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1 g tricellulin and ILDR1 (DFNB42) cause human nonsyndromic deafness.
2 ost are loss-of-function mutations and cause nonsyndromic deafness.
3 orphic allele of BSND as a cause of apparent nonsyndromic deafness.
4 uences are the basis for either syndromic or nonsyndromic deafness.
5 rtholog of the murine Comt2 gene that causes nonsyndromic deafness.
6 e 22q13 cosegregate with autosomal recessive nonsyndromic deafness.
7 nally transmitted aminoglycoside-induced and nonsyndromic deafness.
8 sponsible for both Usher syndrome and DFNB12 nonsyndromic deafness.
9 eles of TBC1D24 can cause either epilepsy or nonsyndromic deafness.
10 ponsible for half of all autosomal recessive nonsyndromic deafness.
11  children diagnosed with autosomal recessive nonsyndromic deafness.
12 ynein genes near loci for different forms of nonsyndromic deafness.
13 ndidate lesion in lhfpl5a predicted to cause nonsyndromic deafness.
14 tion of CEACAM16 leads to autosomal dominant nonsyndromic deafness (ADNSHL) at the autosomal dominant
15 tochondrial DNA causes maternally inherited, nonsyndromic deafness, an extreme case of tissue-specifi
16 protein connexin 26 (CX26) cause prelingual, nonsyndromic deafness and are responsible for as many as
17 s for nearly half of all cases of hereditary nonsyndromic deafness cases.
18 1D; USH1D), whereas missense mutations cause nonsyndromic deafness (DFNB12).
19 lindness (Usher syndrome type 1B, USH1B) and nonsyndromic deafness (DFNB2, DFNA11).
20 gene encoding protocadherin 15, cause either nonsyndromic deafness DFNB23 or Usher syndrome type 1F (
21 tte is a model for studying the mechanism of nonsyndromic deafness DFNB25.
22 passes shaker-2 (sh2), a model for the human nonsyndromic deafness DFNB3.
23 ntegrin-binding protein, are associated with nonsyndromic deafness (DFNB48) and Usher syndrome type 1
24  different recessive mutations of TRIC cause nonsyndromic deafness (DFNB49), a surprisingly limited p
25 rnatively, the dfcr mouse may be a model for nonsyndromic deafness, due to the nonpathologic effect o
26 r the review period, three syndromic and six nonsyndromic deafness genes have been discovered, bringi
27 een discovered, bringing the total number of nonsyndromic deafness genes to 64.
28 halmologic examinations of the patients with nonsyndromic deafness have found asymptomatic RP-like ma
29  for two loci, DFNB12 and USH1D, which cause nonsyndromic deafness, identifying waltzer as a mouse mo
30             Mutations in the OTOF gene cause nonsyndromic deafness in humans, and OTOF knock-out mice
31 n associated with aminoglycoside-induced and nonsyndromic deafness in many families worldwide.
32 tation (p.I12T) in four kindreds segregating nonsyndromic deafness linked to a 4.04-cM interval on ch
33  a chromosomal interval that overlaps with a nonsyndromic-deafness localization, DFNB12.
34 luded localization to four previously mapped nonsyndromic deafness loci but obtained conclusive evide
35                  Here we map a new recessive nonsyndromic deafness locus, DFNB26, to a 1.5-cM interva
36 mutations in other genes that cause USH1 and nonsyndromic deafness may also have distinct effects on
37    A specific allele, previously reported in nonsyndromic deafness, may be associated with a mild ret
38 ve channel gating; and 4), Cx26V84L in M2, a nonsyndromic deafness mutant, retains normal dye couplin
39 mutations known to cause either syndromic or nonsyndromic deafness occur in genes that interact with
40 ond identified gene associated with X-linked nonsyndromic deafness, PRPS1 will be a good candidate ge
41    The DFNB74 locus for autosomal-recessive, nonsyndromic deafness segregating in three families was
42                                              Nonsyndromic deafness segregating in two unrelated consa
43 ons in some dynein genes are associated with nonsyndromic deafness should now be tested.
44 ently mapped DFNB86, a locus associated with nonsyndromic deafness, to chromosome 16p.
45 sher syndrome and 38 probands with recessive nonsyndromic deafness were screened for the presence of
46 of CDH23 have been observed in families with nonsyndromic deafness, whereas nonsense, frameshift, spl
47 tients, they provide a new genetic model for nonsyndromic deafness with enlarged vestibular aqueduct
48 nknown cause, parental nonconsanguinity, and nonsyndromic deafness with hearing loss limited to a sin

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