ライフサイエンスコーパス: lesion site

1 han nonclassical monocytes to migrate to the lesion site.

2 reflected by altered glycosylation at the MS lesion site.

3 a 60% to 70% loss of signal intensity at the lesion site.

4 ributes to MN axonal regeneration across the lesion site.

5 tiple biological pathways within the chronic lesion site.

6 n E2 are elevated in the chronic spinal cord lesion site.

7 and anti-inflammatory metabolites within the lesion site.

8 es both ipsilateral and contralateral to the lesion site.

9 needle deployment to the targeted cancerous lesion site.

10 ction of CRC and adenoma did not differ with lesion site.

11 activation of the myelination program at the lesion site.

12 partial integration with host tissues in the lesion site.

13 esulted in increased axon density within the lesion site.

14 croglia/macrophages and a larger scar at the lesion site.

15 neurons are generated in the vicinity of the lesion site.

16 s slowed polymerase activity at and near the lesion site.

17 a predegenerated PNG (termed I-PNG) into the lesion site.

18 tly to an abasic site than to a hypoxanthine lesion site.

19 mNSCs rapidly migrated (100 mum/day) to the lesion site.

20 post-injury, NRP/GRP were delivered into the lesion site.

21 to PCNA in the replication fork stalled at a lesion site.

22 l regeneration into and beyond a midcervical lesion site.

23 spinal cord and corticospinal axons into the lesion site.

24 ctural features of the DNA duplex around the lesion site.

25 ent of the glial scar established around the lesion site.

26 ol zeta with Pol32 in Pol delta stalled at a lesion site.

27 or the base pairs in the 5' direction to the lesion site.

28 ers and ascending sensory fibers through the lesion site.

29 omotes long-lasting signaling changes at the lesion site.

30 ncorporation, upstream and downstream to the lesion site.

31 atson-Crick base pair alignments outside the lesion site.

32 Cs and in SCs within the nerve distal to the lesion site.

33 inserted into the lateral spinal cord at the lesion site.

34 different NER proteins are assembled at the lesion site.

35 armful mediators diffusing from the original lesion site.

36 maged matrix, which is not restricted to the lesion site.

37 although changes in other measures varied by lesion site.

38 B. burgdorferi to anatomic sites beyond the lesion site.

39 s and for the process of Pol exchange at the lesion site.

40 thout the intervention of scar tissue at the lesion site.

41 and one-base deletions were detected at the lesion site.

42 to more specific localization of NPs at the lesion site.

43 to be a stalled transcription complex at the lesion site.

44 digits within dorsal rootlets bordering the lesion site.

45 ry rapid activation of STAT3 in axons at the lesion site.

46 pinal tract axons also did not grow into the lesion site.

47 ized, which leads to a strand opening at the lesion site.

48 of SCI showed greater NP localization at the lesion site.

49 nal for recruitment of repair enzymes to the lesion site.

50 f the retrograde tracer Fluoro-Gold into the lesion site.

51 astrocyte processes into the margins of the lesion site.

52 ch diminishes with progression away from the lesion site.

53 ministered nanoparticles specifically at the lesion site.

54 ow post-SCI within which NPs localize at the lesion site.

55 ay impair erectile function depending on the lesion site.

56 r surrounded by a reactive glial scar at the lesion site.

57 GG-NER via its interaction with DDB2 at the lesion site.

58 reduction in macrophage accumulation at the lesion site.

59 by newly formed endothelial cells within the lesion site.

60 proliferation of hemocytes which invade the lesion site.

61 nically not related to the symptomatic acute lesion site.

62 as the molecular mechanism of bypass at the lesion site.

63 ased the intensity of reflected light at the lesion sites.

64 on occurs after the nuclease is recruited to lesion sites.

65 substantial frequencies of mutations at the lesion sites.

66 neovascular AMD exhibited NLRP3 staining at lesion sites.

67 potential of (89)Zr-panitumumab at different lesion sites.

68 cues to direct axonal regrowth across nerve lesion sites.

69 that are up-regulated specifically at neural lesion sites.

70 ts to elicit axonal bridging into and beyond lesion sites.

71 inas of adult vldlr(-/-) mice, especially at lesion sites.

72 , yet are not capable of locating the dental lesion sites.

73 or prolonged time periods within spinal cord lesion sites.

74 CI) promotes axon growth into but not beyond lesion sites.

75 he molecule required for T cell migration to lesion sites.

76 ruitment of these cells at neuroinflammatory lesion sites.

77 spectral information required to reveal the lesion sites.

78 ic and DNA repair recognition factors at DNA lesion sites.

79 such as monoubiquitylation of histone H2A at lesion sites.

80 Calcium was uniformly distributed among 48 lesion sites (14%), 43 proximal references (13%), and 42

81 6%) opposite M(1)dG or -1 frameshifts at the lesion site (31%).

82 c spinal tissue implanted immediately at the lesion site, a 10-day delivery of rolipram results in co

83 At the lesion site, a progression in plaque area (8.9+/-25.7%)

84 The phosphodiester backbone twists at the lesion site, accounting for the unusual phosphorus chemi

85 nal projection within and beyond spinal cord lesion sites, achieving a major unmet goal of SCI resear

86 the unmodified bases, including the G at the lesion site, adopt anti glycosidic torsion angles and fo

87 onal cerebral blood volume (rCBV) around the lesion site after 6 h, together with a reduction in the

88 t enhances the recruitment of XPC to the DNA lesion site after irradiation.

89 either the dNaM or d5SICS nucleotides at the lesion site after processing via the base excision repai

90 re, microglia/macrophages accumulated in the lesion site after SCI and expressed the proinflammatory

91 Meningeal cells migrate into the lesion site after undergoing an epithelial-mesenchymal t

92 At the lesion site, alpha-OH-PdG rotates to a syn conformation,

93 al cells (MSCs) or fibroblasts 1 mm from the lesion site also rapidly dispersed into the lesion cavit

94 h Watson-Crick base pairing is intact at the lesion site and (2) the base-displaced intercalation mot

95 cellular fibroblast bridge in a spinal cord lesion site and after a growth factor stimulus at the le

96 ntitative measurements were performed at the lesion site and at the proximal and distal references.

97 vity of inflammatory effector T cells at the lesion site and by an effect in lymphoid tissues that le

98 ively propagates resolution processes at the lesion site and improves neurological outcome.

99 After sacrifice, histological analysis of lesion site and lumbosacral spinal cord regions was perf

100 e function of circuitry in the region of the lesion site and of ascending pathways originating near t

101 l clusters form sequentially adjacent to the lesion site and oxidation spreads between mitochondria.

102 ota incorporates the nucleotide opposite the lesion site and Polkappa carries out the subsequent exte

103 ota incorporates the nucleotide opposite the lesion site and Polkappa performs the extension reaction

104 cultures, the P12 axons failed to cross the lesion site and project to the contralateral P6 IC lobe.

105 cular complexity that are exacerbated at the lesion site and provide structural evidence for the bila

106 ponse occurs both distal and proximal to the lesion site and that the rapid transcriptional activatio

107 helical twist and base pair stacking at the lesion site and the 5'-neighbor dC.dG base pair.

108 ons by reducing subsequent thrombosis at the lesion site and, at least with lipid lowering, by improv

109 LCs occur both at preinvasive lesion sites and elsewhere in the bronchial epithelium o

110 the recruitment of DNA repair factors to the lesion sites and the deposition of histone marks as part

111 n the recruitment of microglial cells at the lesioned site and (b) in the proliferation of neural pro

112 gion, inhibition of protein synthesis at the lesion site, and exposure to ABC chondroitinase.

113 ess to the replication ensemble stalled at a lesion site, and Rad6-Rad18-dependent protein ubiquitina

114 echanisms: local cortical dysfunction at the lesion site, and remote cortical dysfunction due to disr

115 t-off-NT-3 virus was injected rostral to the lesion site, and the intrinsic growth capacity of sensor

116 fect and duration of retention of NPs at the lesion site, and the time window post-SCI within which N

117 s activates calpain, vesicle accumulation at lesion sites, and membrane fusion proteins; Ca(2+) influ

118 raphics, laboratory values, medical history, lesion sites, and previous treatments.

119 apacity to identify and stabilize at the DNA lesion sites, and this function is facilitated in the ge

120 In calcium-containing SVGs, lesion site arc and length of calcium measured 151+/-107

121 Base-pair steps adjacent to the lesion site are overwound.

122 and oligodendrocyte progenitor cells within lesion sites are exposed to secreted products derived fr

123 mmediate, irreversible loss of tissue at the lesion site, as well as a secondary expansion of tissue

124 of lesions; disappearance of amastigotes in lesion sites, as determined by histopathological analysi

125 mild semantic deficits was distinct from the lesion site associated with regularization errors.

126 nor axon regeneration around the optic nerve lesion site at both 8 and 14 days.

127 expression patterns in midcervical contusion lesion sites between 1 and 90 d postinjury of athymic nu

128 Typical herpes lesion site biopsy (TLSB) and cervical biopsy specimens

129 acoronary abciximab delivered to the infarct lesion site but not by manual aspiration thrombectomy.

130 in stimulating axonal growth into or around lesion sites but rarely beyond them.

131 tantly, this dysbiosis is not limited to the lesion site, but is transmissible to normal skin distant

132 Corticospinal axons extend within the lesion site, but not caudal to it, after dorsal hemisect

133 naling is lost in reactive astrocytes at the lesion site, but persists in mild to moderately reactive

134 g from the nucleotides inserted opposite the lesion site by another DNA polymerase.

135 ely unaffected, although repopulation of the lesion site by astrocytes was delayed significantly.

136 although the repopulation of the optic nerve lesion site by astrocytes was significantly delayed upon

137 y attributable to successful crossing of the lesion site by regenerating fibers.

138 incorporation of nucleotides opposite these lesion sites by Poldelta.

139 e, we show that the stalling of PolB1 at the lesion site can be relieved by Dpo4.

140 f this E3 ligase complex directly at the DNA lesion site, causing the assembly of the UV-DDB-CUL4A E3

141 uclear cells [PMNs]) accumulation in culprit lesion site (CLS) thrombus is a predictor of cardiovascu

142 imb corresponding to the sensorimotor stroke lesion site compared with spontaneous recovery and contr

143 icosities increase in density rostral to the lesion site compared with unlesioned controls and are re

144 axons in the connective tissue matrix at the lesion site, confirming previous studies that used prota

145 Smaller tissue bridges at the lesion site correlated with lower ratios of tNAA/mI (R(2

146 clerosis do not include the optic nerve as a lesion site despite frequent involvement.

147 sis showed that NRP/GRP survived, filled the lesion site, differentiated into neurons and glia, and m

148 ulation to enable drug release to a targeted lesion site effectively, maintain coating integrity duri

149 or axons to actively navigate the non-neural lesion site environment.

150 cells, located only at the epicenter of the lesion site, expressed CD200L.

151 icospinal axon regeneration into subcortical lesion sites expressing BDNF.

152 in signaling controls the composition of the lesion site extracellular matrix and we identify Collage

153 tracardiac catheter positioning and ablation lesion sites facilitate increasingly complex catheter ab

154 te and after a growth factor stimulus at the lesion site (fibroblasts genetically modified to secrete

155 se following spinal cord injury in which the lesion site fills in with a connective tissue matrix.

156 Further, NPs were seen to be retained at the lesion site for more than a week.

157 EphB2 is present on fibroblasts invading the lesion site from the adjacent meninges.

158 -3) within and beyond a cervical spinal cord lesion site grafted with autologous bone marrow stromal

159 rted to migrate long distances and to bridge lesion sites, guiding axonal regeneration after spinal c

160 The lesion site had the most BrdU labeling at all times, cor

161 cular zone (SVZ) to generate new OPCs in the lesion site has been debated.

162 fferent protein factors are assembled at the lesion site has remained unclear.

163 ed to the replication machinery stalled at a lesion site has remained unknown.

164 iRNA array of plasma, sampled at the carotid lesion site, identified 8 deregulated miRNAs (miR-15b, m

165 mn sensory axons extend across a spinal cord lesion site if axons are guided by a gradient of neurotr

166 nist NBQX was directly administered into the lesion site immediately after injury.

167 splantation of a human apical papilla at the lesion site improves gait in spinally injured rats and r

168 peripheral origin invaded the center of the lesion site in 129X1Sv/J mice.

169 ivator (EI-tPA), prior to grafting into a T3 lesion site in a clinically relevant severe SCI model, s

170 icient turnover of the NER ensemble from the lesion site in a Rad23-19S proteasomal complex-dependent

171 SCs) into a complete spinal cord transection lesion site in adult female rats.

172 of dorsal column axons across and beyond the lesion site in adult rats.

173 rix +/-one million MSC was injected into the lesion site in all animals.

174 ry axons extended into tissue rostral to the lesion site in animals injected with NT-3 vectors compar

175 axons (2.68%) regenerated >100 mum past the lesion site in crym-GFP ngr1(-/-) mice.

176 abelled neurons above and below the thoracic lesion site in quadrupedally versus bipedally trained ra

177 icles (NPs) as a drug delivery system to the lesion site in rat and pig contusion models of SCI.

178 es between eye and brain, and is the primary lesion site in the age-related disease open angle glauco

179 rograde transport of injury signals from the lesion site in the axon back to the cell soma stimulates

180 lso marked neurodegeneration remote from the lesion site in the chronic phase after stroke in rats.

181 -C4 propriospinal neurons, which crossed the lesion site in the intact half of the spinal cord and re

182 ex facilitates the handover of XPC to the UV-lesion site in the presence of the UV-DDB ligase complex

183 the endogenous or exogenous PARP-1 to the UV-lesion site in vivo after local irradiation.

184 air, at locations corresponding to possible lesion sites in 2D and 3D (590 targets per condition).

185 alignment for the two base pairs between the lesion sites in both duplexes.

186 be able to identify the precise locations of lesion sites in human subjects.

187 mplex specific to DNA repair is remodeled at lesion sites in the global genome nucleotide excision re

188 bacteria, accompanied by significantly fewer lesion sites in the liver.

189 tween deterioration of erectile function and lesion sites in the right occipital and thalamic region,

190 ween stroke-related erectile dysfunction and lesion sites in the right occipito-parietal cortex and t

191 in-associated inhibitors, within spinal cord lesion sites in vivo.

192 amount for the targeting of this nuclease to lesion sites in vivo.

193 ylated cofilin dramatically increases at the lesion site, in a Limk1-dependent manner.

194 r sources of NG2 in SCI and peripheral nerve lesion sites included Schwann cells and endothelial cell

195 compromised because the hostile niche at the lesion site incurs massive astroglial but not neuronal d

196 rd, which in animals with SCI changed to the lesion site, indicating drastic post-injury hemodynamic

197 ferated in injection sites, cell tracts, and lesion sites, indicating that OECs can also accumulate t

198 y facilitates accommodation of the resulting lesion site into the binding pocket, as the enzyme inter

199 inhibitory extracellular matrix in a spinal lesion site is a major impediment to axonal regeneration

200 The lesion site is critical for motor recovery, and lesions

201 enin pathway in fibroblast-like cells in the lesion site is pivotal for axon re-growth and functional

202 We propose that transfer between distal and lesion sites is a critical step in the repair process.

203 e variations in antibody uptake at different lesion sites is demonstrated in this study.

204 The infiltration of monocytes into the lesioned site is a key event in the inflammatory respons

205 The location of the underlying lesion site, known as Wernicke's area, remains controver

206 e maturation of nonneuronal cells within the lesion site lead to failed axon regeneration in mature a

207 n also induced Schwann cell migration to the lesion site, leading to remyelination of regenerating ax

208 -based lesion mapping we also identified the lesion sites linked with such deficits, including some b

209 We show that macrophages arrive at the lesion site long before axon fragmentation, much earlier

210 After injection at the lesion site, lymphoscintigraphy was performed with a 10-

211 igodendrocyte progenitor cells (OPCs) to the lesion site may not be an optimal therapeutic strategy d

212 ve metastatic prostate cancer had at least 1 lesion site of active metabolism for 18F-FDG or 11C-meth

213 rived neural stem cells/progenitors into the lesion site of completely transected rat spinal cord.

214 s in vivo and promotes bone formation at the lesion site of osteomyelitis.

215 of the sample, a second conformation at the lesion site of the duplex emerges, with protonation of t

216 tra indicate compression of the helix at the lesion site of the duplexes, resulting in the formation

217 l traversal across the BBB and accumulate at lesion sites of C. neoformans-infected brains.

218 ts, stroke-afflicted tissue, atherosclerotic lesions, sites of inflammation or infection, or damaged

219 n on DNA, Rad4 may stall preferentially at a lesion site, offering time to open DNA.

220 nd in the extracellular environment at a CNS lesion site, or that are associated with myelin, inhibit

221 extended tens of thousands of axons from the lesion site over virtually the entire length of the rat

222 Irrespective of lesion site, performance on tests of auditory sentence c

223 P]-N(2)-dG, extension of the primer past the lesion site poses the greatest block to polymerase progr

224 xonal damage and may thus help to identify a lesion site precisely, where fractionated nerve conducti

225 Notably, these same cellular sources in lesion sites produced the cell adhesion molecules L1 and

226 bitors AG1478 and PD168393 to an optic nerve lesion site promoting adult retinal ganglion cell axon r

227 Upon recruitment to lesion sites, Rad1-Rad10 removes damaged sequences, enab

228 from dysfunction in regions connected to the lesion site rather than the site itself.

229 hat this degradation event, initiated at the lesion sites, regulates damage recognition by XPC during

230 egenerate and instead die back away from the lesion site, resulting in permanent disability.

231 Denervated Schwann cells distal to the lesion site secrete factors promoting axonal growth and

232 Thus, the 9-1-1 complex at the lesion sites serves as both a damage sensor to activate

233 Thus, the 9-1-1 complex at the lesion sites serves as both a damage sensor to activate

234 substitutions and deletions occurring at the lesion site showed that pol kappaDeltaC was more efficie

235 visual cue was ipsi- or contralateral to the lesion site, showing this is not due simply to an induce

236 ) propagate into brain regions away from the lesion site soon after injury onset.

237 ivered late was ineffective, suggesting that lesion site sparing is insufficient to facilitate activi

238 ns that result from DNA synthesis past a DNA lesion site-specifically embedded in a library of DNA se

239 of any of the severed CST axons crossing the lesion site, suggesting that the recovery of function is

240 EI-tPA-primed hiNPC grafted into lesion sites survived, differentiated, acquired markers

241 ificantly greater localization of NPs at the lesion site than in the remaining uninjured segment of t

242 lantation promoted scaffold formation in the lesion site that facilitated axon regeneration and neuro

243 insic cells contribute to the formation of a lesion site that is refractory to axonal growth.

244 lowing convenient screening of hidden dental lesion sites that are oftentimes omitted by dentists.

245 At the lesion site, the 8-OG residues adopt syn conformations.

246 At the lesion site, the abasic residues and their partner adeni

247 Aside from the lesion site, the helices, including the flanking base pa

248 At the lesion site, the observed (11)C-(R)-PK11195 DVR for each

249 not dissociate from the fork stalled at the lesion site, the replication checkpoint presumably coord

250 chanisms of recovery depend on the task, the lesion site, the time from insult and the distinction be

251 specially interested in the relation between lesion site, therapy-induced recovery, and beneficial re

252 availability of neurotrophic factors in the lesion site, thereby promoting axonal regeneration and l

253 egenerating mossy fibers could not cross the lesion site; those that did were very much shorter than

254 carrier for delivery of therapeutics to the lesion site to minimize the impact of post-SCI response.

255 ntional remodeling was assessed by comparing lesion site to proximal and distal reference arterial ar

256 itized RGCs and caused axons proximal to the lesion site to retract.

257 process that enables DNA replication across lesion sites to ensure timely duplication of genetic inf

258 th state, bone marrow stromal cell grafts in lesion sites to provide permissive matrices for axonal g

259 int independent component analysis to relate lesion sites to therapy-induced brain reorganization, an

260 he biosynthesis of SPM is not induced in the lesion site up to 2 weeks after injury.

261 ore and after stroke was correlated with the lesion site using t-test statistics.

262 ique approach for accurately locating dental lesion sites using a fluorescent mouthguard consisting o

263 erectile dysfunction and cerebral ischaemic lesion sites using voxel-based lesion mapping.

264 al rewiring of axotomized projections at the lesion site versus compensatory outgrowth of spared axon

265 s abciximab delivered locally at the infarct lesion site versus no abciximab and to manual thrombus a

266 ng a 5-nitropyrimidine moiety at the desired lesion site via standard solid-phase procedures.

267 uitment of neural progenitor cells (NPCs) to lesion sites via long-range migration.

268 y abciximab delivered locally at the infarct lesion site vs no abciximab and to manual aspiration thr

269 s 2.2+/-0.3 mm, mean luminal diameter at the lesion site was 2.1+/-0.3 mm (P=0.35).

270 ive CAG, the minimal luminal diameter at the lesion site was compared with the average of the diamete

271 The lesion site was filled with bone marrow stromal cells, t

272 I administration, localization of NPs at the lesion site was reduced but still localize even at four

273 laser-induced DNA damage, less PARylation at lesion sites was observed in Hmgn1(-/-) than in Hmgn1(+/

274 The number of CC1(+) cells in the lesion sites was significantly reduced in Cdk5 cKO compa

275 lyze and quantify localization of NPs to the lesion site, we mapped the entire spinal cord, segment-b

276 d with larger patient numbers and more focal lesion sites, we also argue that clinical diagnosis and

277 tor (BDNF) and neurotrophin-3 (NT-3) into C7 lesion sites, we found both local effects of growth fact

278 al cells located within the epicenter of the lesion site were found to express CD200L at time points

279 Cell tracts extending into the lesion site were not seen when cells were injected eithe

280 Skin swabs obtained from the lesion sites were compared with swabs from identical sit

281 The lesion sites were spatially heterogeneous, including the

282 n accumulates in necrotic caseum, a critical lesion site where persisting tubercle bacilli reside.

283 e brain, react to injury by migrating to the lesion site, where they phagocytose cellular debris.

284 /iNOS(+)/MHCII(+)/CD11c(-) MDMs dominate the lesion site, whereas CCR2(+)/Ly6C(hi)/MHCII(-)/CD11c(+)

285 , but hpol kappa is strongly blocked at this lesion site, whereas hpol iota showed no distinction wit

286 y 26% single-nucleobase substitutions at the lesion site, whereas replication past the cross-linked d

287 t tetrahydroepoxide adduct is unwound at the lesion site, whereas the diol epoxide adduct structure i

288 bust remyelination was found in 62.5% of the lesion sites, whereas there was virtually no remyelinati

289 of a large number of protein factors at the lesion site which then coordinate the dual incision of t

290 rate enhanced microgliosis in and around the lesion site, which accompanies significantly enhanced fu

291 l on T2-weighted images at and distal to the lesion site, which correlates with Wallerian degeneratio

292 ve with pronounced kinking of the DNA at the lesion site, which could serve as a structural element r

293 axons showed no regrowth of axons beyond the lesion site with hnRNP K knockdown.

294 antly more neuronal survival upstream of the lesion site, with some functional improvement.

295 es exhibit a wobble-type base pairing at the lesion site, with thymine shifted toward the major groov

296 t TBI caused substantial degeneration at the lesion site within a few weeks and these did not expand

297 Microglia arrive at the lesion site within minutes of injury, where they rapidly

298 to correspond to the duplex unzipped to the lesion site within the channel.

299 Labeled cells were counted in the lesion site, within 0.5 mm rostral and caudal to the les

300 adable nanoparticles (nano-SOD/CAT) - at the lesion site would protect mitochondria from oxidative st