戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 surrounding the ischemic core, known as the 'glial scar'.
2 xons to penetrate the inhibitory spinal cord glial scar.
3 lycans participating in the formation of the glial scar.
4 itory signals associated with myelin and the glial scar.
5 to the inhibitors associated with myelin and glial scar.
6 CSPGs), the major class of inhibitors in the glial scar.
7 ycans, the major inhibitory molecules in the glial scar.
8 n the pia mater but not in astrocytes in the glial scar.
9 tes become reactive and in many cases form a glial scar.
10 cluding the formation and maintenance of the glial scar.
11 nd versican are not expressed in the chronic glial scar.
12 pregulated by the reactive astrocytes at the glial scar.
13  not be the main CSPG contributory factor in glial scar.
14 restricted to the reactive astrocytes at the glial scar.
15 ate in large numbers among astrocytes in the glial scar.
16 on diet, which reduced their presence in the glial scar.
17  disentangle the arrangement patterns of the glial scar.
18 al cord injury contributing new cells to the glial scar.
19 otentially related to the attenuation of the glial scar.
20 l lobe epilepsy hinges on the removal of the glial scar.
21 rograms and an inhibitory environment from a glial scar.
22 al changes resulting in the formation of the glial scar.
23 t dendrite and the formation of a persistent glial scar.
24 or how single astrocytes combine to form the glial scar.
25 c axons in the inhibitory environment of the glial scar.
26 tory proteins associated with myelin and the glial scar.
27 dystrophic axons in an in vitro model of the glial scar.
28 proteoglycans (CSPGs)-a primary component of glial scars.
29 avities, as well as the number of subretinal glial scars.
30 iated proteins and proteoglycans enriched in glial scars.
31 th, while its appearance on glia may promote glial scarring.
32 n of AQP4 expression or function might alter glial scarring.
33 ry injury processes as well as in diminished glial scarring.
34 d in chronic phase may be due to preexisting glial scarring.
35 lect continuous axons and may instead depict glial scarring.
36  with the NG2 CSPG, a major component of the glial scar, activates PKCzeta, and this activation is bo
37 ng pharmacological target for modulating the glial scar after brain ischemia and facilitating tissue
38 e mechanisms underlying the formation of the glial scar after injury are poorly understood.
39 cans (CSPGs), up-regulated in and around the glial scar after mammalian spinal cord injury, have been
40 y born oligodendrocytes incorporate into the glial scar after optic nerve injury.
41 vivo model of reactive gliosis: that is, the glial scar, after cortical injury.
42 the lesion core that are associated with the glial scar and a cilia-forming astrocyte subtype.
43 -6 could participate in the formation of the glial scar and confer anti-inflammatory properties.
44 s integral to the formation of an inhibitory glial scar and cytoskeleton-mediated astrocyte migration
45 mice expressing MMPs developed a more severe glial scar and enhanced expression of chondroitin sulfat
46 d near the injury site modify the inhibitory glial scar and facilitate axon regeneration past the sca
47 l contusion site with ChABC treatment of the glial scar and glial cell line-derived neurotrophic fact
48 droitin sulfate proteoglycans (CSPGs) at the glial scar and inhibits neuroregeneration.
49 sulted in sensory axon regeneration past the glial scar and into the white matter rostral to the inju
50 in sulphate proteoglycans (CSPGs) within the glial scar and perineuronal net creates a barrier to axo
51 sulfate proteoglycan (CSPG) component of the glial scar and promotes tissue recovery; however, its us
52 of the tumor with the presence of a residual glial scar and reactive changes, mainly presence of hemo
53 SC regeneration, limiting the formation of a glial scar and reducing cell death at the injured site.
54 scades that result in the development of the glial scar and the exclusion of meningeal fibroblasts fr
55 ation results in the formation of the neural/glial scar and the reconstitution of the glial limitans.
56 fter injury by regulating the formation of a glial scar and white matter sparing and/or axonal plasti
57 he peak of acute disease (day 14), prevented glial scarring and ameliorated the disease severity.
58      We also conclude that in the absence of glial scarring and irreversible neuronal injury, in vivo
59                                              Glial scarring and outer limiting membrane integrity, fe
60 2-mediated reprogramming of NG2 glia reduces glial scarring and promotes functional recovery after SC
61 ng and axonal plasticity, the formation of a glial scar, and locomotor recovery after spinal cord inj
62 egeneration, attenuates the formation of the glial scar, and significantly enhances functional recove
63      More than half of the astrocytes in the glial scar are generated by ependymal cells, the neural
64 sic neuronal programs and the formation of a glial scar are the main obstacles.
65 e signals that initiate the formation of the glial scar are unknown.
66 ured area, and astrocytes migrate, forming a glial scar around macrophages.
67 red spinal cord with the formation of a huge glial scar around the macrophages.
68 lized fibrotic scar surrounded by a reactive glial scar at the lesion site.
69 droitin sulfate proteoglycans (CSPG), in the glial scar at the lesion; and (2) the diminished growth
70  physical or molecular barriers presented by glial scarring at the lesion site, it has been suggested
71  NT-3 can achieve axonal bridging beyond the glial scar, but growth for longer distances is not susta
72 levated, indicating that modification of the glial scar by ChABC promotes long-lasting signaling chan
73 egeneration of adult axons in the absence of glial scarring, by using a microtransplantation techniqu
74 lt myelinated white matter tracts beyond the glial scar can be highly permissive for regeneration.
75 osphacan protein levels are decreased in the glial scar compared with the uninjured brain.
76                                The resulting glial scar consists of an irregular array of astrocyte p
77                    At sites of CNS injury, a glial scar develops, containing extracellular matrix mol
78 , and enzymatically modulated the inhibitory glial scar distal to the graft.
79 ctive, we discuss the divergent roles of the glial scar during CNS regeneration and explore the possi
80  be a promising therapeutic target to reduce glial scarring during wound healing after spinal cord in
81 s in the sequence of events that can lead to glial scarring, edema, seizure and neuronal death.
82 as well as the inhibitory environment of the glial scar established around the lesion site.
83 esive interactions between astrocytes at the glial scar, even though reactive gliosis and scar format
84 s a key role in astrogliosis associated with glial scar formation after brain injury.
85 s in cellular responses resulted in abnormal glial scar formation after injury, and significantly inc
86 n deleterious effects of BMPR1b signaling on glial scar formation after SCI.
87  is necessary for neuroprotection and normal glial scar formation after SCI.
88 ith neuronal and oligodendroglial apoptosis, glial scar formation and microglial activation.
89  the nuclear pore complex (NPC) required for glial scar formation and reduced gamma oscillations in m
90           Although astrocytes participate in glial scar formation and tissue repair, dysregulation of
91 s demonstrate that it is possible to inhibit glial scar formation and to facilitate regeneration afte
92                                              Glial scar formation around implanted silicon neural pro
93 nd tissue is suspected to be a key driver of glial scar formation around neural implants.
94                          This contributes to glial scar formation at the lesion border and gliosis in
95 te mainly into glial cells and contribute to glial scar formation at the site of injury.
96 bility of soft hydrogel coatings to modulate glial scar formation by reducing local strain.
97                    The mechanisms underlying glial scar formation have been extensively studied, yet
98 egulation may enable targeted suppression of glial scar formation in diverse neurological disorders.
99 and neuronal cellularity, as well as reduced glial scar formation in response to treatment with EFF-n
100  abolishes the fibrinogen-induced effects on glial scar formation in vivo and in vitro.
101 ation and cell death in the lesion core, and glial scar formation orchestrated by multiple cell types
102                                              Glial scar formation represents a fundamental response t
103 ary and secondary axotomy, inflammation, and glial scar formation that have devastating effects on ne
104 rves as an early signal for the induction of glial scar formation via the TGF-beta/Smad signaling pat
105 coupling while reactive astrocyte markers or glial scar formation was absent.
106 cytokines leads to dramatic inflammation and glial scar formation, affecting brain tissue's ability t
107 ating lesion causes upregulation of gliosis, glial scar formation, and heightened expression of CSPGs
108 ive suppressor of Muller cell proliferation, glial scar formation, and photoreceptor cell death in a
109 ions in the CNS, including the initiation of glial scar formation, angiogenesis, and maintenance of t
110 ding to cell death, axonal degeneration, and glial scar formation, exacerbating the already hostile e
111 ntly, Gsx1 reduces reactive astrogliosis and glial scar formation, promotes serotonin (5-HT) neuronal
112 In brain, AQP4 facilitates water balance and glial scar formation, which are important determinants o
113            Spinal cord injury is followed by glial scar formation, which has positive and negative ef
114 SCI) leads to irreversible neuronal loss and glial scar formation, which ultimately result in persist
115 ferent from focal lesions that would trigger glial scar formation.
116  the response of astrocytes to injury and in glial scar formation.
117  for astrocyte hyperplasia, hypertrophy, and glial scar formation.
118  thus may serve as a novel target to control glial scar formation.
119 the initial molecular mediator that triggers glial scar formation.
120           This cell culture assay mimics the glial scar formed after CNS injury.
121 erotonin-immunoreactive fibers traversed the glial scars formed at both cord-graft interfaces.
122         However, the mechanism through which glial scar-forming astrocytes migrate to the injury site
123                In the injured spinal cord, a glial scar forms and becomes a major obstacle to axonal
124 surprising inability to regenerate even in a glial scar-free environment.
125 nd that degenerating white matter beyond the glial scar has a far greater intrinsic ability to suppor
126 on regeneration, beneficial functions of the glial scar have also been recently identified.
127 n lesions after ablation formed a persistent glial scar in 5 (31.3%) patients.
128 le reducing the inhibitory properties of the glial scar in axon regeneration.
129     We have successfully removed an existing glial scar in chronically contused rat spinal cord using
130 his level may facilitate manipulation of the glial scar in inflammatory disorders of the human CNS.
131 so, BMPR1b knock-out mice have an attenuated glial scar in the chronic stages following injury, sugge
132 y tissue damage, progressive cavitation, and glial scarring in the CNS.
133 l detachment, Muller cells formed subretinal glial scars in the wt mice.
134 lfate proteoglycans (CSPGs) found within the glial scar inhibit axon regeneration but the intracellul
135                                          The glial scar inhibits axonal regeneration, resulting in si
136                             Formation of the glial scar involves migration of astrocytes toward the l
137 he subacute and chronic phases of injury the glial scar is a physical and biochemical barrier to axon
138                                              Glial scar is a significant barrier to neural implant fu
139 nt in astrocyte migration and formation of a glial scar is unknown.
140 migratory potential and ability to penetrate glial scars is higher.
141                       One such response, the glial scar, is a structural formation of reactive glia a
142     Interestingly, astrogliosis demonstrated glial scar-like characteristics at two years post-stroke
143 ory molecules associated with myelin and the glial scar limit axon regeneration in the adult central
144 mical constraints imposed by the periinfarct glial scar may contribute to the limited clinical improv
145 sequences of cranial implants, which include glial scarring, meningeal lymphangiogenesis, and increas
146 r chondroitinase ABC (chABC), tested here in glial scar models, and ability of cervically-patterned s
147 pletion of adult OPCs, inhibition within the glial scar, or damage to the axons that prevents myelina
148 hrough white matter tracts, gray matter, and glial scars, overcoming the inhibitory nature of the CNS
149  and the TSG-6 protein is present within the glial scar, potentially coordinating and stabilizing the
150                                      Whereas glial scarring presents a roadblock for mammalian spinal
151 -21 in regulating astrocytic hypertrophy and glial scar progression after SCI, and suggest miR-21 as
152 ry, suggesting that it has a greater role in glial scar progression.
153                                              Glial scar reformation was effectively prevented after a
154 omoting a permissive microenvironment in the glial scar region.
155  late in chronic phase (day 78), significant glial scarring remained and the clinical severity did no
156 glia largely segregate into the fibrotic and glial scars, respectively; therefore, we used a thymidin
157 an expression increases significantly in the glial scar resulting from cortical injury, including the
158 tional heterogeneity within the cells of the glial scar-specifically, astrocytes, NG2 glia and microg
159                                    Mammalian glial scars supposedly form a chemical and mechanical ba
160 glycans (CSPGs) are a major component of the glial scar that contributes to the limited regeneration
161 hey migrate, undergo hypertrophy, and form a glial scar that inhibits axon regeneration.
162         We now have an in vitro model of the glial scar that may serve as a potent tool for developin
163 have developed a novel in vitro model of the glial scar that mimics the gradient of proteoglycan foun
164                                  It is these glial scars that are associated with epilepsy originatin
165                                              Glial scars that form at CNS injury sites block axon reg
166        Levels of NG2 increase rapidly in the glial scars that form at sites of CNS injury, suggesting
167         While traditionally referred to as a glial scar, the spinal injury scar in fact comprises mul
168        Strikingly, after crossing the distal glial scar, these fibers elongated in white and periaque
169 ajor axon growth inhibitory component of the glial scar tissue that blocks successful regeneration.
170 ognizes tenascin-C, one of the components of glial scar tissue, and an integrin activator.
171 atly enlarged secondary injury surrounded by glial scar tissue, is a poorly understood complication o
172  of CSPGs are highly upregulated by reactive glial scar tissues after injuries and form a strong barr
173 ganglion neurons in an in vitro model of the glial scar to examine macrophage-axon interactions and o
174 m cells were also more efficient in reducing glial scar volume and expression of chondroitin sulfates
175                                          The glial scar was also altered in the absence of acutely di
176 acrophages were widely scattered, and a huge glial scar was formed around the macrophages as in wild-
177                                          The glial scar was identified as a zone with intense cell-ce
178                      Also, demyelination and glial scarring were significantly decreased in MMPI-trea
179 endrocyte lineage cells incorporate into the glial scar, where they are susceptible to the demyelinat
180 sult in the formation of a proteoglycan-rich glial scar, which acts as a barrier to axonal regrowth a
181 ar composition of neural tissue and leads to glial scarring, which inhibits the regrowth of damaged a
182 ns are the principal inhibitory component of glial scars, which form after damage to the adult centra
183 creased CSPG deposition and development of a glial scar, while also increasing axon growth after spin
184       We also hypothesized that treating the glial scar with chondroitinase ABC (ChABC), which digest
185 rimary contributors to the growth-inhibitory glial scar, yet they are also neuroprotective and can fo

 
Page Top