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1 the intervention site (3 stent and 2 balloon injury sites).
2 is, approximately 100-300 mum away from the injury site.
3 ctive loss of the labile SCG10 distal to the injury site.
4 ruitment of endogenous c-kit(+) cells to the injury site.
5 covery by inhibiting axons from crossing the injury site.
6 rombus nor fibrin is generated at the vessel injury site.
7 to extracellular PDI binding at the vascular injury site.
8 howed cardiomyocyte overproliferation at the injury site.
9 or the selective loss of SCG10 distal to the injury site.
10 ardiomyocytes remained localized outside the injury site.
11 greater activity in muscles proximal to the injury site.
12 binding exposed membrane cholesterol at the injury site.
13 mulation of the two nerve branches above the injury site.
14 3 (HDAC3) in the innate immune cells at the injury site.
15 ng cardiomyocytes surrounding and within the injury site.
16 ic contusion site with a second, more distal injury site.
17 grade neuroprotective effect mediated at the injury site.
18 ir motility and direct themselves toward the injury site.
19 ssion of CNTF in cross-sections spanning the injury site.
20 ST collateral branches around and beyond the injury site.
21 ic axons and serotonergic axons spanning the injury site.
22 icantly increased T-cell infiltration at the injury site.
23 4.5mM minimized metabolic derangement at the injury site.
24 n-positive cells along the path and into the injury site.
25 processes were able to grow through a spinal injury site.
26 modeling of the cortical cytoskeleton at the injury site.
27 perfusion and maximize drug delivery at the injury site.
28 car and into the white matter rostral to the injury site.
29 t parenchymal injection, particularly at the injury site.
30 to lymph node CD4+CD25+ T cells draining the injury site.
31 nts dissected from the nerve proximal to the injury site.
32 the percentage area of staining (PAS) at the injury site.
33 frontal-parietal neocortex at or around the injury site.
34 he dendritic tree of motor neurons below the injury site.
35 ctures caused by persistent cartilage at the injury site.
36 Activated microglia persist around the injury site.
37 rout extensively in segments adjacent to the injury site.
38 the spinal cord lesion, often traversing the injury site.
39 pies, could improve cell survival around the injury site.
40 from motor tracts originating rostral to the injury site.
41 egree of preservation of white matter at the injury site.
42 ty of the cells to recruit host cells to the injury site.
43 by providing a permissive environment at the injury site.
44 al damage and limited axonal swelling at the injury site.
45 om abnormal neural activity initiated at the injury site.
46 lation of phagocytic microglial cells at the injury site.
47 cal recordings were made from central to the injury site.
48 a tactile allodynia in areas adjacent to the injury site.
49 odendroglia adjacent to and distant from the injury site.
50 d the survival of VH neurons adjacent to the injury site.
51 orsal column lesions, all fibers stop at the injury site.
52 tly investigating changes which occur at the injury site.
53 blood-brain barrier in areas adjacent to the injury site.
54 release of chemokines that diffuse from the injury site.
55 nt of tissue myofibroblasts to matrix in the injury site.
56 l of the neuropeptides were expressed at the injury site.
57 iber's terminal branches beneath the carious injury site.
58 the adventitia and neointima at the arterial injury site.
59 rticospinal axon growth at and distal to the injury site.
60 ng by preventing adventitial fibrosis at the injury site.
61 was found with increasing distance from the injury site.
62 inal cord perfusion and drug delivery at the injury site.
63 optimum tissue glucose concentration at the injury site.
64 the ringlike structure and then entered the injury site.
65 fically targeted to cells of interest at the injury site.
66 tivated to proliferate and accumulate at the injury site.
67 repair and establish connectivity across the injury site.
68 he surface of other platelets at the primary injury site.
69 ge with targeted process movement toward the injury site.
70 nsient local calcium wave originating at the injury site.
71 s and decreased induction of M2 genes at the injury site.
72 recruits Cxcr4-expressing leukocytes to the injury site.
73 e formation and osteoblast number within the injury site.
74 duces degeneration of neurites distal to the injury site.
75 lets adherent even a small distance from the injury site.
76 howed delayed invasion of macrophages to the injury site.
77 ced by a proliferative burst surrounding the injury site.
78 wth-inhibitory environment that forms at the injury site.
79 e localizing epicardial Fn1 synthesis to the injury site.
80 depletion of inflammatory macrophages at the injury site.
81 ceptor is induced in cardiomyocytes near the injury site.
82 ow defective trafficking of MG53 to membrane injury sites.
83 lity of growth-promoting biomolecules at CNS injury sites.
84 ion inhibitors (ARIs) that accumulate at CNS injury sites.
85 mboembolism without increasing bleeding from injury sites.
86 lls to injured tissue probably direct MSC to injury sites.
87 nsive cells (i.e. microglia) accumulating in injury sites.
88 module is the form specifically recruited to injury sites.
89 equire Schwann cells for their attraction to injury sites.
90 lls expressing Dcx migrating from SVZ to the injury sites.
91 uitin ligase that shows rapid recruitment to injury sites.
93 of 14C-label was mainly concentrated at the injury site (2.5 times greater) although uninjured brain
99 sibility that axonal STAT3, activated at the injury site, acts as a retrograde signaling transcriptio
100 ncrease in phosphorylated ERK1 at the spinal injury site after in vivo ChABC treatment, indicating th
102 ecomes localized to endocardial cells at the injury site, an area that is supplemented with raldh2-ex
103 nd found that macrophages recruited into the injury site and adult retinal ganglion cell (RGC) axons,
104 he sparing of 20% of the white matter at the injury site and complete recovery of detrusor-EUS coordi
105 spared ventral motor neurons adjacent to the injury site and distal to it, with other AMPA subunit mR
106 regulates multiple signaling cascades at the injury site and exerts protective effects on axotomized
107 e regenerating growth cones have crossed the injury site and have grown along distal Schwann cells ou
108 y in rats, and occur early in neurons in the injury site and hours to days later in oligodendroglia a
109 h wild type yet frequently fail to cross the injury site and instead stray along aberrant trajectorie
110 brainstem and propriospinal axons across the injury site and is followed by markedly improved urinary
111 such as tenascin are upregulated around the injury site and may be involved in inhibition of axon gr
112 nerating peripheral axons is to traverse the injury site and navigate toward their original trajector
113 patic injury, neutrophils also penetrate the injury site and perform the critical tasks of dismantlin
114 els of tyrosinated alpha-tubulin at the axon injury site and plays an important role in injury signal
115 elevation of podocyte [Ca(2)(+)]i around the injury site and promoted cell-to-cell propagating podocy
116 GF) is rapidly induced in MG residing at the injury site and that pro-HB-EGF ectodomain shedding is n
117 ds on regeneration of these axons through an injury site and the formation of functional synaptic con
118 tion, the accumulation of macrophages at the injury site and the increase in immunostaining of these
119 ding anterograde Mn transport at the primary injury site and the perilesional tissues secondarily ove
121 um wave only disrupted mitochondria near the injury site and was not altered by expression of the pro
122 nts' (TREEs) that trigger gene expression in injury sites and can be engineered to modulate the regen
123 llular matrix component commonly elevated at injury sites and detected immunochemically in activated
124 inC72-rich vesicles are rapidly recruited to injury sites and fuse with plasma membrane compartments
126 duces ectopic discharges originating at both injury sites and related dorsal root ganglia (DRG).
127 ic cytoskeleton reorganization occurs at the injury site, and microtubules have been implicated in th
128 with significantly less white matter at the injury site, and morphometric comparisons of injured Tg
129 xonal tracing of these fibers from the nerve injury site, and no evidence of sprouting into adjacent
130 m, depolymerization of microtubules near the injury site, and subsequent formation of local new micro
131 cles located both proximal and distal to the injury site ( approximately 30% decrease in fibre cross-
132 s from the myelin and the scar tissue at the injury site are considered major impediments to axon reg
133 al relay connections that bypass one or more injury sites are able to mediate spontaneous functional
134 ebral cortex, astroglial reaction begins and injury sites are infiltrated by activated mononuclear ph
136 microinjected TTX or vehicle (VEH) into the injury site at 15 min after a standardized contusive SCI
137 lood vessels increases within 11 mm from the injury site at 3 days post-injury and remains prominent
138 et interactions may be localized to vascular injury sites because integrins must be activated before
140 te infiltration and axonal growth within the injury site, but the mechanisms of these effects are not
141 Mac1-positive macrophages accumulated at the injury site by 4 days and immunostaining of these cells
143 iciently delivered to a cervical hemisection injury site by intrathecal delivery at the lumbar cord.
144 le that subdural intraspinal pressure at the injury site can be measured safely after traumatic spina
145 clear axonal regeneration beyond spinal cord injury sites can be achieved by combinatorial approaches
146 and, in turn, can promote debridement of the injury site, cell proliferation and angiogenesis, collag
147 emaphorin 3A messenger RNA expression within injury sites compared with saline-treated control animal
148 , the number of growing MTs increases at the injury site, concomitant with local downregulation of KL
149 dase (or saline solution) was infused to the injury site continuously for 2 wk and then motor behavio
151 repair, reducing neutrophil influx into the injury site, decreasing proinflammatory mediators, incre
152 nsient collapse of identity distant from the injury site, demonstrating the biological relevance of a
153 of injury, some of the damaged axons at the injury site developed spontaneous activity (up to 36% of
154 rating sympathetic fibers extending from the injury site -- did not change the density of sympathetic
158 JNK signaling promotes regrowth through the injury site, enabling regeneration of the axonal tract.
159 o-associated virus injection adjacent to the injury site enhances cell proliferation, alters astrocyt
160 at a local increase of Wnt activation at the injury site enhances reactionary dentine secretion.
163 t 3 days and most prominently, 1 mm from the injury site, followed by a significant reduction at 7 da
165 ccumulated in the adventitia surrounding the injury site from 2 hours to 3 days, followed by macropha
166 ) whether delivery of salmon fibrin into the injury site further enhances CST regeneration and motor
167 tissue and delivery of neurotrophin-3 at the injury site further increased spine density when combine
168 bris and altered extracellular matrix at the injury site, grow along the residual distal nerve sheath
170 rial passages and were transplanted into the injury site immediately after complete transection of th
172 through GFAP-positive tissue bridges at the injury site implicates GFAP-negative lesion areas as esp
173 pressure probe was placed subdurally at the injury site in 18 patients who had isolated severe traum
174 ther normal spinal cord of adult rats or the injury site in a dorsal column hemisection model of spin
175 tended distally into closer proximity to the injury site in AAV-L1-treated compared with control mice
176 trates that cardiomyocytes migrated into the injury site in control hearts but that migration was inh
177 ncement of 5-HT axon regeneration beyond the injury site in either Nogo/MAG/NgR1 triple mutants or Ng
178 ries and salmon fibrin was injected into the injury site in half the rats, yielding four groups (AAVs
180 mRNA expression was observed locally at the injury site in multiple forms of sciatic nerve injury, i
182 nal transport of this ion channel across the injury site in regenerated fibres, as well as decreased
185 se directed manner across great distances to injury sites in the CNS, where they might engage niches
186 ivated antigen-specific T-cells at traumatic injury sites, in addition to antigen-containing areas, c
188 Beginning with immediate changes at the injury site, including death of neural cells and release
189 -derived cells localize to areas outside the injury site, including intact spinal cord and brain.
192 at local adenosine generated by cells at the injury site is critical for protection from IRI through
194 egy that delivers cells and biologics to IVD injury site is needed to limit the progression of disc d
195 ther than diffusible factors released at the injury site is primarily involved in this enhancement.
196 hat the migration of cardiomyocytes into the injury site is regulated independently of proliferation,
198 , the number of axons that regrow beyond the injury site is substantially reduced, even when the tumo
200 with strategies to alter the terrain at the injury site itself suggests that there are important int
202 of Clostridium perfringens sialidase to the injury site markedly increased the number of spinal axon
204 hat the accumulation of neuropeptides at the injury site may play a role in the initiation or modulat
205 e appearance of matricryptic sites within an injury site may provide important new signals to regulat
206 propriate bioactive matrices relative to the injury site may stimulate the innate regenerative stem c
207 ion of Na+ channels in the membrane at nerve injury sites may contribute to the development of ectopi
208 Targeted inactivation of JNK1 at arterial injury sites may represent a potential therapeutic inter
212 ones that develop quickly at the peripheral injury site, move centrally by axon transport, and initi
213 stress and the inflammatory reaction at the injury site, neuronal and oligodendrocyte survival and a
215 In situ FN--FN made by tissue cells at the injury site--often contains an extra domain A (EDA) inse
216 he absence of axonal regeneration across the injury site, olfactory cell transplants led to improved
217 ral nerve that was grafted to span a chronic injury site or (2) a PNG that bridged a chronic contusio
220 ce to suggest that ectopic activity from the injury site plays a crucial role in the initiation of th
221 waves in the hemisphere contralateral to the injury site prompted us to examine whether corpus callos
224 myelin and Remak Schwann cells distal to the injury site reorganize and modify their properties to fo
225 ation, there is local loss of axons near the injury site, scar formation, a rapid impact on the cytos
226 meability and immune cell recruitment at the injury site, since both of these events have been linked
228 tion, and limiting vascular perfusion of the injury site, subsequently leading to incomplete function
230 concentration of radioactive lactate at the injury site suggests that the injured brain may use the
231 linC72 intensely labels the circumference of injury sites, supporting a key role for dysferlinExon40a
232 there is extension of glial membranes to the injury site (termed activation), and then axonal debris
233 scar tissue and inhibitory molecules at the injury site that block the regenerating axons, a lack of
234 cruitment of skeletal progenitor cells to an injury site, the differentiation of these cells into bon
235 at intensely labels exposed phospholipids of injury sites, then infiltrates and stabilizes the membra
236 of tyrosinated alpha-tubulin locally at the injury site to facilitate the retrograde transport of in
238 l cells following pONC, propagating from the injury site to the optic nerve head and finally the enti
239 s reveal a signaling mechanism from the axon injury site to the soma that controls neuronal growth co
240 promote adhesion of platelets to endothelial injury sites to assure wound healing, simultaneously dam
242 ools of the innate immune system employed at injury sites to protect the host from invading microbes
244 treatment with ChABC degraded CS-GAG at the injury site, upregulated a regeneration-associated prote
245 s of the kinetics of individual platelets at injury sites using intravital microscopy demonstrates th
246 modulation of the immune environment at the injury site via fractalkine delivery resulted in a drama
247 oration of anatomical connections across the injury site was associated with recovery of function wit
248 sprouting of reticulospinal axons above the injury site was demonstrated by anterograde tracing.
251 e yet Schwann cell-less scaffolds across the injury site was insufficient to direct regenerating grow
252 a 5-mm-long segment of cord centered at the injury site was spared, significantly more tissue was sp
253 y GFAP-negative meningeal fibroblasts at the injury site, we analyzed mice deficient in PlexinA3 and
254 phage and osteoclast distribution within the injury site were not compromised by the absence of B cel
256 expression, MG53 cannot translocate to acute injury sites, whereas rescue of NM-IIA expression in the
257 tic response and fewer micro-cavities at the injury site, which appear to create a more growth-permis
258 ed active synapses with graft neurons at the injury site with the signal propagating by graft axons t
259 ages showed specific accumulation around the injury site, with consistent expression during the study
260 ent significantly reduced tissue loss at the injury site, with greater effect on sparing of WM than g
261 nd found that cells integrated well into the injury site, with little migration away from the graft.
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