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1 d the development of retinal function in the normal retina.
2 ctivity in the rd1 retina was similar to the normal retina.
3 genin-6 during degeneration when compared to normal retina.
4 her than in the lesion but lower than in the normal retina.
5 e regions with functionally and structurally normal retina.
6  pericyte-containing microvasculature of the normal retina.
7 t of non-neurogenic environment of the adult normal retina.
8 ions of the empirically observed patterns in normal retina.
9 in CRB1 mutations resembles that of immature normal retina.
10 ld yield photoreceptor deficits in otherwise normal retina.
11 achments, increased to 180% of the amount in normal retina.
12 I activity also promotes RGC survival in the normal retina.
13 ss sensitive but otherwise resemble those of normal retina.
14 lowed by functional maturation by P30 in the normal retina.
15 d significant differences between AMD versus normal retinas.
16 ere more frequent in the AMD retinas than in normal retinas.
17 reased mtDNA control region SNPs compared to normal retinas.
18 reased blood flow due to vasodilation in the normal retinas.
19 ound in photoreceptor and RPE cell layers in normal retinas.
20 ntrast to the lightly stained glial cells in normal retinas.
21 ger blood vessels, compared with age-matched normal retinas.
22 clear layers of diabetic retinas, but not in normal retinas.
23 munoreactivity; these swellings were rare in normal retinas.
24 vertheless, significantly lower than that of normal retinas.
25 urvey for novel peroxidases expressed within normal retinas.
26 cular membranes in comparison with levels in normal retinas.
27 s no detectable level of the active forms in normal retinas.
28 gher levels in neovascular membranes than in normal retinas.
29 as switched to base medium preconditioned by normal retinas.
30 er between the junctional zone and adjacent "normal" retina.
31  approach has enabled us to show that in the normal retina a single ribbon and arciform density oppos
32                         The effect of PDT on normal retina and choroid (with no CNV) was studied in 9
33                           Forty spots on the normal retina and choroid were treated with PDT and were
34    Molecular biological analyses of RNA from normal retina and from proliferative and myofibroblastic
35 Full-length CRMP-5 protein was identified in normal retina and optic nerve by Western blot analyses.
36 on and three-dimensional (3D) imaging of the normal retina and optic nerve head were performed.
37                                       In the normal retina and optic nerve, immunocytochemical staini
38 f, are more crucial than others in effecting normal retina and pigment epithelium development.
39  enzyme (BACE1) is strongly expressed in the normal retina and that BACE1(-/-) mice develop pathologi
40 ed in innate immunity that is present in the normal retina and that is activated by optic nerve crush
41   Here, we determine which cell types in the normal retina and the optic nerve express OPA1.
42  serve as a marker for RGC quantification in normal retinas and for estimation of RGC loss in ocular
43 ility to modulate cell proliferation in both normal retinas and retinas with lesions.
44  overall pattern of immunoreactivity between normal retinas and retinas with severe loss of ganglion
45 tion at the tissue level is regulated in the normal retina, and how retinal diseases may affect oxyge
46 holesterol metabolism for maintenance of the normal retina, and suggest new targets for diseases affe
47 but the intrinsic survival mechanisms in the normal retina are poorly understood.
48 of the compensatory dilation observed in the normal retina, arterioles constrict in response to an ox
49         An additional Zone 4 was defined as "normal" retina, at least 500 mum from the edge of the GA
50  33D1(+) dendritic cells were present in the normal retina but were MHC class II(low/-).
51 e demonstrate that BBS2 retinopathy involves normal retina development followed by apoptotic death of
52 , it is imperative that we better understand normal retina development.
53 CS retinas were significantly larger than in normal retinas due to lower basal blood flow in the RCS
54 survival pathway in retinal neurons and that normal retina expresses a highly active basal insulin re
55 ed a custom retinal microarray to analyze 33 normal retinas from 19 donors, aged 29-90 years.
56                            We found that the normal retina has a baseline expression of the LPA recep
57 ogy, diabetic patients with angiographically normal retinas have been found to exhibit subtle defects
58                                           In normal retina, IMPG1 and IMPG2 occupy distinct IPM compa
59 egment optical coherence tomography showed a normal retina in all patients, but the subfoveal choroid
60                 Two types of transition from normal retina into intercalary membrane (ICM) were noted
61 ells, when retrospectively enriched from the normal retina, like their radial glial counterparts in t
62 scribed here that attempt to identify in the normal retina of goldfish neuronal progenitors intrinsic
63 I (+) dendriform cells could be found in the normal retinas of highly EAU-susceptible B10.RIII mice.
64 but revealed no evidence of retinal waves in normal retina or during regeneration.
65                                       Within normal retina, OX2R was not detected on myeloid-derived
66 ntly longer for OFF RGCs than for ON RGCs in normal retinas (P = 0.025).
67 ot statistically different from those in the normal retinas (P>0.05).
68                                           In normal retinas, reflectance spectra were similar along t
69  images of the retinas of mice (B6/SJLF2 for normal retina, rhodopsin-deficient Rho(-/-) for photorec
70 unohistochemistry and electron microscopy of normal retinas showed that Mueller cells, which synthesi
71 inoblastomas was more similar to that of the normal retina than that of retina-derived iPSCs, and we
72 confined to the apical retinal surface as in normal retinas, the planar organization of cone photorec
73 X binding and dynamic epigenetic profiles in normal retinas, the up-regulated cone-enriched genes do
74 e produced a rapid and prolonged decrease in normal retina TrkB.FL.
75                   Myeloid-derived cells from normal retina were programmed similar to TGF-beta-stimul
76            Expression profiles of mutant and normal retinas were compared by using canine retinal cus
77 l significance of Hmgb1 release, ischemic or normal retinas were treated with the neutralizing anti-H
78  to cone photoreceptor outer segments in the normal retina, whereas no Tgamma c immunoreactivity was
79 understanding of these signaling pathways in normal retina will provide a firm basis for targeting th
80          CD81 was found in all layers of the normal retina with a distinct absence of labeling in the
81 ave regions of structurally and functionally normal retina with definable transitions to severe lamin