New discovery on how the inner ear works

Researchers have found that the parts of the inner ear that process sounds such as speech and music seem to work differently than other parts of the inner ear.

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New discovery on how the inner ear works

Researchers have found that the parts of the inner ear that process sounds such as speech and music seem to work differently than other parts of the inner ear.

from #Audiology via ola Kala on Inoreader http://ift.tt/29Dgo5X
via IFTTT

New discovery on how the inner ear works

Researchers have found that the parts of the inner ear that process sounds such as speech and music seem to work differently than other parts of the inner ear.

from #Audiology via xlomafota13 on Inoreader http://ift.tt/29Dgo5X
via IFTTT

Head wave correlations in ambient noise

Ambient ocean noise is processed with a vertical line array to reveal coherent time-separated arrivals suggesting the presence of head wave multipath propagation. Head waves, which are critically propagating water waves created by seabed waves traveling parallel to the water-sediment interface, can propagate faster than water-only waves. Such eigenrays are much weaker than water-only eigenrays, and are often completely overshadowed by them. Surface-generated noise is different whereby it amplifies the coherence between head waves and critically propagating water-only waves, which is measured by cross-correlating critically steered beams. This phenomenon is demonstrated both experimentally and with a full wave simulation.

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WFS1 in Optic Neuropathies: Mutation Findings in Nonsyndromic Optic Atrophy and Assessment of Clinical Severity.

WFS1 in Optic Neuropathies: Mutation Findings in Nonsyndromic Optic Atrophy and Assessment of Clinical Severity.

Ophthalmology. 2016 Jul 7;

Authors: Grenier J, Meunier I, Daien V, Baudoin C, Halloy F, Bocquet B, Blanchet C, Delettre C, Esmenjaud E, Roubertie A, Lenaers G, Hamel CP

Abstract
PURPOSE: To search for WFS1 mutations in patients with optic atrophy (OA) and assess visual impairment.
DESIGN: Retrospective molecular genetic and clinical study.
PARTICIPANTS: Patients with OA followed at a national referral center specialized in genetic sensory diseases.
METHODS: Mutation screening in WFS1 was performed by Sanger sequencing. WFS1-positive patients were evaluated on visual acuity (VA) and retinal nerve fiber layer (RNFL) thickness using time-domain (TD) or spectral-domain (SD) optical coherence tomography (OCT). Statistical analysis was performed.
MAIN OUTCOME MEASURES: Mutation identification, VA values, and RNFL thickness in sectors.
RESULTS: Biallelic WFS1 mutations were found in 3 of 24 unrelated patients (15%) with autosomal recessive nonsyndromic optic atrophy (arNSOA) and in 8 patients with autosomal recessive Wolfram syndrome (arWS) associated with diabetes mellitus and OA. Heterozygous mutations were found in 4 of 20 unrelated patients (20%) with autosomal dominant OA. The 4 WFS1-mutated patients of this latter group with hearing loss were diagnosed with autosomal dominant Wolfram-like syndrome (adWLS). Most patients had VA decrease, with logarithm of the minimum angle of resolution (logMAR) values lower in arWS than in arNSOA (1.530 vs. 0.440; P = 0.026) or adWLS (0.240; P = 0.006) but not differing between arNSOA and adWLS (P = 0.879). All patients had decreased RNFL thickness that was worse in arWS than in arNSOA (SD OCT, 35.50 vs. 53.80 μm; P = 0.018) or adWLS (TD-OCT, 45.84 vs. 59.33 μm; P = 0.049). The greatest difference was found in the inferior bundle. Visual acuity was negatively correlated with RNFL thickness (r = -0.89; P = 0.003 in SD OCT and r = -0.75; P = 0.01 in TD-OCT).
CONCLUSIONS: WFS1 is a gene causing arNSOA. Patients with this condition had significantly less visual impairment than those with arWS. Thus systematic screening of WFS1 must be performed in isolated, sporadic, or familial optic atrophies.

PMID: 27395765 [PubMed - as supplied by publisher]

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