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1 the intervention site (3 stent and 2 balloon injury sites).
2 duces degeneration of neurites distal to the injury site.
3 lets adherent even a small distance from the injury site.
4 howed delayed invasion of macrophages to the injury site.
5 ced by a proliferative burst surrounding the injury site.
6 wth-inhibitory environment that forms at the injury site.
7 e localizing epicardial Fn1 synthesis to the injury site.
8 depletion of inflammatory macrophages at the injury site.
9 ceptor is induced in cardiomyocytes near the injury site.
10 ctive loss of the labile SCG10 distal to the injury site.
11 ruitment of endogenous c-kit(+) cells to the injury site.
12 covery by inhibiting axons from crossing the injury site.
13 rombus nor fibrin is generated at the vessel injury site.
14 to extracellular PDI binding at the vascular injury site.
15 or the selective loss of SCG10 distal to the injury site.
16 ey signalling protein SLC6/SNF-12 toward the injury site.
17 ardiomyocytes remained localized outside the injury site.
18 binding exposed membrane cholesterol at the injury site.
19 mulation of the two nerve branches above the injury site.
20 ng cardiomyocytes surrounding and within the injury site.
21 ic contusion site with a second, more distal injury site.
22 grade neuroprotective effect mediated at the injury site.
23 ir motility and direct themselves toward the injury site.
24 e first innate immune cells to arrive at the injury site.
25 ssion of CNTF in cross-sections spanning the injury site.
26 ST collateral branches around and beyond the injury site.
27 ic axons and serotonergic axons spanning the injury site.
28 icantly increased T-cell infiltration at the injury site.
29 ropelling axon growth well beyond the spinal injury site.
30 n-positive cells along the path and into the injury site.
31 processes were able to grow through a spinal injury site.
32 modeling of the cortical cytoskeleton at the injury site.
33 car and into the white matter rostral to the injury site.
34 t parenchymal injection, particularly at the injury site.
35 to lymph node CD4+CD25+ T cells draining the injury site.
36 nts dissected from the nerve proximal to the injury site.
37 the percentage area of staining (PAS) at the injury site.
38 frontal-parietal neocortex at or around the injury site.
39 tion promotes colon cancer metastasis at the injury site.
40 he dendritic tree of motor neurons below the injury site.
41 ctures caused by persistent cartilage at the injury site.
42 or recruitment of innate immune cells at the injury site.
43 Activated microglia persist around the injury site.
44 rout extensively in segments adjacent to the injury site.
45 the spinal cord lesion, often traversing the injury site.
46 from motor tracts originating rostral to the injury site.
47 egree of preservation of white matter at the injury site.
48 by providing a permissive environment at the injury site.
49 al damage and limited axonal swelling at the injury site.
50 om abnormal neural activity initiated at the injury site.
51 lation of phagocytic microglial cells at the injury site.
52 ophages and microglia to the traumatic brain injury site.
53 cal recordings were made from central to the injury site.
54 a tactile allodynia in areas adjacent to the injury site.
55 odendroglia adjacent to and distant from the injury site.
56 d the survival of VH neurons adjacent to the injury site.
57 orsal column lesions, all fibers stop at the injury site.
58 tly investigating changes which occur at the injury site.
59 blood-brain barrier in areas adjacent to the injury site.
60 release of chemokines that diffuse from the injury site.
61 nt of tissue myofibroblasts to matrix in the injury site.
62 l of the neuropeptides were expressed at the injury site.
63 the adventitia and neointima at the arterial injury site.
64 rticospinal axon growth at and distal to the injury site.
65 ng by preventing adventitial fibrosis at the injury site.
66 nfiltration of myeloid cells at the vascular injury site.
67 o localize pro-regenerative signaling at the injury site.
68 ith a reduction of intracellular Ca2+ at the injury site.
69 otaxis (DeltacheY) did not accumulate at the injury site.
70 is, approximately 100-300 mum away from the injury site.
71 he surface of other platelets at the primary injury site.
72 howed cardiomyocyte overproliferation at the injury site.
73 greater activity in muscles proximal to the injury site.
74 3 (HDAC3) in the innate immune cells at the injury site.
75 orimotor cortex dysfunction above the spinal injury site.
76 4.5mM minimized metabolic derangement at the injury site.
77 perfusion and maximize drug delivery at the injury site.
78 pies, could improve cell survival around the injury site.
79 ty of the cells to recruit host cells to the injury site.
80 iber's terminal branches beneath the carious injury site.
81 inal cord perfusion and drug delivery at the injury site.
82 optimum tissue glucose concentration at the injury site.
83 the ringlike structure and then entered the injury site.
84 fically targeted to cells of interest at the injury site.
85 tivated to proliferate and accumulate at the injury site.
86 repair and establish connectivity across the injury site.
87 ge with targeted process movement toward the injury site.
88 cally relevant dose of growth factors at the injury site.
89 nsient local calcium wave originating at the injury site.
90 s and decreased induction of M2 genes at the injury site.
91 recruits Cxcr4-expressing leukocytes to the injury site.
92 e formation and osteoblast number within the injury site.
93 module is the form specifically recruited to injury sites.
94 ges and the removal of cellular corpses from injury sites.
95 equire Schwann cells for their attraction to injury sites.
96 lls expressing Dcx migrating from SVZ to the injury sites.
97 uitin ligase that shows rapid recruitment to injury sites.
98 ow defective trafficking of MG53 to membrane injury sites.
99 ion inhibitors (ARIs) that accumulate at CNS injury sites.
100 lls to injured tissue probably direct MSC to injury sites.
101 nsive cells (i.e. microglia) accumulating in injury sites.
102 by guiding growing neuronal processes across injury sites.
103 lity of growth-promoting biomolecules at CNS injury sites.
104 mboembolism without increasing bleeding from injury sites.
106 of 14C-label was mainly concentrated at the injury site (2.5 times greater) although uninjured brain
112 sibility that axonal STAT3, activated at the injury site, acts as a retrograde signaling transcriptio
113 ncrease in phosphorylated ERK1 at the spinal injury site after in vivo ChABC treatment, indicating th
114 the times to first clot at a saphenous vein injury site after the infusions of the FIX agents are si
116 ecomes localized to endocardial cells at the injury site, an area that is supplemented with raldh2-ex
117 nd found that macrophages recruited into the injury site and adult retinal ganglion cell (RGC) axons,
118 he sparing of 20% of the white matter at the injury site and complete recovery of detrusor-EUS coordi
119 absorbable dressings that can be left in the injury site and degrade to reduce the duration of interv
120 spared ventral motor neurons adjacent to the injury site and distal to it, with other AMPA subunit mR
121 regulates multiple signaling cascades at the injury site and exerts protective effects on axotomized
122 e regenerating growth cones have crossed the injury site and have grown along distal Schwann cells ou
123 y in rats, and occur early in neurons in the injury site and hours to days later in oligodendroglia a
124 h wild type yet frequently fail to cross the injury site and instead stray along aberrant trajectorie
125 brainstem and propriospinal axons across the injury site and is followed by markedly improved urinary
127 such as tenascin are upregulated around the injury site and may be involved in inhibition of axon gr
128 nerating peripheral axons is to traverse the injury site and navigate toward their original trajector
129 patic injury, neutrophils also penetrate the injury site and perform the critical tasks of dismantlin
130 els of tyrosinated alpha-tubulin at the axon injury site and plays an important role in injury signal
132 elevation of podocyte [Ca(2)(+)]i around the injury site and promoted cell-to-cell propagating podocy
134 GF) is rapidly induced in MG residing at the injury site and that pro-HB-EGF ectodomain shedding is n
135 ds on regeneration of these axons through an injury site and the formation of functional synaptic con
136 ding anterograde Mn transport at the primary injury site and the perilesional tissues secondarily ove
138 um wave only disrupted mitochondria near the injury site and was not altered by expression of the pro
139 nts' (TREEs) that trigger gene expression in injury sites and can be engineered to modulate the regen
140 llular matrix component commonly elevated at injury sites and detected immunochemically in activated
141 inC72-rich vesicles are rapidly recruited to injury sites and fuse with plasma membrane compartments
143 telets roll along exposed collagen at vessel injury sites and respond with filipodia protrusion, shap
144 twork plasticity in CNS regions removed from injury sites and that might prevent full recovery of fun
145 ic cytoskeleton reorganization occurs at the injury site, and microtubules have been implicated in th
146 with significantly less white matter at the injury site, and morphometric comparisons of injured Tg
147 xonal tracing of these fibers from the nerve injury site, and no evidence of sprouting into adjacent
148 m, depolymerization of microtubules near the injury site, and subsequent formation of local new micro
149 cles located both proximal and distal to the injury site ( approximately 30% decrease in fibre cross-
150 s from the myelin and the scar tissue at the injury site are considered major impediments to axon reg
151 al relay connections that bypass one or more injury sites are able to mediate spontaneous functional
153 microinjected TTX or vehicle (VEH) into the injury site at 15 min after a standardized contusive SCI
154 lood vessels increases within 11 mm from the injury site at 3 days post-injury and remains prominent
155 et interactions may be localized to vascular injury sites because integrins must be activated before
157 processes taking place not just at the focal injury site but also rostral and caudal to the spinal in
158 te infiltration and axonal growth within the injury site, but the mechanisms of these effects are not
160 iciently delivered to a cervical hemisection injury site by intrathecal delivery at the lumbar cord.
161 le that subdural intraspinal pressure at the injury site can be measured safely after traumatic spina
162 clear axonal regeneration beyond spinal cord injury sites can be achieved by combinatorial approaches
163 and, in turn, can promote debridement of the injury site, cell proliferation and angiogenesis, collag
164 emaphorin 3A messenger RNA expression within injury sites compared with saline-treated control animal
165 , the number of growing MTs increases at the injury site, concomitant with local downregulation of KL
166 cell sequencing, we found that the wild-type injury site consists of Runx1-positive endocardial cells
167 dase (or saline solution) was infused to the injury site continuously for 2 wk and then motor behavio
170 repair, reducing neutrophil influx into the injury site, decreasing proinflammatory mediators, incre
171 nsient collapse of identity distant from the injury site, demonstrating the biological relevance of a
172 of injury, some of the damaged axons at the injury site developed spontaneous activity (up to 36% of
173 rating sympathetic fibers extending from the injury site -- did not change the density of sympathetic
176 how Runx1 is specifically upregulated at the injury site during zebrafish heart regeneration, and tha
178 JNK signaling promotes regrowth through the injury site, enabling regeneration of the axonal tract.
179 o-associated virus injection adjacent to the injury site enhances cell proliferation, alters astrocyt
180 at a local increase of Wnt activation at the injury site enhances reactionary dentine secretion.
182 y in vitro including co-encapsulation of the injury site extracellular matrix modifier chondroitinase
184 t 3 days and most prominently, 1 mm from the injury site, followed by a significant reduction at 7 da
186 ccumulated in the adventitia surrounding the injury site from 2 hours to 3 days, followed by macropha
187 ) whether delivery of salmon fibrin into the injury site further enhances CST regeneration and motor
188 tissue and delivery of neurotrophin-3 at the injury site further increased spine density when combine
189 bris and altered extracellular matrix at the injury site, grow along the residual distal nerve sheath
192 rial passages and were transplanted into the injury site immediately after complete transection of th
194 through GFAP-positive tissue bridges at the injury site implicates GFAP-negative lesion areas as esp
195 pressure probe was placed subdurally at the injury site in 18 patients who had isolated severe traum
196 ther normal spinal cord of adult rats or the injury site in a dorsal column hemisection model of spin
197 tended distally into closer proximity to the injury site in AAV-L1-treated compared with control mice
198 trates that cardiomyocytes migrated into the injury site in control hearts but that migration was inh
199 ncement of 5-HT axon regeneration beyond the injury site in either Nogo/MAG/NgR1 triple mutants or Ng
200 elerated egress of neutrophils from the tail injury site in fish, whereas neutrophil-specific deletio
201 ries and salmon fibrin was injected into the injury site in half the rats, yielding four groups (AAVs
203 mRNA expression was observed locally at the injury site in multiple forms of sciatic nerve injury, i
205 nal transport of this ion channel across the injury site in regenerated fibres, as well as decreased
208 se directed manner across great distances to injury sites in the CNS, where they might engage niches
210 ivated antigen-specific T-cells at traumatic injury sites, in addition to antigen-containing areas, c
212 Beginning with immediate changes at the injury site, including death of neural cells and release
213 -derived cells localize to areas outside the injury site, including intact spinal cord and brain.
218 at local adenosine generated by cells at the injury site is critical for protection from IRI through
220 egy that delivers cells and biologics to IVD injury site is needed to limit the progression of disc d
221 ther than diffusible factors released at the injury site is primarily involved in this enhancement.
222 hat the migration of cardiomyocytes into the injury site is regulated independently of proliferation,
224 , the number of axons that regrow beyond the injury site is substantially reduced, even when the tumo
226 with strategies to alter the terrain at the injury site itself suggests that there are important int
228 of Clostridium perfringens sialidase to the injury site markedly increased the number of spinal axon
230 hat the accumulation of neuropeptides at the injury site may play a role in the initiation or modulat
231 e appearance of matricryptic sites within an injury site may provide important new signals to regulat
232 propriate bioactive matrices relative to the injury site may stimulate the innate regenerative stem c
233 Targeted inactivation of JNK1 at arterial injury sites may represent a potential therapeutic inter
236 ones that develop quickly at the peripheral injury site, move centrally by axon transport, and initi
237 stress and the inflammatory reaction at the injury site, neuronal and oligodendrocyte survival and a
239 M2 macrophages and CD133+ stem cells in the injury sites of peritoneal surface at day 5 post-operati
240 In situ FN--FN made by tissue cells at the injury site--often contains an extra domain A (EDA) inse
241 he absence of axonal regeneration across the injury site, olfactory cell transplants led to improved
242 ral nerve that was grafted to span a chronic injury site or (2) a PNG that bridged a chronic contusio
245 ce to suggest that ectopic activity from the injury site plays a crucial role in the initiation of th
247 waves in the hemisphere contralateral to the injury site prompted us to examine whether corpus callos
250 cate that RN-NSCs grafted into a spinal cord injury site relay supraspinal control of serotonergic re
251 myelin and Remak Schwann cells distal to the injury site reorganize and modify their properties to fo
252 qualitatively demonstrate graft survival and injury site retention using a rat C4 hemi-contusion mode
253 jury, single-cell (sc) RNA sequencing of the injury site reveals an early increase in MPC genes assoc
254 ation, there is local loss of axons near the injury site, scar formation, a rapid impact on the cytos
255 meability and immune cell recruitment at the injury site, since both of these events have been linked
257 tion, and limiting vascular perfusion of the injury site, subsequently leading to incomplete function
259 ees of spinal cord pathology remote from the injury site, suggesting the involvement of similar secon
260 concentration of radioactive lactate at the injury site suggests that the injured brain may use the
262 linC72 intensely labels the circumference of injury sites, supporting a key role for dysferlinExon40a
264 there is extension of glial membranes to the injury site (termed activation), and then axonal debris
265 scar tissue and inhibitory molecules at the injury site that block the regenerating axons, a lack of
266 cruitment of skeletal progenitor cells to an injury site, the differentiation of these cells into bon
267 at intensely labels exposed phospholipids of injury sites, then infiltrates and stabilizes the membra
268 of tyrosinated alpha-tubulin locally at the injury site to facilitate the retrograde transport of in
270 sis catheter were placed intradurally at the injury site to monitor intraspinal pressure (ISP), spina
271 l cells following pONC, propagating from the injury site to the optic nerve head and finally the enti
272 s reveal a signaling mechanism from the axon injury site to the soma that controls neuronal growth co
273 promote adhesion of platelets to endothelial injury sites to assure wound healing, simultaneously dam
275 ools of the innate immune system employed at injury sites to protect the host from invading microbes
276 DRG macrophages, but not those at the nerve injury site, to both the initiation and maintenance of t
277 occurred at the NMJ, distant from the nerve injury site, to support functional recovery at the muscl
279 treatment with ChABC degraded CS-GAG at the injury site, upregulated a regeneration-associated prote
280 s of the kinetics of individual platelets at injury sites using intravital microscopy demonstrates th
281 w that entraining endogenous stem cells into injury sites using the combined effect of AMD3100 and lo
282 modulation of the immune environment at the injury site via fractalkine delivery resulted in a drama
283 oration of anatomical connections across the injury site was associated with recovery of function wit
284 sprouting of reticulospinal axons above the injury site was demonstrated by anterograde tracing.
287 e yet Schwann cell-less scaffolds across the injury site was insufficient to direct regenerating grow
288 a 5-mm-long segment of cord centered at the injury site was spared, significantly more tissue was sp
289 y GFAP-negative meningeal fibroblasts at the injury site, we analyzed mice deficient in PlexinA3 and
290 phage and osteoclast distribution within the injury site were not compromised by the absence of B cel
292 expression, MG53 cannot translocate to acute injury sites, whereas rescue of NM-IIA expression in the
293 tic response and fewer micro-cavities at the injury site, which appear to create a more growth-permis
294 ion of a neuroinhibitory microenvironment at injury sites, which includes neuroinflammatory signaling
295 ed active synapses with graft neurons at the injury site with the signal propagating by graft axons t
296 ages showed specific accumulation around the injury site, with consistent expression during the study
297 ent significantly reduced tissue loss at the injury site, with greater effect on sparing of WM than g
298 nd found that cells integrated well into the injury site, with little migration away from the graft.
299 tinct monocyte/macrophage populations at the injury site, with their dynamic changes over time elucid