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1 is specifically induced in these cells after retinal damage.
2  part, plays a causative role in KCl-induced retinal damage.
3  to a significant attenuation of KCl-induced retinal damage.
4 ptors is implicated as a causative factor to retinal damage.
5  used to treat ophthalmic infections without retinal damage.
6 n activator (uPA)] in excitotoxicity-induced retinal damage.
7 -antiplasmin, failed to attenuate KA-induced retinal damage.
8 l-glutamate have been implicated in ischemic retinal damage.
9 diffuse to the posterior segment, triggering retinal damage.
10 offer protection against excitotoxin-induced retinal damage.
11 ived neurotrophic factor (BDNF) reduces this retinal damage.
12  the material in vitreous and variable local retinal damage.
13  in parallel with the increasing severity of retinal damage.
14 stantial, and there was little other obvious retinal damage.
15 ing, and CCR1 expression was correlated with retinal damage.
16 ve any long-term safety benefit from reduced retinal damage.
17  refinement, angiogenesis, and recovery from retinal damage.
18  its protective effect against light-induced retinal damage.
19 ression were dynamically regulated following retinal damage.
20 d genes were dynamically regulated following retinal damage.
21 st common and may be due to neurotoxicity or retinal damage.
22 evealed prominent choroiditis with extensive retinal damage.
23 ion of proliferating MGPCs in the absence of retinal damage.
24 nts were inaccurate in the presence of outer retinal damage.
25  damage or by CNTF or FGF2 in the absence of retinal damage.
26 s been reported to play an important role in retinal damage.
27 equired to prevent the voriconazole-mediated retinal damage.
28 ociated with Muller glia and MGPCs following retinal damage.
29 -consuming, and carry risks of infection and retinal damage.
30 uller glia to reenter the cell cycle without retinal damage.
31 predictor for stereopsis in populations with retinal damage.
32 trols, as well as to identify early signs of retinal damage.
33 ts and by histopathologic evidence of severe retinal damage.
34 um that was mainly responsible for secondary retinal damage.
35 1 predispose mice to age- and light-mediated retinal damage.
36 in increased susceptibility to light-induced retinal damage.
37 se to intrinsic signals remain despite inner retinal damage.
38 nd exacerbated visual function defects after retinal damage.
39 dies against retinal antigens and results in retinal damage.
40 eared to vary with the severity of the laser retinal damage.
41 an important factor in toxoplasmosis-induced retinal damage.
42 eurogenic potential capable of responding to retinal damage.
43 n of photoreceptors or ouabain-induced inner retinal damage.
44  defense mechanism against pressure-mediated retinal damage.
45 betic macular edema without visible signs of retinal damage.
46 therapeutic approach to dyslipidemia-induced retinal damage.
47 issue and was protective from photooxidative retinal damage.
48 filtration, therefore contributing to reduce retinal damage.
49 se provides early evidence of stress-related retinal damage.
50 gy examination was also performed to confirm retinal damage.
51 mice display increased retinal apoptosis and retinal damage.
52 own to block diabetes- and endotoxin-induced retinal damage.
53 response and those that result in extraneous retinal damage.
54 tine, factors besides SAG1 are important for retinal damage.
55 important cortical reorganizations following retinal damages.
56 eutralizing antibody significantly decreased retinal damage after IR, whereas treatment of retinas or
57 s provide evidence that Hmgb1 contributes to retinal damage after IR.
58 even at relatively low intensities, leads to retinal damage and blindness in wild-type animals.
59 y has been suggested to cause ON-independent retinal damage and contribute to changes particularly in
60                     Oxidative stress induces retinal damage and contributes to vision loss in progres
61 dence that Muller glia can proliferate after retinal damage and generate new rods; however, the evide
62 te the mechanism by which alkali burns cause retinal damage and may have importance in designing ther
63           OCT provides objective measures of retinal damage and may offer clues toward understanding
64 g of pathogenic T cells or for effecting the retinal damage and photoreceptor loss typical of EAU.
65 insulin-deficient diabetes, or light-induced retinal damage and protects ganglion cells from apoptosi
66 retinal progenitors that migrate to areas of retinal damage and regenerate lost neurons.
67 n either RGCs or retinal glia would increase retinal damage and RGC death in a mouse model of glaucom
68 istology and ERG analysis revealed increased retinal damage and significant loss of retinal function.
69 l studies, acute blue light exposure induces retinal damage and the use of blue-blocking IOLs lessens
70 ents and prescribing physicians to potential retinal damage and uses readily available OCT measuremen
71 cotherapies may well be able to mitigate the retinal damage and vision loss associated with geographi
72 ogression and limit or eliminate irreparable retinal damage and vision loss associated with progressi
73 serum RBP4 levels could be a risk factor for retinal damage and vision loss in nondiabetic as well as
74 on of subclinical multiple sclerosis-related retinal damage and visual dysfunction.
75 ation prevented diabetes-induced increase in retinal damage, and increases in VEGF and ICAM-1.
76 he effects of metipranolol, known to prevent retinal damage, and of other antiglaucoma drugs were det
77 nal damage, but the mechanisms that underlie retinal damage are not clearly understood.
78 the mechanisms that lead to ischemia-induced retinal damage are poorly understood.
79 xicity"), the downstream events that lead to retinal damage are poorly understood.
80 ll-deficient mice developed profound RPE and retinal damage at doses that caused minimal effects in w
81 y, which includes conditions associated with retinal damage attributable to blockage of its blood sup
82 can be specified to avoid not only the inner retinal damage, but also permanent disorganization and s
83  has been proposed to play a pivotal role in retinal damage, but the mechanisms that underlie retinal
84                        He may have permanent retinal damage, but this is still unclear because the op
85                     Dark-rearing potentiated retinal damage by light.
86 BDNF) rescues photoreceptors from collateral retinal damage caused by photodynamic therapy (PDT).
87 ty of cone arrestin to prevent light-induced retinal damage caused by prolonged activation of the pho
88 ence that AA MS patients exhibit accelerated retinal damage compared to CA MS patients.
89 limit also predicts whether individuals with retinal damage due to macular degeneration will have ste
90 d Arr-1 evolution in animals at high risk of retinal damage due to periodic bright-light exposure of
91  caspase-independent apoptosis contribute to retinal damage during murine cytomegalovirus (MCMV) reti
92  atypical p38 activity (Tab1(KI)) to explore retinal damage during OIR.
93 sion strikingly increased with the extent of retinal damage, especially at the photoreceptors, in con
94 s a protective role by preventing additional retinal damage from accumulation of cellular debris.
95 cient diet rats exhibited protection against retinal damage from either intermittent or hyperthermic
96 tamate have been suggested to play a role in retinal damage in a number of blinding diseases such as
97 tive in preventing or reducing light-induced retinal damage in all transgenic rats.
98 on of plasminogen activators might attenuate retinal damage in blinding retinal diseases in which hyp
99 a can serve as a source of new neurons after retinal damage in both fish and birds.
100 hondria initiate the subsequent irreversible retinal damage in experimental uveitis.
101                     There was no evidence of retinal damage in eyes treated with insulin and FGF2.
102           These changes seem consistent with retinal damage in human glaucoma (focal field defects),
103 eneration in fish but is not expressed after retinal damage in mice.
104                 Although glutamate can cause retinal damage in part by hyperstimulating its receptors
105 l Intelligence (AI) algorithms for detecting retinal damage in patients undergoing (hydroxy-)chloroqu
106                                              Retinal damage in teleosts, unlike mammals, induces robu
107 topathologic findings emphasize the risk for retinal damage in these highly myopic eyes, indicating t
108                                Light-induced retinal damage in transgenic rats depends on the time of
109 tion factor Ascl1 is upregulated in MG after retinal damage in zebrafish and is necessary for regener
110                                    Following retinal damage, in which MGPCs are known to form, mTor s
111  retina which may contribute to ameliorating retinal damage induced by HFD.
112 retinal glial cells contribute critically to retinal damage induced by RD and provide a new avenue fo
113                            In the absence of retinal damage, insulin, IGF1 and FGF2 induced pS6 in Mu
114 tis (EAU), recent work has demonstrated that retinal damage involves oxidative stress early in uveiti
115        The time course of light-induced T17M retinal damage is biphasic, with an initial decline in r
116                     Visual field loss due to retinal damage is considered irreversible, and methods a
117           The experiments confirmed that the retinal damage is not mediated by direct effect of the a
118 precisely how inefficient autophagy promotes retinal damage is unclear.
119       In conclusion, we propose that central retinal damage leads to enhanced peripheral vision by se
120 ensity (20 000 lux for 30 min) light-induced retinal damage (LIRD) as compared with WT, indicating im
121 ansient amplification of Wnt signaling after retinal damage may unlock the latent regenerative capaci
122                                    Following retinal damage, microglia undergo morphological changes,
123                                              Retinal damage models suggested that rod cell death indu
124 LB(gld) mice, correlating with the increased retinal damage observed in BALB(gld) mice.
125                                              Retinal damage occurred as a direct result of total aver
126 d in Muller glia in response to NMDA-induced retinal damage or by CNTF or FGF2 in the absence of reti
127                            No differences in retinal damage or parasite growth were observed, indicat
128 ession levels of Pax2 are increased by acute retinal damage or treatment with growth factors.
129          OCT and OCT-A showed no evidence of retinal damage, or vascular or microvascular events.
130                                    To assess retinal damage, outer nuclear layer (ONL) thickness was
131 jection-induced retinal detachment can cause retinal damage, particularly when SR vector bleb include
132 stly, inhibiting CCR1 reduced photic-induced retinal damage, photoreceptor cell apoptosis, and retina
133 m permissible exposure safety limit produces retinal damage preceded by a transient reduction in the
134 infiltration in the inner retina, leading to retinal damage primarily localized to the ganglion cells
135 of the retina showed no evidence of residual retinal damage resulting from the colchicine injections
136  improvement and avoid potentially permanent retinal damage, retina specialists should be familiar wi
137 nflammatory protein production, leukostasis, retinal damage, signs of anterior uveitis, and uncouplin
138 retinal pigment epithelium (RPE) may lead to retinal damage similar to that associated with the early
139  After either kainate- or colchicine-induced retinal damage, some of the newly generated cells expres
140     Although high levels of glutamate induce retinal damage, subtoxic levels of glutamate directly st
141                                  Much of the retinal damage that characterizes the disease results fr
142 rovides an alternative rod-dominant model of retinal damage that shares a surprising number of featur
143                            This mechanism of retinal damage through neuroglia remodeling may be clini
144            Further, the relationship of this retinal damage to a primary astrocytopathy in NMOSD is u
145               In the postnatal retina, acute retinal damage transiently induces transitin expression
146 significant contribution to inflammation and retinal damage triggered by IR.
147 g potential therapeutic approaches to reduce retinal damages upon DR progression.
148 expressing mononuclear cells contributing to retinal damage via recruitment of CD4(+) T cells.
149                                              Retinal damage was also observed but only from postnatal
150                                              Retinal damage was assessed by immunolocalization studie
151                                              Retinal damage was assessed by measuring outer nuclear l
152                                              Retinal damage was assessed in quail fed a carotenoid-de
153                                The degree of retinal damage was assessed morphologically by measuring
154 ere measured to assess retinal function, and retinal damage was evaluated by light microscopy.
155              In this study, the potential of retinal damage was investigated by using radiant exposur
156 rix metalloproteinase (MMP)-9 in KCl-induced retinal damage was investigated.
157 x metalloproteinases in excitotoxin-mediated retinal damage was investigated.
158                                  Progressive retinal damage was quantified by direct counting of rod
159      No clinically apparent warning of outer retinal damage was seen in the SD-OCT images of long-ter
160                                     However, retinal damage was still evident at 6 months after supra
161 g required for regeneration after widespread retinal damage were not required for RGC regeneration.
162 he inflamed retina, CD4(+) T cells can cause retinal damage when they are not properly regulated.
163  that IL-8 is upregulated upon laser-induced retinal damage, which recapitulates enhanced vasculariza
164 ances in OCT have enabled early detection of retinal damage, with studies suggesting that thinning of
165                 This demonstrates that inner retinal damage, without extensive photoreceptor damage,
166                              Following acute retinal damage, zebrafish possess the ability to regener
167                  The decreasing width of the retinal damage zone suggests that photoreceptors migrati

 
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