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1 r in very old CBA mice (which do not exhibit severe hearing loss).
2 listening devices, and cochlear implants for severe hearing loss.
3 zed by retinitis pigmentosa (RP) and mild-to-severe hearing loss.
4 e absent in patients with a moderate or more severe hearing loss.
5 uditory evoked responses in 13 patients with severe hearing loss.
6 retinal degeneration as well as moderate to severe hearing loss.
7 on of a dominant-negative erbB receptor show severe hearing loss and 80% postnatal loss of type-I SGN
10 distortion product otoacoustic emission and severe hearing loss at high frequencies, the shift is la
13 d the proportion of infants with moderate-to-severe hearing loss diagnosed by age 10 months (57% vs 1
20 in the CN of middle-aged C57 mice (with less-severe hearing loss) or in very old CBA mice (which do n
21 tor impairment, cognitive or language delay, severe hearing loss, or bilateral blindness at 18 months
22 tor disability, cognitive or language delay, severe hearing loss, or bilateral blindness at a correct
24 The T(-4128) SNP may be contributing to the severe hearing loss phenotype in the HL2 pedigree by red
25 None of the p.Cys759Phe patients exhibited a severe hearing loss phenotype, and more than 60% had onl
26 cell-level molecular defects responsible for severe hearing loss, the genetics responsible for less s
27 In the CN of old C57 mice (18 months) with severe hearing loss, the number of glycine-immunoreactiv
31 sses of 10 listeners with bilateral, mild-to-severe hearing loss were simulated in 10 corresponding g
32 t some individuals with these mutations have severe hearing loss, whereas their maternal relatives wi
33 ected, patients receiving cisplatin had more severe hearing loss with concurrent carboplatin administ
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