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1    Lack of pendrin during this period led to endolymphatic acidification, loss of the endocochlear po
2  different ionic compositions, including the endolymphatic and perilymphatic spaces of the organ of C
3 d in an intact cochlear epithelium where the endolymphatic and perilymphatic surfaces could be separa
4  involving failure of the development of the endolymphatic appendage.
5 undles were exposed to the estimated in vivo endolymphatic Ca(2+) concentration (0.3 mm) present in t
6 eir hair bundles were exposed to the in vivo endolymphatic Ca(2+) concentration (40 microM), all mani
7 owed for the first physiological estimate of endolymphatic Ca2+ near the MET channel (56 +/- 11 micro
8 encies (CF) and found that, at physiological endolymphatic calcium concentrations, approximately half
9 nificantly higher than those in the adjacent endolymphatic compartment and also higher than those of
10 sult in either collapse or distension of the endolymphatic compartment in the cochlea, with concomita
11 2X2 receptors on epithelial cells lining the endolymphatic compartment.
12 abel density significantly above that of the endolymphatic compartment.
13 her cells lining the cochlear and vestibular endolymphatic compartments express TRPML3.
14 mpairment, which is associated with enlarged endolymphatic compartments of the inner ear.
15 a P2X(2) receptors, which would regulate the endolymphatic concentration of the current-carrying ion
16 il embryonic day 15, after which time severe endolymphatic dilatation occurs, reminiscent of that see
17 ntire dorsal rim of the otic cup becomes the endolymphatic duct (ED), while the posteroventral rim be
18  ears often lack a distinct saccule, and the endolymphatic duct and common crus are invariably fused.
19 , the most common phenotype being failure of endolymphatic duct and common crus formation, accompanie
20  central vestibule, a coiled cochlea, and an endolymphatic duct and sac allowing fluid balance with t
21 e loss of dorsal otic structures such as the endolymphatic duct and sac is attributable to the downre
22 cular canals were the most sensitive and the endolymphatic duct and sac most resistant to exogenous N
23 cells in the thyroid gland as well as in the endolymphatic duct and sac of the inner ear, whereas pre
24 ed effects of VHL deficiency on "tumor-free" endolymphatic duct and sac of VHL patients.
25 alysis of clinically uninvolved "tumor-free" endolymphatic duct and sac tissues of VHL patients, we d
26 lar canals, utricle, saccule, cochlear duct, endolymphatic duct and sac, and neurons of the eighth cr
27   Pds expression was detected throughout the endolymphatic duct and sac, in distinct areas of the utr
28 2 normally promotes dorsal fates such as the endolymphatic duct and semicircular canals by positively
29                               Absence of the endolymphatic duct and swelling of the membranous labyri
30 e ventromedial otic vesicle, the base of the endolymphatic duct and the fusion plates of the semicirc
31 ivatives, including the semicircular canals, endolymphatic duct and utricle, are malformed or absent.
32 r work has shown that sensory organs and the endolymphatic duct each arise near the boundaries of bro
33 ing that leads to dorsal otic patterning and endolymphatic duct formation.
34 in the hindbrain from otic induction through endolymphatic duct outgrowth, and in the prospective neu
35 hat may be critical for the specification of endolymphatic duct outgrowth.
36 inner ears lack a non-sensory structure, the endolymphatic duct, and the membranous labyrinth is poor
37 selected topographical sites within the CNS, endolymphatic duct/sac epithelia are preferentially and
38 he primary effect of VHL deficiency on human endolymphatic duct/sac epithelium seems to be the genera
39 arise within the intraosseous portion of the endolymphatic duct/sac, the vestibular aqueduct.
40 be placed in the intraosseous portion of the endolymphatic duct/sac.
41 5 revealed that mtl and bsd homozygotes lack endolymphatic ducts and semicircular canals and have sho
42 (facial nerve exiting through jugular canal, endolymphatic ducts exiting posterior to the skull roof)
43 or growth and morphogenesis of the embryonic endolymphatic epithelium, a precursor of the endolymphat
44  and epithelial folding at the origin of the endolymphatic epithelium.
45 hought to be related to the shear motion and endolymphatic flow between the tectorial membrane (TM) a
46  in the larva, apparently owing to a loss of endolymphatic fluid in the ear, together with an over-in
47  supporting cells, secretory cells that make endolymphatic fluid or otolithic membranes, and simple e
48  several regions thought to be important for endolymphatic fluid resorption in the inner ear, consist
49  walls fuse together as normal; however, the endolymphatic fluid space in the semicircular canals is
50 determined by examining 3D T2 sequences, and endolymphatic hydrops was identified on delayed post-con
51  hemorrhage, or insidiously, consistent with endolymphatic hydrops.
52 e membranous labyrinth with the formation of endolymphatic hydrops.
53 nt fibrocytes and a significant reduction of endolymphatic potential in high-frequency cochlear regio
54 ation selective stereociliary process or the endolymphatic potential, our data lend additional suppor
55 ring loss associated with enlargement of the endolymphatic sac (EES).
56 endolymphatic epithelium, a precursor of the endolymphatic sac (ES) and duct (ED), which mediate endo
57                                          The endolymphatic sac (ES) is a cystic organ that is a part
58                 Here, we show that the mouse endolymphatic sac absorbs fluid in an SLC26A4-dependent
59 otocyst and gradually becomes limited to the endolymphatic sac by stage 30.
60 (ELST) have been proposed to be derived from endolymphatic sac epithelium, but other possible structu
61   Slc26a4 expression in the developing mouse endolymphatic sac is required for acquisition of normal
62          Vasopressin hypersensitivity of the endolymphatic sac may be implicated in the pathogenesis
63 erapy, intratympanic gentamicin therapy, and endolymphatic sac surgery.
64                                              Endolymphatic sac tumors (ELST) have been proposed to be
65                                              Endolymphatic sac tumors (ELSTs) are associated with von
66                                              Endolymphatic sac tumors (ELSTs) occur sporadically or i
67 ed reports suggest a possible association of endolymphatic sac tumors (ELSTs), which are extremely ra
68 blastomas (the most common tumor in VHL) and endolymphatic sac tumors (ELSTs).
69                                    Papillary endolymphatic sac tumors are destructive, hypervascular
70 s) with histopathologically proved papillary endolymphatic sac tumors were retrospectively reviewed.
71 creatic cysts and tumors, pheochromocytomas, endolymphatic sac tumors, and epididymal cystadenomas.
72 araganglioma, cerebral hemangioblastoma, and endolymphatic sac tumors.
73 drenal medullae and sympathetic paraganglia, endolymphatic sac, epididymis, and broad ligament.
74 onstrate expression of ATP6B1 in cochlea and endolymphatic sac.
75  glands, epididymis, broad ligament, and the endolymphatic sac/petrous bone.
76 nd cysts of the pancreas, pheochromocytomas, endolymphatic-sac tumors, and papillary cystadenomas of
77 -cell RNA-seq analysis of pre- and postnatal endolymphatic sacs demonstrates two types of differentia
78                      Gross structures of the endolymphatic space and stria vascularis observed at the
79 e cupula of each vertical canal occludes the endolymphatic space, its displacement should be proporti
80 ula extending only a small distance into the endolymphatic space.
81  well as a fusion of the utricle and saccule endolymphatic spaces into a common utriculosaccular cavi
82 roughout the forming semicircular canals and endolymphatic structures.

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