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1 xposing these mutants and normal siblings to cuprizone.
2 could be carefully controlled using a toxin, cuprizone.
3  and IGF-1 tg mice 3 weeks after exposure to cuprizone.
4 formation of blue complex between copper and cuprizone.
5 mice experiencing chronic demyelination from cuprizone.
6 onse to demyelinating agents in both chronic cuprizone and acute lysolecithin rodent animal models.
7 IP-1alpha knockout mice (MIP-1alpha(-/-)) to cuprizone and comparing pathology to wild-type mice.
8 ain during cuprizone toxicity, mice were fed cuprizone and evaluated at 3-, 4-, and 6-week cuprizone
9  Increased CD38 expression is present in the cuprizone and experimental autoimmune encephalomyelitis
10 We used a novel MS mouse model that combines cuprizone and experimental autoimmune encephalomyelitis
11                   We further determined that cuprizone and inhibition of mTOR cooperatively compromis
12 ouse models of demyelination (treatment with cuprizone and injections of lysolecithin).
13 tration and withdrawal of the combination of cuprizone and rapamycin (Cup/Rap) in C57BL/6J male mice
14 Then, we administered demyelination-inducing cuprizone and stimulated axon regeneration by Pten knock
15 croscopic studies performed in mice fed with cuprizone and treated with anacardic acid showed lower g
16 demyelination by feeding the copper chelator cuprizone, and correlated our results with detailed hist
17 phodiesterase-EGFP(+) mice were treated with cuprizone, and OPCs were sorted from the corpus callosum
18  chronically demyelinated lesions induced by cuprizone appears to be the result of oligodendrocyte de
19 proinflammatory cytokines, lysolecithin, and cuprizone) are associated with strongly impaired mitocho
20 ction of BDNF on OLG lineage cells following cuprizone, BDNF(+/-) mice were evaluated.
21                                           In cuprizone-challenged mice, substantial numbers of NPCs m
22           C57BL/6J mice were maintained on a cuprizone-containing or control diet and sacrificed at s
23                        It was found that the cuprizone content in chow could varied significantly bet
24                 C57BL/6 mice were given 0.2% cuprizone (CPZ) for 2 to 6 weeks while controls ate the
25                                              Cuprizone (CPZ) is a neurotoxic agent acting as a copper
26                                    Using the cuprizone (CPZ) model of demyelination and mice of eithe
27                            Following chronic cuprizone (CPZ)-induced demyelination (male and female m
28 n-mediated, nonautoimmune MS animal model of cuprizone (Cup) intoxication.
29  in a non-T-cell model of demyelination, the cuprizone (cupr) model in C57BL/6 mice.
30 erosis and CNS injury.SIGNIFICANCE STATEMENT Cuprizone (CZ) is a copper chelator that induces demyeli
31                                              Cuprizone (CZ), a copper chelator, is widely used to stu
32 to overcome the metabolic dysfunction in the cuprizone-demyelinated adult brain.SIGNIFICANCE STATEMEN
33 to selectively kill SVZ-derived eNPCs in the cuprizone demyelination model, we observed migration of
34 ntify myelin loss in brain tissues using the cuprizone demyelination model.
35 as Ind-Cl increased remyelination within the cuprizone diet-induced demyelinating model.
36 ental autoimmune encephalomyelitis (EAE) and cuprizone diet-induced demyelination.
37 erosis and in two experimental mouse models, cuprizone diet-related demyelination and experimental au
38  cells undergo apoptosis if mice remain on a cuprizone diet.
39     It is important to control the amount of cuprizone dosed in animals to be consistent as different
40                                    Following cuprizone-elicited demyelination in mice, astrocytes con
41                              Hindbrains from cuprizone-exposed mice showed reduced Abcd1, Cat, and Pe
42 es, but also oligodendrocytes, in short-term cuprizone-exposed mice.
43 nd peroxisomal thiolase immunostaining after cuprizone exposure was increased by 4-PBA.
44 ament heavy chain immunoreactivity caused by cuprizone exposure.
45 ated following demyelination in the brain of cuprizone-fed mice and spinal cord lesions of mice injec
46                                              Cuprizone-fed mice had reduced [(18)F]7a brain uptake, r
47                                           In cuprizone-fed mice, IL-17 was produced by CNS CD3(+) T c
48 nd Th17 CD4(+) T cells infiltrate the CNS of cuprizone-fed mice, with infiltration of Th17 cells bein
49 neration and loss compared to non-irradiated cuprizone-fed mice.
50             For mice of susceptible strains, cuprizone feeding results in oligodendrocyte cell loss a
51 d with that in wild-type mice in response to cuprizone feeding, demonstrating the essential role of I
52 lly demyelinated lesion of mice treated with cuprizone for 12 weeks, mature oligodendrocyte regenerat
53 cuprizone for 27 days and mice that were fed cuprizone for 25 days, followed by normal diet for 2 day
54 brains from control mice, mice that were fed cuprizone for 27 days and mice that were fed cuprizone f
55 dant in the brains of mice that had consumed cuprizone for 27 days, and the numbers of O4-positive ce
56                 Female C57BL/6 mice were fed cuprizone for 3 weeks, followed by a period of 2 weeks o
57 ollowing exposure to the demyelinating agent cuprizone, however, GALC +/- animals had significantly r
58 plied to the quantification of low levels of cuprizone in chow formulations.
59 thod was developed for the quantification of cuprizone in cuprizone pre-clinical formulations.
60 nificant challenge for the quantification of cuprizone in the mixture.
61 ecific chelators (bathocuproine disulfonate, cuprizone) induced nondesensitizing NMDAR currents even
62                    In adult mice with toxin (cuprizone)-induced demyelination, oral GlcNAc prevents n
63 ntiation in fibronectin aggregate containing cuprizone-induced demyelinated lesions in male mice.
64 linated axons and oligodendrocyte numbers in cuprizone-induced demyelinated lesions.
65 , as well as a mouse model that incorporates cuprizone-induced demyelination along with CNS delivery
66           First, we fate mapped SVZ-eNPCs in cuprizone-induced demyelination and found that SVZ endog
67 hat Tmem106b-/- mice are more susceptible to cuprizone-induced demyelination and have a reduced capac
68 trated that n-3 PUFA supplementation reduced cuprizone-induced demyelination and improved motor and c
69 ed glial chimeras was greatly accentuated by cuprizone-induced demyelination and its associated mobil
70  the Nlrp3 gene was increased >100-fold in a cuprizone-induced demyelination and neuroinflammation mo
71 erived microglia exhibit dynamic response to cuprizone-induced demyelination and species-specific tra
72 eceptor (CXCR2) were relatively resistant to cuprizone-induced demyelination and that circulating CXC
73     When we ablated SVZ-derived eNPCs during cuprizone-induced demyelination in female mice, the anim
74                                              Cuprizone-induced demyelination in mice is a frequently
75                      These data suggest that cuprizone-induced demyelination is useful for modeling c
76  channels in GFAP-positive astrocytes during cuprizone-induced demyelination leads to a significant r
77 ly study its effects on remyelination in the cuprizone-induced demyelination model and in experimenta
78 ms during myelination and remyelination in a cuprizone-induced demyelination model.
79                                              Cuprizone-induced demyelination remains incompletely cha
80              Remarkably, ponesimod prevented cuprizone-induced demyelination selectively in the cingu
81 the present study, we used a murine model of cuprizone-induced demyelination to broaden the applicati
82 l delay, myelination at the onset and during cuprizone-induced demyelination was unaffected in male N
83 to control mice in the corpus callosum after cuprizone-induced demyelination, followed by chronic red
84 ans with multiple sclerosis and of mice with cuprizone-induced demyelination, in ex vivo models of de
85                          We show that during cuprizone-induced demyelination, in vivo CXCR7 antagonis
86             During early remyelination after cuprizone-induced demyelination, mice lacking mTOR in ad
87    Our findings support a two-hit process of cuprizone-induced demyelination, supporting the idea tha
88 yelin repair as well as motor recovery after cuprizone-induced demyelination.
89 he corpus callosi (CCs) of mice subjected to cuprizone-induced demyelination.
90 xamined the importance of IL-17 signaling in cuprizone-induced demyelination.
91 of CNS resident cells in the pathogenesis of cuprizone-induced demyelination.
92  of IL-17-induced Act1-mediated signaling in cuprizone-induced demyelination.
93 us callosum of mice infused with BMP4 during cuprizone-induced demyelination.
94 XCR2-positive neutrophils were important for cuprizone-induced demyelination.
95 s accelerated in lysophosphatidylcholine- or cuprizone-induced demyelination.
96 tion followed by longitudinal studies in the cuprizone-induced demyelination/remyelination mouse mode
97 tive demyelinating MS lesions, as well as in cuprizone-induced lesions, and that this phosphorylation
98                              Evidence from a cuprizone-induced model of demyelination, in vitro and i
99 l and clozapine, also significantly improved cuprizone-induced motor impairment.
100                                              Cuprizone-induced neurobehavioral deficits were improved
101 he histological level, siponimod ameliorated cuprizone-induced oligodendrocyte degeneration, demyelin
102  SOCS3-deficient mice were protected against cuprizone-induced oligodendrocyte loss relative to wild-
103               Siponimod also ameliorated the cuprizone-induced pathologies in Rag1-deficient mice, de
104 ations test revealed that ponesimod reversed cuprizone-induced working memory deficits.
105 he molecular and cellular mechanism by which cuprizone induces demyelination remains unclear.
106                                              Cuprizone inhibits mitochondrial function and induces de
107 mulated axon regeneration and that localized cuprizone injection promoted axon regeneration.
108 l compared to non-transplanted, X-irradiated cuprizone-intoxicated mice.
109 the brain to 40 Gy of X-irradiation prior to cuprizone intoxication and this resulted in a significan
110 lammatory protein-1alpha (MIP-1alpha) during cuprizone intoxication, a model where demyelination of t
111 ouse white matter following subdemyelinating cuprizone intoxication, as well as normal-appearing whit
112                    We demonstrate that after cuprizone intoxication, CCR2-dependent infiltration of m
113 However, upon induction of demyelination via cuprizone intoxication, neuroantigen-specific CD8+ T cel
114 hat continuously express IGF-1 (IGF-1 tg) to cuprizone intoxication.
115 ligodendrocytes, might be interrupted during cuprizone intoxication.
116 ental autoimmune encephalomyelitis (EAE) and cuprizone intoxication.
117                 Demyelination on exposure to cuprizone is accompanied by predictable microglial activ
118                                              Cuprizone is an amide compound that has been wildly used
119                                              Cuprizone is usually administrated as a minor component
120 s efficient remyelination of the brain after cuprizone-mediated demyelination but has no effect on re
121  remyelination and functional recovery after cuprizone-mediated demyelination in mice.
122  (male and female), human cell cultures, and cuprizone-mediated demyelination mice (female) were exam
123 ment of an innovative animal model combining cuprizone-mediated demyelination with transfer of myelin
124 ntravital imaging, single-cell ablation, and cuprizone-mediated demyelination, in both female and mal
125 n injury and repair, that is lysolecithin or cuprizone-mediated demyelination, showed that PAR1 knock
126 q) gene expression, and in vivo using murine cuprizone-mediated demyelination.
127 okines, among them Cxcl10, Ccl2, and Ccl3 in cuprizone-mediated oligodendrocyte apoptosis.
128 ocyte death and remyelination failure in the cuprizone model (male mice).
129               ERbeta-ligand treatment in the cuprizone model further increased cholesterol synthesis
130  lesion to a chronic state, we have used the cuprizone model of chronic demyelination.
131  by ponesimod increases remyelination in the cuprizone model of demyelination and significantly incre
132                   In this study, we used the cuprizone model of demyelination in mice to investigate
133                   The neurotoxicant-induced, cuprizone model of demyelination is ideally suited for t
134                                    Using the cuprizone model of demyelination, a noninflammatory mode
135                   In this study, we used the cuprizone model of demyelination, characterized by oligo
136 tors ex vivo and faster remyelination in the cuprizone model of demyelination/remyelination.
137 ental allergic encephalitis (EAE) and in the cuprizone model of demyelination/remyelination.
138 tic Cav1.2 knock-out mouse was tested in the cuprizone model of myelin injury and repair which causes
139 t OPCs to remyelinate the adult brain in the cuprizone model of myelin injury and repair.
140 (-/-) and Nlrp3(-/-) mice are studied in the cuprizone model of neuroinflammation and demyelination.
141                                       In the cuprizone model of oligodendrocyte degeneration and demy
142                   In this study, we used the cuprizone model to investigate the temporal and causal r
143 in the repair of a demyelinating lesion, the cuprizone model was used and the corpus callosum was exa
144  during the remyelination phase of a chronic cuprizone model with axonal damage.
145                                       In the cuprizone model, acute disease reduces serum cholesterol
146                            In EAE and in the cuprizone model, areas of myelin loss, which are likely
147       When guanabenz was administered in the cuprizone model, in which demyelination is less dependen
148 bition promotes in vivo remyelination in the cuprizone model, which is accompanied by improved spatia
149 ration across the remyelination phase of the cuprizone model.
150                                 With EAE and cuprizone models combined, we uncovered that TNFR2 does
151                    In this study, we use the cuprizone mouse model of demyelination to investigate lo
152                                       In the cuprizone mouse model of demyelination, we found ponesim
153  of neuroinflammatory lesions in vivo in the cuprizone mouse model of MS.
154 lin pathology in primary cultures and in the cuprizone mouse model of multiple sclerosis (MS), a deva
155                                    Using the cuprizone mouse model, we combined electrophysiological
156  in experimental autoimmune encephalitis and cuprizone MS mouse models without affecting basal neurot
157                                          The cuprizone neurotoxicant model causes extensive corpus ca
158 loped for the quantification of cuprizone in cuprizone pre-clinical formulations.
159 ing a chow placebo with various amounts of a cuprizone reference standard to achieve target concentra
160 ormal diet following 12 weeks of exposure to cuprizone, remyelination and oligodendrocyte regeneratio
161 vels in unchallenged animals, treatment with cuprizone revealed that Tmem106b-/- mice are more suscep
162 ns specifically in a pathway dysregulated by cuprizone to promote remyelination efficiency.
163 icient mice, resulting in an amelioration of cuprizone toxicity at later time points.
164       To evaluate Axl's role in brain during cuprizone toxicity, mice were fed cuprizone and evaluate
165 in prolonged axonal damage and recovery from cuprizone toxicity.
166 ion were performed on the corpus callosum of cuprizone treated mice.
167 n vivo on an 11.7T animal MRI scanner from 7 cuprizone-treated and 7 control capital ES, Cyrillic57BL
168      Significant (p < 0.05) demyelination in cuprizone-treated animals was found according to both LF
169 ong-term locomotor performance of previously cuprizone-treated animals was monitored using the motor
170 old nanocrystals improved motor functions of cuprizone-treated mice in both open field and kinematic
171                   Moreover, we found that in cuprizone-treated mice the detrimental actions of IFN-ga
172  chemokine transcripts in both untreated and cuprizone-treated MIP-1alpha(-/-) mice.
173 e found that OPC-targeted Notch1 ablation in cuprizone-treated Plp-creER Notch1(lox/lox) transgenic m
174 ovel data revealing that mTOR inhibition and cuprizone treatment additively affect the metabolic prof
175 uprizone and evaluated at 3-, 4-, and 6-week cuprizone treatment and 3- and 5-week post-cuprizone wit
176 on of pharmacological HDAC inhibitors during cuprizone treatment and is consistent with in vitro resu
177 reased as a function of dose and duration of cuprizone treatment and it was detectable prior to obser
178 dipine during the demyelination stage of the cuprizone treatment displayed a reduced number of reacti
179 numerous chemokines were up-regulated during cuprizone treatment in wild-type, C57BL/6 mice.
180                        Consistent with this, cuprizone treatment initiated a caspase-3-dependent form
181 s, and motor recovery after the cessation of cuprizone treatment were compromised.
182                       Following cessation of cuprizone treatment, animals showed an initial recovery
183       BDNF protein levels were reduced after cuprizone treatment, suggesting that the demyelinating l
184                                    At 4-week cuprizone treatment, the corpora callosa of wildtype (WT
185                                    At 6-week cuprizone treatment, there was significantly more Oil Re
186 d that Sfmbt2 family miRNAs decreased during cuprizone treatment.
187 and persistent demyelination after prolonged cuprizone treatment.
188 ls, suggesting a source of IL-17 in CNS upon cuprizone treatment.
189 ease in the NG2 response at 4 and 5 weeks of cuprizone treatment.
190         Bis-cyclohexanone oxalyldihydrazone (cuprizone) was administered to young adult mice in order
191 emyelination mediated by the copper chelator cuprizone, we evaluated the expression of CXCL12 and its
192 on microscopy determined that at 3-week post-cuprizone withdrawal the number of dystrophic axons and
193 nificantly more SMI-32+ axons at 3-week post-cuprizone withdrawal, indicative of axonal damage in the
194       In Axl-/- corpora callosa, 5-week post-cuprizone withdrawal, the number of mature oligodendrocy
195 lial activation and astrogliosis, and, after cuprizone withdrawal, this activation reproducibly dimin
196 k cuprizone treatment and 3- and 5-week post-cuprizone withdrawal.

 
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