transmission electron microscopy (TEM) showed that HCLCs converted from pillar cells maintained the pillar cell shape and that subsurface cisternae, normally observed underneath the cytoskeleton in outer hair cells (OHCs), was not present in Deiters' cells-derived HCLCs. Voltage-clamp recordings showed that whole-cell currents from Deiters' cells-derived HCLCs retained the same kinetics and magnitude seen in normal Deiters' cells and that nonlinear capacitance (NLC), an electrical hallmark of OHC electromotility, was not detected from any HCLCs measured. Taken together, these results suggest that while Notch inhibition is sufficient for promoting stereocilia bundle formation, it is insufficient to convert neonatal supporting cells to mature hair cells. The fact that Notch inhibition led to stereocilia formation in supporting cells and supernumerary stereocilia in existing hair cells appears to suggest that Notch signaling may regulate stereocilia formation and stability during development.
PMID: 29662441 [PubMed]
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Hearing, self-motion perception, mobility, and aging.
Related Articles |
Hearing, self-motion perception, mobility, and aging.
Hear Res. 2018 Mar 31;:
Authors: Campos J, Ramkhalawansingh R, Pichora-Fuller MK
Abstract
Hearing helps us know where we are relative to important events and objects in our environment and it allows us to track our changing position dynamically over space and time. Auditory cues are used in combination with other sensory inputs (visual, vestibular, proprioceptive) to help us perceive our own movements through space, known as self-motion perception. Whether we are maintaining standing balance, walking, or driving, audition can provide unique and important information to help optimize self-motion perception, and consequently to support safe mobility. Recent epidemiological and experimental studies have provided evidence that hearing loss is associated with greater walking difficulties, poorer overall physical functioning, and a significantly increased risk of falling in older adults. Importantly, the mechanisms underlying the associations between hearing status and mobility are poorly understood. It is also critical to consider that age-related hearing loss is often concomitant with declines in other sensory, motor, and cognitive functions and that these declines may interact, particularly during realistic, everyday tasks. Overall, exploring the role of auditory cues and the effects of hearing loss on self-motion perception specifically, and mobility more generally, are important to both building fundamental knowledge about the perceptual processes underlying the ability to perceive our movements through space, as well as to optimizing mobility-related interventions for those with hearing loss so that they can function better when confronted by everyday, real-world, sensory-motor challenges. The goal of this paper is to explore the role of hearing in self-motion perception across a range of mobility-related behaviors. First, we briefly review the ways in which auditory cues are used to perceive self-motion and how sound inputs affect behaviors such as standing balance, walking, and driving. Next, we consider age-related changes in auditory self-motion perception and the potential consequences to performance on mobility-related tasks. We then describe how hearing loss is associated with declines in mobility-related abilities and increased adverse outcomes such as falls. We describe age-related changes to other sensory and cognitive functions and how these may interact with hearing loss in ways that affect mobility. Finally, we briefly consider the implications of the hearing-mobility associations with respect to applied domains such as screening for mobility problems and falls risk in those with hearing loss and developing interventions and training approaches targeting safe and independent mobility throughout the lifespan.
PMID: 29661612 [PubMed - as supplied by publisher]
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Short and Long-Term Outcomes of Titanium Clip Ossiculoplasty
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Active Transcutaneous Bone Conduction Implant: Middle Fossa Placement Technique in Children With Bilateral Microtia and External Auditory Canal Atresia
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Vestibular Manifestations in Subjects With Enlarged Vestibular Aqueduct
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Long-term Hearing Outcome of Canaloplasty With Partial Ossicular Replacement in Congenital Aural Atresia
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