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1 r in very old CBA mice (which do not exhibit severe hearing loss).
2 icated for recessively inherited moderate to severe hearing loss.
3 listening devices, and cochlear implants for severe hearing loss.
4 zed by retinitis pigmentosa (RP) and mild-to-severe hearing loss.
5 e absent in patients with a moderate or more severe hearing loss.
6 uditory evoked responses in 13 patients with severe hearing loss.
7 (SISA) questionnaire, to detect moderate to severe hearing loss.
8 nversations, even for those with moderate to severe hearing loss.
9 retinal degeneration as well as moderate to severe hearing loss.
11 f cognitive functioning in older adults with severe hearing loss after cochlear implantation; however
12 on of a dominant-negative erbB receptor show severe hearing loss and 80% postnatal loss of type-I SGN
13 arly-onset, usually non-progressive, mild-to-severe hearing loss and generally good central vision un
14 The data suggest that the combination of severe hearing loss and old age results in deficits in o
16 to evaluate the apps' ability to detect less severe hearing loss and the diagnostic performance of 2
17 Defects in ear canal development can cause severe hearing loss as sound waves fail to reach the mid
18 terozygous mutant mice were found to develop severe hearing loss at 6 months of age without balance d
19 distortion product otoacoustic emission and severe hearing loss at high frequencies, the shift is la
20 lear implant activation in older adults with severe hearing loss at risk for MCI, suggesting that coc
23 d the proportion of infants with moderate-to-severe hearing loss diagnosed by age 10 months (57% vs 1
26 A consecutive sample of older adults with severe hearing loss eligible for cochlear implantation w
27 ed in patients with post-lingual moderate to severe hearing loss, failed to prevent hearing loss.
28 glia, we found that loss of Med12 results in severe hearing loss in adult animals through rapid degen
29 ber of genes are responsible for moderate to severe hearing loss in sporadic individuals born to cons
34 ighboring supporting cells, many humans with severe hearing loss lack both hair cells and supporting
37 in the CN of middle-aged C57 mice (with less-severe hearing loss) or in very old CBA mice (which do n
38 tor impairment, cognitive or language delay, severe hearing loss, or bilateral blindness at 18 months
39 tor disability, cognitive or language delay, severe hearing loss, or bilateral blindness at a correct
42 The T(-4128) SNP may be contributing to the severe hearing loss phenotype in the HL2 pedigree by red
43 None of the p.Cys759Phe patients exhibited a severe hearing loss phenotype, and more than 60% had onl
44 cell-level molecular defects responsible for severe hearing loss, the genetics responsible for less s
45 In the CN of old C57 mice (18 months) with severe hearing loss, the number of glycine-immunoreactiv
51 sses of 10 listeners with bilateral, mild-to-severe hearing loss were simulated in 10 corresponding g
52 t some individuals with these mutations have severe hearing loss, whereas their maternal relatives wi
53 ected, patients receiving cisplatin had more severe hearing loss with concurrent carboplatin administ