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1 ry cortex remained unchanged in animals with congenital deafness.
2 rise to disorders of the cardiac rhythm and congenital deafness.
3 manifested as both retinitis pigmentosa and congenital deafness.
4 altzer locus result in circling behavior and congenital deafness.
5 me, which causes both cardiac arrhythmia and congenital deafness.
6 ly occurring cochlear pathology presented by congenital deafness.
7 r-order auditory cortex remained auditory in congenital deafness.
11 sher syndrome type 1C (USH1C), a syndrome of congenital deafness and progressive blindness, as well a
12 disorder characterized by moderate to severe congenital deafness and progressive retinitis pigmentosa
14 into thyroid physiology, the pathogenesis of congenital deafness and the role of altered sulphate tra
17 study demonstrates differences in effects of congenital deafness between supragranular and other cort
18 for several months, providing evidence that congenital deafness can be effectively overcome by treat
21 en (Bth) mutant mice are models for profound congenital deafness (DFNB7/B11) and progressive hearing
23 ass XV unconventional myosin, cause profound congenital deafness in humans and both deafness and vest
24 ant mouse models for the most common form of congenital deafness in humans, which are knock-outs for
25 ant mouse models for the most common form of congenital deafness in humans, which are knockouts for t
26 odel for the most prevalent form of X-linked congenital deafness in man, which is associated with mut
30 py from cohorts of cats with normal hearing, congenital deafness, or congenital deafness with a cochl
31 animal models and humans have indicated that congenital deafness produces degenerative changes in the
34 ereditary disorder characterized by profound congenital deafness, retinitis pigmentosa, and vestibula
35 ically heterogeneous disorder causing severe congenital deafness, retinitis pigmentosa, and vestibula
37 l impact on cells in the cochlear nucleus to congenital deafness, suggesting selective processing imp
38 ion have been studied using animal models of congenital deafness that include surgical ablation of th
39 ion factor 1 (Pit1(dw)), which has profound, congenital deafness that is rescued by oral TH replaceme
40 r syndrome type 1, characterized by profound congenital deafness, vestibular arreflexia, and progress
41 a recessive autosomal disorder manifested by congenital deafness, vestibular dysfunction, and progres
44 mutation can be offered to individuals with congenital deafness with high sensitivity and specificit
46 , Pendred first described the association of congenital deafness with thyroid goitre (MM#274600).
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