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The issue of mitochondrial dysfunction in tinnitus, along with specific damage to proteins involved in the motility of SC of OHC, calls for an in-depth analysis of metabolic dysfunctions in degenerative tinnitus and presbyacusis, which may relate to the sophisticated mechanisms of sound transduction of the inner ear with molecular dysfunctions leading to altered sound perception in the course of inner ear degeneration

1).6 It is certainly the case that in the summer of 1886, while at Walberswick, Llewellyn crossed over to Southwold on the Blyth ferry

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