ライフサイエンスコーパス: lesion site

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

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

3 activation of the myelination program at the lesion site.

4 esulted in increased axon density within the lesion site.

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

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

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

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

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

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

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

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

13 l regeneration into and beyond a midcervical lesion site.

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

15 spinal cord and corticospinal axons into the lesion site.

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

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

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

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

20 ers and ascending sensory fibers through the lesion site.

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

22 ncorporation, upstream and downstream to the lesion site.

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

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

25 reduction in macrophage accumulation at the lesion site.

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

27 different NER proteins are assembled at the lesion site.

28 armful mediators diffusing from the original lesion site.

29 by newly formed endothelial cells within the lesion site.

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

31 although changes in other measures varied by lesion site.

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

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

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

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

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

37 digits within dorsal rootlets bordering the lesion site.

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

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

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

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

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

43 astrocyte processes into the margins of the lesion site.

44 ch diminishes with progression away from the lesion site.

45 proliferation of hemocytes which invade the lesion site.

46 reduction in axonal growth (P < 0.01) at the lesion site.

47 a fraction of T cells expand locally at the lesion site.

48 are observed along the duplex, except at the lesion site.

49 royed when a thin film was inserted into the lesion site.

50 for recruitment of the repair enzymes to the lesion site.

51 lic changes in brain regions remote from the lesion site.

52 acts to stop the migrating microglia at the lesion site.

53 oxidative changes are not restricted to the lesion site.

54 nically not related to the symptomatic acute lesion site.

55 ay impair erectile function depending on the lesion site.

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

57 han nonclassical monocytes to migrate to the lesion site.

58 reflected by altered glycosylation at the MS lesion site.

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

60 ributes to MN axonal regeneration across the lesion site.

61 tiple biological pathways within the chronic lesion site.

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

63 and anti-inflammatory metabolites within the lesion site.

64 es both ipsilateral and contralateral to the lesion site.

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

66 cues to direct axonal regrowth across nerve lesion sites.

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

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

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

70 or prolonged time periods within spinal cord lesion sites.

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

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

73 ruitment of these cells at neuroinflammatory lesion sites.

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

75 such as monoubiquitylation of histone H2A at lesion sites.

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

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

78 substantial frequencies of mutations at the lesion sites.

79 neovascular AMD exhibited NLRP3 staining at lesion sites.

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

81 nits NR1 and NR2A mRNAs in VMN caudal to the lesion site 24 h after SCI.

82 6%) opposite M(1)dG or -1 frameshifts at the lesion site (31%).

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

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

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

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

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

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

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

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

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

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

93 hat A-T base pairs flanking the [BP]-N(2)-dG lesion site allow for local flexibility consistent with

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

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

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

97 The lesion site and a proximal reference site were analyzed.

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

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

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

101 per colon by sampling CT attenuation at the lesion site and discarding sites having attenuation less

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

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

104 right-handed helix with a slight bend at the lesion site and no severe distortions of the sugar-phosp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

130 The lesion site (at low thoracic level) in severed adult rat

131 d, and the major groove is compressed at the lesion site because of the location of the bulky PhIP-N-

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

133 Chronic TTX infusion into the lesion site blocked the synchronous neuronal activity af

134 r of neuronal injury not only at the primary lesion site but also in the antero- and retrograde proje

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

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

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

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

139 y produced dose-limiting inflammation at the lesion sites, but the other regimens were well tolerated

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

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

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

143 incorporation of nucleotides opposite these lesion sites by Poldelta.

144 ce segment and lesion site plaque burden and lesion site calcium occurred in the groups with CK-MB el

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

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

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

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

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

150 ase-pair step parameter roll adjacent to the lesion site could be extracted.

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

152 ous variable was defined as VA at the target lesion site divided by that of average reference segment

153 deling index was defined as VA at the target lesion site divided by that of average references.

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

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

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

157 icospinal axon regeneration into subcortical lesion sites expressing BDNF.

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

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

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

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

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

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

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

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

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

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

168 the dominant parietal cortex, but many other lesion sites have been implicated suggesting that the pr

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

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

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

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

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

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

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

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

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

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

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

180 component of atheroma, are attracted to the lesion site in response to chemotactic signals, particul

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

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

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

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

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

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

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

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

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

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

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

192 y approximately 50% mutagenesis at epsilon C lesion sites in untreated cells.

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

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

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

196 ession arose from multiple cell types at the lesion site, including reactive microglia, macrophages,

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 se to the replication machinery stalled at a lesion site is achieved via this association.

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

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

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

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

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

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

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

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

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

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

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

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

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

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 fts that were placed into either subcortical lesion sites or sites of thoracic spinal cord injury fai

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

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

223 ofiles in close proximity to the spinal cord lesion site, peaking 3 d after injury.

224 There was a mean of six false-positive lesion sites per colon.

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

226 US, progressively more reference segment and lesion site plaque burden and lesion site calcium occurr

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

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

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

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

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

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

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

234 ed to the replication machinery stalled at a lesion site remains unknown.

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

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

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

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

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

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

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

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

243 with UvrABC proteins of the following three lesions site-specifically positioned in DNA, and of know

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

245 s a larger magnitude of curvature around the lesion site than for the duplexes with the purines flank

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

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

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

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

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

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

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

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

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

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

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

257 ted by partially unwinding the duplex at the lesion site to produce a bulge and tipping the guanine r

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

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

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

261 aemic profile and have beneficial effects at lesion sites to prevent or regress atherosclerosis, a co

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

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

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

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

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

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

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

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

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

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

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

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

274 Such a sheared base-pair alignment at the lesion site was previously observed for epsilondC.dG and

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

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

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

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

279 Large chemical shifts at the lesion site were consistent with ring current shielding

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

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

282 The lesion sites were spatially heterogeneous, including the

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

284 tructures show remarkable differences at the lesion site where the extrahelical location of the tetra

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

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 n when OVA was injected into a newly created lesion site with extensive BBB leakage.

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

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

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

297 he structure of the duplex is perturbed near lesion sites, with the local unwinding of the double hel

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

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

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