ライフサイエンスコーパス: postinjury

1 stay and at long-term follow-up (up to 2 yrs postinjury).

2 imit reparative processes in the early-phase postinjury.

3 t hospital admission and 3, 6, and 12 months postinjury.

4 ry outcome was mortality within 7 to 9 years postinjury.

5 e status and less hyperchloremia at 24 hours postinjury.

6 jury, with another probe test performed 3 mo postinjury.

7 ic episodes increasing as a function of time postinjury.

8 ere euthanized at 2 hours, 1 day, and 3 days postinjury.

9 ed Glasgow Outcome Scale (GOS-E) at 3 months postinjury.

10 was strongly expressed in odontoblasts 4 wk postinjury.

11 eo-electrocorticography (ECoG) 2 to 16 weeks postinjury.

12 current is larger for intact neurons at 2 d postinjury.

13 onocytes rolled on a thrombus 3 to 5 minutes postinjury.

14 5 degrees C) initiated approximately 2.0 hrs postinjury.

15 n of CD68, CCL-2, TNF-alpha, and IL-6 at 1 d postinjury.

16 how these changes at 1 d, but recover by 2 d postinjury.

17 one interview at 6-, 12-, 24-, and 36-months postinjury.

18 decreased in axotomized neurons at 1 and 2 d postinjury.

19 antly increased in axotomized neurons at 1 d postinjury.

20 rebral blood flow were measured 30 min-6 hrs postinjury.

21 ward regained size back to normal by 2 weeks postinjury.

22 roup) or at 1, 2, and 3 days (EPO-24h group) postinjury.

23 thymidine analog incorporation was observed postinjury.

24 and repeated subsequently for up to 32 days postinjury.

25 Similar results were seen at 1-year postinjury.

26 muscle action potential starting at 14 days postinjury.

27 stered intraperitoneally at days 1, 2, and 3 postinjury.

28 rn-injured mice was 50 x 10(3) CFU at 7 days postinjury.

29 in modulating phrenic function normally and postinjury.

30 th unilateral ACL insufficiency, 32-364 days postinjury.

31 Outcome was assessed 6-9 months postinjury.

32 e aerosolized every 4 hrs, starting at 2 hrs postinjury.

33 IB4 vascular profiles decreasing by 21 days postinjury.

34 atio, and decreased shunt fraction at 48 hrs postinjury.

35 itive dysfunction persisted for up to 16 wks postinjury.

36 tients survived, 9 (47%) developed infection postinjury.

37 s performed at baseline and at 24 and 48 hrs postinjury.

38 cular samples obtained over the first 48 hrs postinjury.

39 tion, gender, and time (p = .0035) by 24 hrs postinjury.

40 red cell viability to control values at 24 h postinjury.

41 time (p = .0045) throughout the first 48 hrs postinjury.

42 n admission, compared to only 33 at 24 hours postinjury.

43 lammation were similar during the first week postinjury.

44 rome c release peaked at approximately 4-8 h postinjury.

45 rom injured samples between 1 day and 7 days postinjury.

46 ) and restored cognitive performance 14 days postinjury.

47 mor necrosis factor alpha) peaked by 12-24 h postinjury.

48 Sheep were killed 48 hrs postinjury.

49 were collected on admission, 24, and 48 hrs postinjury.

50 expressed in the same direction at 24 hours postinjury.

51 immune cell activation between 1 and 8 weeks postinjury.

52 activity during intestinal epithelium repair postinjury.

53 hysical activity participation within 7 days postinjury.

54 f axons and neurons during the first 2 weeks postinjury.

55 uestionnaires in the ED and at days 7 and 28 postinjury.

56 ric moderate-to-severe TBI sample 1-5 months postinjury.

57 wounds were aggravated or minimally handled postinjury.

58 evels differentially in the initial 24 hours postinjury.

59 005) or 1 month (neuropsychiatric; P < .005) postinjury.

60 fer-treated animals at 18 hours and 24 hours postinjury.

61 crophage polarization markers at 3 h and 7 d postinjury.

62 ortex as early as few hours and up to 5 days postinjury.

63 ionally injured patients within 7 to 9 years postinjury.

64 disability, vegetative, or dead) at 6 months postinjury.

65 nning 30 minutes and persisting up to 1 week postinjury.

66 mechanism may drive sex outcome differences postinjury.

67 m injured and control mice collected at 3 mo postinjury.

68 e happens almost entirely in the first weeks postinjury.

69 ve mechanism responsible for sex differences postinjury.

70 lood samples were obtained from days 1 to 14 postinjury.

71 (TLR) pathway thought to drive inflammation postinjury.

72 ce compared with wild-type mice at 2-4 weeks postinjury.

73 For 30-45 mins postinjury, 1 L of normal saline was administered.

74 At 6 months postinjury, 133 (19%) patients had a fatal outcome; of t

75 For 30-60 mins postinjury, 500 mL of either normal saline (control, n =

76 Serum C-tau concentrations at 5 days postinjury, a biomarker of brain injury, were reduced by

77 lined from 4.6 preinjury to 3.7 at 12 months postinjury, a decline of nearly 1 full ADL (P < .05).

78 ated genes (false discovery rate <2) at d 14 postinjury, a subset of which were enriched for T-cell-r

79 rimotor function, evident as early as 1 week postinjury, a time point when increased neuronal surviva

80 Postinjury abdominal compartment syndrome (ACS) is an ex

81 aparotomy was followed by growing reports of postinjury abdominal compartment syndrome and prophylact

82 Postinjury administration of sulforaphane reduced the lo

83 vels were drawn twice daily for up to 9 days postinjury; AI was defined as two consecutive cortisols

84 tudes of both CAP components were suppressed postinjury, although this deficit was 16% greater for th

85 subsequently demonstrated that pharmacologic postinjury AMPK activation was sufficient to delay muscl

86 T cells were determined on days 2, 5, and 10 postinjury and compared with similar measurements made i

87 ll numbers were highest between 3 and 7 days postinjury and declined by 50% over the next 3 weeks.

88 tions (PTSR) were assessed at 4 and 12 weeks postinjury and depression at baseline and week 4.

89 icipation in physical activity within 7 days postinjury and incidence of persistent postconcussive sy

90 synthase inhibitor, during the first 12 hrs postinjury and infusion of BBS-2, a specific inducible n

91 Late phase of healing occurs a few days postinjury and involves interaction of injured myofibers

92 Fibrinolysis shutdown is common postinjury and predicts poor outcomes.

93 g independent predictor of MOF and mortality postinjury and represents a common variant with prognost

94 ing pathways that govern cartilage responses postinjury and suggest that delivery of NF-kappaB siRNA

95 demonstrate the importance of TLR signaling postinjury and supports that a genetic mechanism may dri

96 within physiologic ranges for a certain time postinjury and then suddenly deteriorate.

97 ary vascular hyperpermeability peaked 12 hrs postinjury and was related to vascular endothelial growt

98 pregulated during the repair phase (2-3 days postinjury) and returned to the control level when repai

99 ht microscopy at intervals from 1 to 56 days postinjury, and the area of damaged tissue (termed lesio

100 e collection was performed on days 17 and 29 postinjury, and urinary C-terminal telopeptide of type I

101 n that in controls during the first 24 hours postinjury, and was not affected by inhibitors of biosyn

102 At 70 days postinjury, animals implanted with scaffold-plus-cells e

103 r discomfort increased from 24- to 36-months postinjury (ARR 1.06, 95% CI: 1.01, 1.12).

104 is both necessary and sufficient to inhibit postinjury arterial VSMC proliferation, whereas membrane

105 rotein immunoreactive clusters 7 and 14 days postinjury, as compared with nontreated rats.

106 (+) astrocytes that persisted for >/=6 weeks postinjury, as well as increased intraspinal GLT1 protei

107 SD and depression were assessed at 12 months postinjury, as were the following functional outcomes: a

108 ts were observed at the 6-, 9-, and 12-month postinjury assessments.

109 pproximating 1:1:1 during the first 24 hours postinjury, based on US military retrospective experienc

110 hippocampal-onset seizures began 16-25 days postinjury, before hippocampal atrophy developed, as dem

111 n heavy chain 2) were increased on d 2 and 4 postinjury but later returned to baseline levels on d 8

112 ain constant in the SVZ and RMS until 5 days postinjury but then rapidly expanded by 150,000 cells by

113 medial VSMCs from injured vessels at 2 weeks postinjury but was restored when the up-regulation of ei

114 ever, MAC was down-regulated on days 5 and 7 postinjury but was still higher than in non-injured mice

115 0%) were known to have survived to 36-months postinjury but were lost to follow-up at all time points

116 han free-electron laser incisions up to 36 d postinjury, but at day 45 they became similar.

117 The mechanisms that dictate postinjury cardiomyocyte proliferation early in life rem

118 s were developed and implemented to optimize postinjury care.

119 tepped care that consisted of (1) continuous postinjury case management, (2) motivational interviews

120 n of IL-10 amplified the Th1 response at 1 d postinjury, causing increases in IL-6 and CCL2, while pr

121 FR2(+) cells and suppressed replenishment of postinjury CD34(+)/VEGFR2(+) cells in peripheral blood (

122 Postinjury changes in gut microbiota persist for at leas

123 Control over postinjury CNS plasticity is a major frontier of science

124 ality that allows 'point-of-care' testing of postinjury coagulopathy and monitoring of transfusion st

125 Existing limitations in the management of postinjury coagulopathy include the lack of a uniform de

126 Progressive postinjury coagulopathy remains the fundamental rational

127 with life threatening hemorrhage at risk for postinjury coagulopathy should receive component therapy

128 secutive patients over 14 months at risk for postinjury coagulopathy were stratified by transfusion r

129 PF occurs early in severe shock, leading to postinjury coagulopathy, and ultimately hemorrhage-relat

130 This review examines the current approach to postinjury coagulopathy, including identification of pat

131 he injured rat groups (B, EF, B+EF) on day 1 postinjury compared with sham.

132 tion of spinal neurons and axons at 12 weeks postinjury, compared with control (LV-GFP)-treated anima

133 moderate-to-severe TBI (msTBI) at 1-5 months postinjury, compared with well matched healthy control c

134 Six months postinjury, comparing good outcome (PCPC < or = 3, n = 2

135 h a lower GCS score at 24 hrs, in those with postinjury complications, in those with 6-wk mortality,

136 ophysiological recordings, conducted at 24 h postinjury, compound action potentials (CAPs) were evoke

137 care on mortality at discharge and 12 months postinjury, controlling for injury severity.

138 ns in monocyte and T-cell responses on day 2 postinjury correlates with the development of adverse cl

139 xamine synaptic profiles in Vc/C2 at 3 weeks postinjury, corresponding to the time of peak behavioral

140 Minocycline alone attenuated postinjury cortical lesion volume, hippocampal CA3 neuro

141 n lactulose permeability from day 1 to day 2 postinjury could not be demonstrated in the B and EF gro

142 ion on computed tomography and a complicated postinjury course.

143 CD4(-/-) mice with WT CD4(+) T cells reduced postinjury cytokine production to WT levels.

144 p were euthanized for histologic analysis at postinjury day 3 and day 28.

145 During postinjury days 1-8, 65 neurological wake-up tests were

146 s was 40% to 70% lower in trauma patients on postinjury days 2, 5, and 10 than in healthy control sub

147 o was significantly lower in patients on all postinjury days than in the control subjects.

148 The postinjury decrease in SGC tonic GABA currents is in dir

149 0.9% of tracer-flooded neurons revealed only postinjury dextran uptake, consistent with delayed membr

150 age that normally occurred between 1 and 4 d postinjury did not occur in IL-10 mutants.

151 xotomy, we reveal a critical period of 4-5 h postinjury during which the course of Wallerian axonal d

152 Postinjury epilepsy (PIE) is a devastating sequela of va

153 spontaneous seizures.SIGNIFICANCE STATEMENT Postinjury epilepsy is an unpreventable and devastating

154 Postinjury etomidate attenuated water maze deficits, but

155 Lastly, postinjury etomidate did not exacerbate neurologic or hi

156 The ineffectiveness of postinjury etomidate on motor and histologic tasks sugge

157 rd heightened fear learning during stressful postinjury events and provides a potential molecular mec

158 rate injury, accelerate recovery, or prevent postinjury fibrosis after AKI.

159 which resulted in a concomitant increase in postinjury functional recovery.

160 , plasma cfDNA levels, and IG count at day 1 postinjury gave good discriminatory power for the identi

161 Desensitization is most marked immediately postinjury, generally resolving by Day 7.

162 r studies suggest that Olig2 is critical for postinjury gliosis.

163 Our research sheds light on postinjury heterogeneity.

164 present a network-level mechanism underlying postinjury hippocampal dysfunction and epileptic network

165 The process of postinjury hippocampal epileptogenesis may involve gradu

166 ormant basket cell" hypothesis suggests that postinjury hippocampal network hyperexcitability results

167 tate/pyruvate ratio remained elevated beyond postinjury hour 100 in the seizure group but not the non

168 After 7 days postinjury, however, the cellular responses differed bet

169 The mechanisms underlying postinjury immune suppression are not known.

170 Reversal of postinjury immune suppression in SCI mice can be achieve

171 25+ T cells contribute to the development of postinjury immune suppression.

172 sought to determine if differences in early postinjury immune-related gene expression are associated

173 o and production of M-CSF and contributes to postinjury immunoaberrations.

174 This could contribute to postinjury immunosuppression.

175 , indicated that FK506 reduced the extent of postinjury impairments to axonal transport and subsequen

176 served reduced cortical cell loss at 5 weeks postinjury in mannose-binding lectin (-/-) mice compared

177 significantly elevated over the first 7 days postinjury in the hypotensive versus normotensive patien

178 studied the population of cells that divide postinjury in the injury epicenter by delivering BrdU or

179 The postinjury increase in alveolar-arterial oxygen tension

180 erlines a pathogenic contribution of sterile postinjury inflammation in APAP-induced acute liver inju

181 ical and basic science literature related to postinjury inflammation in childhood, focusing on the de

182 Postinjury inflammation markedly reduces newborn neuron

183 d by HMGB1 neutralization and attenuation of postinjury inflammation.

184 vival of young neurons is sharply reduced by postinjury inflammation.

185 ventions for the prevention and treatment of postinjury inflammatory dysregulation depends on continu

186 ealing how OPCs themselves contribute to the postinjury inflammatory milieu by producing cytokines th

187 The postinjury inflammatory response in the CNS leads to neu

188 l mice, and those microglia present at early postinjury intervals retained their resting morphology.

189 At 2 d postinjury, intrinsic bursting activity is lost within t

190 he prevalence of ongoing problems at 3-years postinjury is high, confirming that serious injury is fr

191 ated neural control of systemic inflammation postinjury is likely exaggerated in patients with trauma

192 Four days postinjury, laser-injured mouse retinas injected with IG

193 In pediatric burn patients at 6 months postinjury, leg muscle protein net deposition is unrespo

194 Administered starting 4 h postinjury, LM11A-31 promotes functional recovery withou

195 lose permeability in the B+EF group on day 2 postinjury markedly decreased from day 1 but was still s

196 g the early molecular and cellular responses postinjury may provide targets for therapeutic intervent

197 l experiments for a further understanding of postinjury mechanisms of motor control and recovery.

198 adverse inflammatory responses that lead to postinjury MOF.

199 Thirty-day postinjury motor function determined by CatWalk (Noldus

200 monocyte (Mphi) dysfunctions could result if postinjury Mphi differentiation preferentially favored i

201 This M1 to M2 sequence is observed during postinjury muscle regeneration, which provides an excell

202 e neuroscore and beam walk tests for 4 weeks postinjury (n = 11).

203 uring hospitalization and at 3 and 12 months postinjury (N=826).

204 tropium bromide 1 hr before injury (n=6) and postinjury nebulization protocols of 18 mug (n=6), 36 mu

205 treated groups, including both preinjury and postinjury nebulization protocols.

206 Postinjury neurogenesis occurs as a burst of proliferati

207 as injected into the T9 dorsal horns 2 weeks postinjury/nontransection.

208 her regional brain edema formation at 24 hrs postinjury nor the extent of cortical tissue loss assess

209 al contusion lesion sites between 1 and 90 d postinjury of athymic nude (AN) and Sprague Dawley (SD)

210 increased in all injured rat groups on day 1 postinjury; on day 2 it remained elevated post-B, decrea

211 4 administration schedules (preinjury only, postinjury only, for 24 hr postsurgery, or for 72 hr pos

212 PC) score at hospital discharge and 6 months postinjury or at death.

213 ocking cPLA2 pharmacologically at 30 minutes postinjury or genetically deleting cPLA2 in mice amelior

214 between admission levels of Gc-globulin and postinjury organ dysfunction and infection.

215 hildren with traumatic brain injury, 6-month postinjury outcome inversely correlated with Glasgow Com

216 There is considerable heterogeneity in postinjury outcome, which is only partially explained by

217 lyses, blood lead levels increased with time postinjury (p < 0.0005) up to 3 months, with number of r

218 er PTSR than the assessment group at 4 weeks postinjury, p < .01, and at 12 weeks postinjury, p < .05

219 4 weeks postinjury, p < .01, and at 12 weeks postinjury, p < .05, and significantly lower depressive

220 nd longitudinal (1 day and 1 week vs 1 month postinjury; P < .001) evidence of CBF recovery in the ri

221 useful for follow-up evaluation of secondary postinjury pathologies.

222 onsidered when designing acute and long-term postinjury patient intervention strategies aimed to enha

223 nt guidelines advocate rest in the immediate postinjury period until symptoms resolve, no clear evide

224 Over the acute postinjury period, patients with AI had lower trough mea

225 UCH-L1 performed best in the early postinjury period.

226 We hypothesized that postinjury PF occurs early in severe shock, leading to p

227 e immune status of patients in the immediate postinjury phase and how this might influence patient ou

228 tissue loss increases throughout the chronic postinjury phase.

229 on brain injury in untreated, preinjury, and postinjury phenylephrine (1 microg/kg/min intravenously)

230 ogrammed NIH3T3 cells significantly improved postinjury physiological functions and showed anatomic e

231 a), which modulates these two aspects of the postinjury physiological response.

232 ogen protein signals remodel the progressive postinjury (PI) niche.

233 One day postinjury, PP mixed cells were cultured in the presence

234 lation of NMDA receptors by NMDA 24 and 48 h postinjury produced a significant attenuation of neurolo

235 ovide one molecular mechanism underlying the postinjury protective effects of oligodendrocytes by str

236 tionship of preinjury psychiatric status and postinjury PTSD with conflicting results, but no prospec

237 Animals were euthanized at five timepoints postinjury, ranging from 6 hours to 9 weeks after BrdU d

238 ction (i.e., the point at which the earliest postinjury recovery of phrenic activity has been reporte

239 vivo evidence that FGF signaling facilitates postinjury recovery of the mouse hematopoietic system by

240 suppressed after injury and increased during postinjury recovery, whereas chlorzoxazone metabolism wa

241 rophylactic measures, PE remains a threat to postinjury recovery.

242 hat would be considered the normal period of postinjury recovery.

243 peritoneal cholecalciferol treatment 6 hours postinjury reduced alveolar inflammation, cellular damag

244 n of RANKL, given either prophylactically or postinjury, reduces liver injury in a manner associated

245 n, which are a subset of cells necessary for postinjury regeneration of gut epithelium.

246 esponsible for sex-based outcome differences postinjury remain conflicting.

247 ia enhanced revascularization and/or altered postinjury remodeling.

248 sed by the lesion or by processes related to postinjury reorganization.

249 opulation maintenance and crypt regeneration postinjury require mTOR.

250 in 81% and 85% of subjects at 3 and 6 months postinjury, respectively.

251 amined the effect of gender on the immediate postinjury response to major trauma.

252 se leads to activation of glia, which govern postinjury responses in the nervous system.

253 a therapeutic target for atherosclerosis and postinjury restenosis.

254 mg/kg) by subcutaneous injection 30 minutes postinjury restores levels of barrier sealing glucocorti

255 tested the function of Wnt signaling in the postinjury retina, focusing on its ability to influence

256 Ultrastructural analyses of axons postinjury revealed immediate breakage and buckling of m

257 Interestingly, after halting GCV at 14 d postinjury, scar elements and vessels entered the lesion

258 pacity of monocyte IL-12 production on day 2 postinjury showed a statistically significant correlatio

259 uggest the possibility of rapid, transmedian postinjury signals between homologous mirror-image neuro

260 At 1 month postinjury, smaller lesion area and midsagittal tissue b

261 ypothermia group showed significantly higher postinjury somatosensory-evoked potential amplitudes wit

262 In the acute postinjury stage, equine SF exhibits poor boundary lubri

263 ny interlimb constraints in promoting robust postinjury stepping behavior.

264 cAMP into the L4 dorsal root ganglion, and a postinjury stimulus to the injured axon was administered

265 ater than that for the N1 CAPs, and improved postinjury strength-duration and refractoriness properti

266 rophages than scalpel wounds at days 2 and 7 postinjury, suggesting that free-electron laser irradiat

267 reach the wound decreased after the first h postinjury, suggesting that the knockdown specifically a

268 sion increased in IL-10 mutant muscle at 1 d postinjury, suggesting that the mutation amplified the t

269 Maintenance of postinjury T-lymphocyte immune paralysis or anergy could

270 Eleven rats were controls with postinjury temperature maintained at 37 +/- 0.5 degrees

271 nd CD-1 were significantly larger at 56 days postinjury than in the KA-resistant strains C57Bl/6 and

272 time) and neuropsychiatric symptoms at 1 day postinjury that resolved at either 1 week (cognitive; P

273 oach can be adapted to systemic therapy in a postinjury therapeutic time window.

274 Over a postinjury time course of 1 week, alphaCT1-treated IBZs

275 y BLT1 receptor were suppressed at the 3-day postinjury time point, but recovered by 1 wk.

276 regeneration is achievable at unprecedented postinjury time points.

277 In this study, we showed how the hyperacute postinjury time window contained a focused, specific sig

278 -155 deletion improves locomotor function at postinjury times corresponding with the arrival and maxi

279 We transduced neurons postinjury to express a constitutively active Rheb to en

280 Postinjury treatments with tiotropium bromide were as ef

281 ice, treatment accelerated recovery, reduced postinjury tubular atrophy and interstitial fibrosis, an

282 The two groups underwent preinjury, weekly postinjury (up to 4 wks) somatosensory-evoked potential

283 haAF1 is necessary and sufficient to inhibit postinjury VSMC proliferation.

284 Cumulative mortality at 3 years postinjury was 16% (95% confidence interval [CI], 15.8%-

285 revalence of reporting problems at 36-months postinjury was 37% for mobility, 21% for self-care, 47%

286 the phagocytic macrophage marker CD68 at 3 d postinjury was followed by increased CD206 expression at

287 dmission with systemic disease preinjury and postinjury was higher in both injury groups than in CC a

288 Continued improvement to 36-months postinjury was only present for the usual activities ite

289 t of cortical tissue loss assessed at 7 days postinjury was significantly aggravated by superimposed

290 GAG release during the period 24-72 hours postinjury was similar to that in uninjured controls, bu

291 cipants with adjustment disorder at 3 months postinjury were significantly more likely to meet criter

292 Immediate neurologic symptoms postinjury were used to identify mild TBI.

293 in the first 24 hr and then from days 1 to 7 postinjury) were assessed for 24 inflammatory mediators

294 loping major depressive episode by 3 months' postinjury, which could facilitate selective referral fo

295 cyte growth factor in hepatic stellate cells postinjury, which, in turn, results in an earlier onset

296 ontinuous infusion of ZK 234238 started 1 hr postinjury with a dose of 100 microg/kg/hr.

297 uma and could be administered at least 3 hrs postinjury with only a small reduction in efficacy.

298 netic resonance imaging (MRI) out to 30 days postinjury, with a subset of animals selected for histop

299 t T-cell entry was not evident until 14 days postinjury, with T-cell numbers doubling between 2 and 6

300 enous repair continues beyond the first week postinjury (wpi), however, is unknown.