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1 melanocyte-derived intermediate cells in the stria vascularis.
2 , forming the intermediate cell layer of the stria vascularis.
3 ner hair cells or a reduced thickness of the stria vascularis.
4 stemic circulation and the fluids inside the stria vascularis.
5 egions medial to inner HCs as well as in the stria vascularis.
6 e progressive appearance of large lesions in stria vascularis.
7  maintained in scala media, generated by the stria vascularis.
8 articular in the cochlear organ of Corti and stria vascularis.
9 nd structurally damaged blood vessels in the stria vascularis.
10 at Kir4.1 confers the outflow of K(+) in the stria vascularis.
11 endocochlear potential due to atrophy of the stria vascularis.
12 y regions between the sensory tissue and the stria vascularis.
13 in the potassium-secreting epithelium of the stria vascularis.
14 lt animals through rapid degeneration of the stria vascularis.
15 , spiral ganglia, the spiral limbus, and the stria vascularis.
16 lesions in the cochlea were found within the stria vascularis, a barrier epithelium containing the pr
17 s to spindle, root, and basal cells from the stria vascularis, a structure in the cochlea necessary f
18  In the previously reported S1pr2(-/-) mice, stria vascularis abnormalities, organ of Corti degenerat
19 cytes (intermediate cells) in the developing stria vascularis, all of which are significantly diminis
20 ts principally from degeneration of cochlear stria vascularis and decline of the endocochlear potenti
21 ortance of basal cell tight junctions in the stria vascularis and directly verify the two-cell hypoth
22                   Both marginal cells of the stria vascularis and hair cells express Trpml3 mRNA.
23 on by altering ion channel expression in the stria vascularis and inducing blood-labyrinth barrier (B
24 artery, which supplies blood directly to the stria vascularis and protects its capillary bed from hig
25 tissues, increased E2F1 and apoptosis in the stria vascularis and spiral ganglion neurons of the inne
26                   Ngb was not present in the stria vascularis and the inner and outer hair cells.
27 tribution of nonsensory cell networks in the stria vascularis and the sensory region toward the matur
28 gentamicin (GTTR) enters the cochlea via the stria vascularis and then HCs selectively.
29 ing was restricted to the basal cells in the stria vascularis and was also detectable in the spiral g
30 an of Corti, in the basal cell region of the stria vascularis, and in type 1 fibrocytes of the spiral
31  We found that hair cells, marginal cells of stria vascularis, and other cells lining the cochlear an
32 was observed to leak from capillaries of the stria vascularis, and pericytes lost their tight associa
33 barrier properties of tight junctions of the stria vascularis appeared intact in a biotin tracer assa
34  in the human cochlea, and they point to the stria vascularis as an important therapeutic target for
35 licated apoptosis in the spiral ganglion and stria vascularis because of mitochondrial reactive oxyge
36 megalin, the candidate AG transporter in the stria vascularis, by binding competitor cilastatin preve
37 ments (organ of Corti, afferent neurons, and stria vascularis) can degenerate independently, and exer
38  cells and will facilitate future studies of stria vascularis cell function.
39  either to cochlear sensory epithelial or to stria vascularis cells as the cell types most prominentl
40 paratus of renal glomerular podocytes and in stria vascularis cells of the inner ear, consistent with
41  we show that cochlear epithelial cells, not stria vascularis cells, are the main inner-ear cells rel
42  high throughput of K(+) across cells of the stria vascularis, conferred partly by the activity of Ki
43      Gelatin zymography of extracts from the stria vascularis confirmed these findings.
44 berrations in outer and inner hair cells and stria vascularis defects, leading to deafness in the var
45  hepatocyte growth factor (HGF) signaling in stria vascularis development for the first time and that
46 ochlear potential, indicative of significant stria vascularis dysfunction, but without obvious signs
47           Aberrant splicing of Fgfr2 blocked stria vascularis formation due to erroneous ligand usage
48 he relation of this developmental process to stria vascularis function is currently unknown.
49 n of transcripts in the WT versus Nr3b2(-/-) stria vascularis has identified a set of genes that is l
50                                          The stria vascularis, however, does not sustain permanent da
51 le's loop and for potassium secretion by the stria vascularis in the inner ear.
52  Our findings indicate the importance of the stria vascularis in the mechanism of hearing impairment,
53 elements (e.g., glial cells and cells in the stria vascularis) in auditory impairment in ASD.
54  of the cochlea revealed degeneration of the stria vascularis, in conjunction with disorganization of
55  neural crest cells fail to migrate into the stria vascularis intermediate layer, resulting in a sign
56 n proteins in the endothelial barrier of the stria vascularis (intrastrial fluid-blood barrier) throu
57                                          The stria vascularis is a nonsensory structure that is essen
58              Vascular disturbance within the stria vascularis is a potential mechanism that leads to
59 ent increase in macrophage activation in the stria vascularis is associated with a decline in auditor
60 embranes in the cochlea, suggesting that the stria vascularis is the primary site of cochlear pathoge
61                                  Explants of stria vascularis, 'mini-chips', are selectively cultured
62 ss structures of the endolymphatic space and stria vascularis observed at the light microscope level
63 acrophage-like melanocytes (PVM/Ms) from the stria vascularis of mice aged between P10 and P15 (P, po
64 anently impaired expression of KCNJ10 in the stria vascularis of Pit1(dw) mice, which likely contribu
65 rporation of the melanocytes into the future stria vascularis of the cochlear duct requires c-MET sig
66 owth factor (Hgf) is expressed in the future stria vascularis of the cochlear epithelium.
67 ll barriers and the capillary bed within the stria vascularis of the S1P(2) receptor-null mice showed
68                  Cochlear melanocytes in the stria vascularis originated from Pax3-traced melanoblast
69 y preserving the structural integrity of the stria vascularis.SIGNIFICANCE STATEMENT Mutations in Med
70 y outer hair cells (OHCs), inner hair cells, stria vascularis, spiral ganglia, and surrounding nerves
71 tivity to 8-isoprostane was increased in the stria vascularis, spiral ganglion cells and the organ of
72 vity delineated blood vessels located in the stria vascularis, spiral ligament, sub-basilar region, s
73 ing that the intermediate cells (ICs) of the stria vascularis (StV) express outward K+ current that r
74                                          The stria vascularis (StV) of the cochlear duct is the stati
75  early pathophysiological alterations in the stria vascularis (SV) are associated with increased macr
76                                          The stria vascularis (SV) in the cochlea generates and maint
77                                          The stria vascularis (SV) is a stratified epithelium in the
78 e organ of Corti (OC), spiral ganglion (SG), stria vascularis (SV), and afferent nerve fibres.
79 dependent on ion homeostasis mediated by the stria vascularis (SV).
80 ar melanocytes are intermediate cells in the stria vascularis that generate endocochlear potentials r
81 ibration into electrical signals, versus the stria vascularis, the cellular battery that powers trans
82 tin accumulation is consistently high in the stria vascularis, the region of the cochlea that maintai
83 used a decrease in VEGF expression levels in stria vascularis vessels.
84 evealed that pericytes on capillaries of the stria vascularis were closely associated with the endoth
85 permeability of a biotin-based tracer in the stria vascularis were unaltered.
86 hin the organ of Corti, spiral ganglion, and stria vascularis, which are known targets of cisplatin o
87 ced by 4 and 8 weeks old in mutants, and the stria vascularis, which generates the EP, showed degener
88      The primary lesion was localized to the stria vascularis, which houses the main vasculature of t