ライフサイエンスコーパス: injure

1 f rib 7 (21.3%, 47 of 221) was most commonly injured.

2 surface only if the cornea was superficially-injured.

3 capable of extensive body regeneration when injured.

4 Among 307 people aboard the flight, 192 were injured; 63 of the injured patients were initially evalu

5 Congruent with this, injured A/J fibres produced Ca(2+) sparks and Ca(2+) wav

6 Among 29613 injured adolescents (mean [SD] age, 17.3 [1.4] years; 72

7 ng drugs have gained popularity for treating injured adult axons, the rationale being that increased

8 al hepatocytes can engraft and repopulate an injured adult liver.

9 the predominant source of myofibroblasts in injured adult lung.

10 tion of recovery neurobiology components for injured adult mammalian spinal cord that are different f

11 9(+) progenitors that were transplanted into injured adult mouse lungs differentiated into all major

12 suppressed p53 acetylation and apoptosis in injured AECs, and prevented pulmonary fibrosis (PF).

13 Neuronal cells dissociated from SNE-injured and contralateral L4 and L5 dorsal root ganglia

14 tored after injury.SIGNIFICANCE STATEMENT In injured and diseased nerves, the transcription factor c-

15 Chondrocytes in injured and diseased situations frequently re-express ph

16 issection to specifically collect individual injured and non-injured nociceptive DRG neurons and to d

17 nced the engraftment of muscle stem cells in injured and noninjured muscles in mice.

18 omponents of the BMP signaling pathway, were injured and then tested for nocifensive responses to a n

19 anatomic and functional improvements in the injured animals emerged over the course of a year.

20 ur combinatorial strategy in the chronically injured animals prevented a decline in locomotor behavio

21 Transfer of blood-borne EVs from brain-injured animals was also enough to suppress exploratory

22 s were found in cerebrospinal fluid (CSF) of injured animals with a CSF/serum ratio of 20% at peak,

23 spread out over the tissues adjacent to the injured area in certain diseases, including brain tumors

24 , we show that angiogenic sprouting into the injured area starts as early as 15 h after injury.

25 s, facilitates the neuronal migration toward injured areas, and shows survival properties due to its

26 ly for its therapeutic potential on severely injured areas.

27 onstrate effective siRNA transfection of the injured arterial wall and provide a clinically effective

28 esveratrol attenuated Akt phosphorylation in injured arteries.

29 e formation of dystrophic growth cone at the injured axonal tip, the subsequent axonal dieback, and t

30 Injured axons are able to quickly re-grow thus to restor

31 function after injury relies on whether the injured axons can find their target cells.

32 The injured axons exhibited enrichment of mRNAs related to p

33 gthening of 3'UTRs was more prevalent in the injured axons, including the newly discovered alternativ

34 ways related to RNA granule formation in the injured axons.

35 ronal responses that support regeneration of injured axons.

36 We followed up 2,757 adult patients, injured between July 2011 and June 2012, through deaths

37 mark problems: in vivo thrombus growth in an injured blood vessel and in vitro thrombus deposition in

38 of platelets to the subendothelial matrix of injured blood vessels.

39 w-derived G-CSF-responsive cells home to the injured brain and are critical for altering neural proge

40 tion times and increased accumulation in the injured brain compared to generation 4 dendrimers (G4,

41 etitive (r)TBI mouse model and harvested the injured brain extracts from the acute to the chronic pha

42 uitment order of these subpopulations to the injured brain largely remains unknown.

43 ly decreased by chronic hyperglycemia in the injured brain of fish.

44 Monocytes purified from the injured brain stimulated the proliferation of naive T ly

45 High-resolution images of naive and injured brain tissue facilitated the comparison of CL sp

46 t the direct impact of transplanted cells on injured brain tissue.

47 negative implications for the ability of the injured brain to clear edema.

48 tivated microglia and damaged neurons in the injured brain, and deliver therapeutics in small and lar

49 of early inflammatory infiltrate within the injured brain, and whether their depletion attenuates se

50 in rapid recruitment of leukocytes into the injured brain.

51 al and structural organization in normal and injured brain.

52 d abrogated neutrophil infiltration into the injured brain.

53 hils infiltrate the intracerebral hemorrhage-injured brain.

54 strategy to promote synaptic recovery in the injured brain.

55 ting fluids and proinflammatory cells in the injured brain.

56 ircuitry and neurodegeneration in normal and injured brains.

57 They never got injured but also had low prospective reproductive succes

58 This process takes place in injured, but not in normal, SECs.

59 ilities who fall may not be seriously ill or injured, but policies often require immediate transport

60 cents treated at PTCs were more likely to be injured by a blunt than penetrating injury mechanism (91

61 dds of underreporting in the NVSS than those injured by firearms (odds ratio [OR]: 68.2; 95% CI: 15.7

62 ry response that ensues when hepatocytes are injured by lipids (lipotoxicity).

63 dual- and county-level covariates, decedents injured by non-firearm mechanisms had higher odds of und

64 that the expression of 5-HTT was elevated in injured carotid arteries and over-expression of 5-HTT in

65 elets inhibited endothelial recovery in wire-injured carotid arteries, but this effect was also abrog

66 nd vascular cell adhesion molecule 1 in wire-injured carotid arteries.

67 In response to the loss of CCR2, injured Ccr2(-/-) sciatic nerves demonstrate prolonged e

68 membrane vesicles released from activated or injured cells and are detectable by flow cytometry.

69 Furthermore, only a few injured cells were found along the edge of the circular

70 that acts primarily to remove pathogens and injured cells.

71 embrane-based cell-cell interaction with the injured cells.

72 opulation-based, consecutive sample of 67047 injured children and adults served by EMS (1971 rural an

73 ission fibrinolytic derangement is common in injured children and adults, and is associated with poor

74 Prospective study of severely injured children at a level 1 pediatric trauma center.

75 AST examination during initial evaluation of injured children improves clinical care.

76 period of maturation for human NSCs in adult injured CNS is not well defined, posing fundamental ques

77 tion in the adult CNS.SIGNIFICANCE STATEMENT Injured CNS nerves fail to regenerate spontaneously.

78 o potentiate the regenerative outcome in the injured CNS.

79 and requires validation in other critically injured cohorts.

80 in vivo High-concentration thrombin directly injured conditionally immortalized human and rat podocyt

81 of hedgehog activation, consistent with non-injured controls.

82 Results Myeloid cells infiltrated into the injured cord at 6 and 24 hours after TAR.

83 ized with adherent bacteria in superficially-injured corneas.

84 ate-to-pyruvate ratios were increased in the injured cortex at acute (12/24 hours) and sub-acute (7 d

85 protein (GFAP)-breakdown product (GBDPs) in injured cortex were also attenuated by MSCs.

86 Similarly, directly injured corticospinal neurons in vivo also exhibit a spe

87 toxic molecules from dying cells pass to and injure coupled neighbors.

88 o unmask distinguishing features of severely injured DCD hearts.

89 Using microfluidic chambers to separate and injure distal axons, we show that axotomy causes retrogr

90 r region and rescues Kcna2 expression in the injured DRG and attenuates neuropathic pain.

91 ockdown fully reversed MOR expression in the injured DRG and potentiated the morphine effect on pain

92 n of the DNA methyltransferase DNMT3a in the injured DRG neurons via the activation of the transcript

93 KChIP1, and DPP10 were transfected into the injured DRGs (defined as DRGs with injured spinal nerves

94 4.3, KChIP1, and DPP10 surface levels in the injured DRGs.

95 Injured DRs of induced animals also contained far more a

96 Two weeks after injury, injured DRs of induced animals contained far more SCs an

97 cating that caErbB2 enhanced regeneration of injured DRs, without aberrantly activating SCs and axons

98 The ankle and foot are commonly injured during sporting activities.

99 and KKO selectively bound to photochemically injured endothelium at sites where surface glycocalyx wa

100 Immature injured entheses retained high levels of Gli1 expression

101 e effect of Smo deletion was examined in the injured entheses.

102 Injured femoral arteries showed a 20% increase in neoint

103 At physical examination, the injured finger was swollen and purple.

104 duction in hippocampal neural density in the injured group compared to controls.

105 an attractive therapeutic option to cure the injured heart and prevent heart failure.

106 nd P2 receptors on T cells isolated from the injured heart revealed profound upregulation of the enzy

107 T cells infiltrating the injured heart significantly upregulated at the gene (qua

108 Injured heart tissue exposed to WNT-974 exhibits decreas

109 re under development for regeneration of the injured heart.

110 ene expression signature identified severely injured hearts during EVHP (upregulation of c-Jun, 3.19

111 elevations in cardiac Troponin-I in severely injured hearts during EVHP, and may also detect injury a

112 Histochemical assessment identified severely injured hearts during EVHP.

113 Lastly, injured hearts failed to fully regenerate as evidenced b

114 eloid cell numbers markedly increased in the injured hearts, and histamine levels were up-regulated i

115 ignal was found to be 24 +/- 6% lower in the injured hemisphere compared with the non-injured hemisph

116 the injured hemisphere compared with the non-injured hemisphere, while the hyperpolarized bicarbonate

117 -to-lactate ratio was 33 +/- 8% lower in the injured hemisphere.

118 ) lymphocytes, were reduced and migration to injured hepatocytes prevented.

119 e expression was investigated in healthy and injured human and rodent liver.

120 Severely injured human blunt trauma patients (n = 472, average in

121 1 in the nuclei of renal proximal tubules of injured human kidney allografts, but not in those of sta

122 ologous human SCs could be transplanted into injured human spinal cord.

123 on SCI in rats, and importantly, also in the injured human spinal cord.

124 Further, BLEO-injured il17a(-/-) mice had diminished levels of circula

125 low, there was responder bias with patients injured in intentional events, younger, and less serious

126 Most high-risk trauma patients injured in rural areas were cared for outside of major t

127 d access to major trauma care among patients injured in rural regions.

128 e surrounding surgical resection site can be injured inadvertently due to procedures such as incision

129 ood vessels within the skin of the thermally injured/infected mice.

130 Retrospective cohort study of severely injured (injury severity score >15) patients from the Na

131 ically limits macrophage accumulation in the injured kidney during RAS activation by constraining the

132 Lgals3, Pdgfb, Egf, and Tgfb In comparison, injured kidneys from mice lacking BRP-39 had significant

133 production and improved energy metabolism in injured kidneys from mPGC-1alpha mice.

134 cortex, medulla and pelvis of the normal and injured kidneys, we found that ureteral obstruction not

135 l IRI in mice induced miR-146a expression in injured kidneys.

136 al structure and reduced oxidative stress in injured kidneys.

137 The ligation-injured lacrimal glands temporarily decreased in weight

138 shown to extensively repopulate chronically injured liver tissue.

139 ctivation, which was not the case in acutely injured liver.

140 insight into the microscopic behavior of the injured lung and provide a means of testing protective-v

141 ntiinflammatory and pro-resolving effects on injured lung endothelium and alveolar epithelium, includ

142 r processes at specific locations within the injured lung.

143 Injured mature CNS axons do not regenerate in mammals.

144 In contrast, injured mature entheses had few Gli1+ cells early in the

145 sociated with shorter hospital LOS in mildly injured Medicaid recipients.

146 sp1-EYFP+ CPCs improved the survivability of injured mice and restored the functional performance of

147 Conditional ablation of MSLN+ aPFs in BDL-injured mice attenuated liver fibrosis by approximately

148 Traumatic brain injured mice receiving human amniotic mesenchymal stroma

149 Intraperitoneal inoculation of the thermally injured mice, bypassing the need for translocation, prod

150 reduced inflammation and lung injury in LPS-injured mice.

151 -derived EVs before adoptive transfer to LPS-injured mice.

152 type-B receptor 1 (EphB1) is upregulated in injured motor neurons, which in turn can activate astroc

153 survival in the bloodstream of the thermally injured mouse during sepsis.

154 s, NMN deamidase reduces NMN accumulation in injured mouse sciatic nerves and preserves some axons fo

155 at trkB.T1 is significantly increased in the injured mouse spinal cord, where it is predominantly fou

156 Restitution of injured mucosa involves the recruitment of immune cells,

157 ex quantitative proteomics screen of acutely injured murine kidneys.

158 descendant populations, which fuse with the injured muscle fiber.

159 Such cells failed to accumulate in acutely injured muscle of old mice, known to undergo ineffectual

160 ently proliferate upon injury and regenerate injured muscles, but continually decline during regenera

161 ed myoblasts and impairs the regeneration of injured muscles.

162 ice exhibited fewer suppressive Tregs in the injured myocardium and decreased expression of the gene

163 on as a result of increased myeloid invading injured myocardium in response to MI.

164 lowing MI rescued Treg infiltration into the injured myocardium of YAP/TAZ mutants and decreased fibr

165 However, the mechanisms by which injured myocardium recruits suppressive immune cells rem

166 (+) M2-like macrophages predominantly in the injured myocardium, compared to the control.

167 cells (CPCs), and their potential to recover injured myocardium.

168 vel and promising approach to regenerate the injured myocardium.

169 a novel clinical approach to regenerate the injured myocardium.

170 hich impair overall reparative potential for injured myocardium.

171 on promotes fusion of exogenous myoblasts to injured myofibers.

172 ring the endogenous molecules to salvage the injured neighboring cells by regulating apoptosis, infla

173 However, in the injured nerve it was detrimental and resulted in delayed

174 ich maintains macrophage infiltration to the injured nerve, and sends paracrine signals to activate T

175 ts define novel morphological transitions in injured nerves and show that repair Schwann cells have a

176 elongated cells that build Bungner bands in injured nerves and that such cells can transform to myel

177 red nerve conduit that was applied to bridge injured nerves in a rat sciatic nerve transection model.

178 rowth of axons through the proximal parts of injured nerves repair, Schwann cells gradually lose rege

179 ent with the fact that tumors do not form in injured nerves, although they contain proliferating Schw

180 In injured nerves, this transcription factor promotes the r

181 We visualize these injured neural dynamics by mapping them onto the worm's

182 xplored in prospective studies of critically injured neurological patients.

183 gy and secrete inflammatory factors that can injure neurons directly or via activation of neurotoxic

184 ctions of C3 on regeneration and survival of injured neurons after SCI.

185 reduction in positive Fluoro-Jade B stained injured neurons and microglial activation.

186 found minimal transcriptional changes in non-injured neurons at 7 days after SNI.

187 the impact of microglial exosomal miRNAs on injured neurons in this research.

188 coordinate regulation of gene expression in injured neurons involving multiple pathways was central

189 euronal functions, as cytoskeleton dynamics, injured neurons regeneration, synaptic plasticity.

190 mediates a cross talk between astrocytes and injured neurons that promotes synaptic recovery in the i

191 s with elimination of inhibitory inputs onto injured neurons, including those formed onto dendritic s

192 that axonal fusion restores full function to injured neurons, is dependent on exposure of phospholipi

193 s to form cells that support the survival of injured neurons, promote axon growth, remove myelin-asso

194 navigation, plasticity, and regeneration of injured neurons.

195 p inhibited neuronal inflammation in scratch-injured neurons.

196 ng nicotinamide adenine dinucleotide flux in injured neurons.

197 aptic excitability, and inhibitory inputs at injured neurons.

198 cifically collect individual injured and non-injured nociceptive DRG neurons and to define their gene

199 nalysis of the transcriptomic profile of the injured nociceptors revealed oxidative stress as a key b

200 t, several novel transcripts were altered in injured nociceptors, and the global signature of these L

201 y and demonstrate layer-by-layer analysis of injured ocular vasculature.

202 These findings link phagocytosis of injured oligodendrocytes, a pathological hallmark of MS

203 Intratracheal delivery of stem cells into injured or diseased lungs can provide a variety of thera

204 that remodeling of the fibronectin matrix in injured or diseased tissue elicits an EDA-dependent fibr

205 ploiting endogenous stem cells to regenerate injured or diseased tissue may circumvent these challeng

206 ies for long-term repair and regeneration of injured or diseased tissues and organs.

207 dily applied to image wound healing in other injured or diseased tissues, or to monitor tissue change

208 More men were injured or killed by landmines or UXO than were women (0

209 however, it is unclear how the type of cells injured or the mechanism of injury activates these pathw

210 In the commonly injured orbitofrontal and temporal pole regions CoV was

211 investigate that BMSCs deliver miR-9 to the injured pancreas or peripheral blood mononuclear cell (P

212 c the effects of pri-miR-9-BMSCs and protect injured pancreas.

213 r topical application, the MSCs homed to the injured parenchyma and improved the neurological functio

214 s not feasible or proves unacceptable to the injured patient.

215 , including the highest number of critically injured patients (10 of 12).

216 tometry analyses on a total of 70 critically injured patients (Injury Severity Score [ISS] >/= 25) at

217 med flow cytometry analyses in 34 critically injured patients and compared findings with those of 9 h

218 is still a common cause of death in severely injured patients and is characterized by impairment of o

219 Severely injured patients frequently suffer compromised fracture

220 In the transcriptome cohort, 20 critically injured patients later developed MODS.

221 entional events, younger, and less seriously injured patients less likely to participate; therefore,

222 ng overtime hours were required to treat the injured patients on the day of the event.

223 f care, injury severity, and mortality among injured patients served by 9-1-1 emergency medical servi

224 fection and organ dysfunction than similarly injured patients that did not (P < 0.05).

225 Of the 53487 injured patients transported by EMS (17633 patients in t

226 oard the flight, 192 were injured; 63 of the injured patients were initially evaluated at San Francis

227 ared transcriptome findings in 36 critically injured patients with those of 6 patients with minor inj

228 e the longer-term health status of seriously injured patients, identify predictors of outcome, and es

229 As PIE affects as many as 20% of brain-injured patients, reliable biomarkers are imperative bef

230 In cohorts of severely injured patients, there are distinct, identifiable trans

231 equal numbers of violently and nonviolently injured patients.

232 were differentially expressed in critically injured patients.

233 of inflammation and coagulation in severely injured patients.

234 teria prescribe specific transport rules for injured patients.

235 l population.SIGNIFICANCE STATEMENT Although injured peripheral nerves contain repair Schwann cells t

236 environment.SIGNIFICANCE STATEMENT Repair of injured peripheral nerves remains a critical clinical pr

237 Functional recovery of injured peripheral neurons often remains incomplete, but

238 to CD4(+) T cells following phagocytosis of injured, phosphatidylserine-exposing oligodendroglial ce

239 Although fusion between injured proximal axon and distal fragment has been obser

240 on of the C5a active receptor (C5aR/CD88) by injured pulp fibroblasts controls the direction of neuri

241 nterface in direct contact with irreversibly injured pulp tissue.

242 retrograde dendritic spine loss at directly injured pyramidal neurons followed by retrograde presyna

243 oral changes of the elastic stiffness of the injured rat neocortex and spinal cord at 1.5 and three w

244 ate or NMDA was injected directly into crush-injured rat sciatic nerves, ERK1/2 phosphorylation was o

245 l MSCs transplanted onto the cortex of brain injured rats with TBI.

246 ng respiration-competent mitochondria to the injured region.

247 at is seen in other mammals, the majority of injured retinal ganglion cells (RGCs) survive with relat

248 py may serve to replace or resurrect dead or injured retinal neurons.

249 Furthermore, injured RGCs display activated signal transducer and act

250 of maturation, despite implantation into the injured rodent spinal cord, yet they support delayed fun

251 motor function in motor complete spinal cord injured (SCI) individuals is poor.

252 iously reported that myelin clearance in the injured sciatic nerve proceeds unhindered in the Ccr2(-/

253 In injured SECs, endothelin-1 blocked CAV1 phosphorylation

254 1, and CAV1 phosphorylation was increased in injured SECs, resulting in increased GRK2-CAV1 interacti

255 expansions of hepatocyte stem/progenitors at injured sites that are lineage but not fate restricted.

256 Injured skeletal muscle regenerates, but with age or in

257 types; hence, it may affect regeneration of injured skeletal muscle.

258 tion, lead to concomitant compression of the injured spinal cord and neuronal death.

259 d macrophage-specific mRNA directly from the injured spinal cord and performed RNA sequencing to inve

260 n macrophage-specific mRNA directly from the injured spinal cord in mice and performed RNA sequencing

261 y molecule associated with scar formation in injured spinal cord.

262 upportive environment for axon growth in the injured spinal cord.

263 majority of myelinating Schwann cells in the injured spinal cord; invasion of peripheral myelinating

264 stronger in those sections from mechanically injured spinal cords.

265 into the injured DRGs (defined as DRGs with injured spinal nerves) of living SNL rats.

266 trix proteins not previously associated with injured spinal tissue, including small proteoglycans inv

267 n and an overall healthier and less severely injured study population than previously reported.

268 150 healthy controls and communicative brain-injured subjects in various states of conscious wakefuln

269 propriate inflammatory conditions where they injure the host, leading to the death of the neutrophils

270 A total of 10 Gy irradiation was used to injure the intestinal epithelium and induce subsequent c

271 gastric refluxate is a noxious material that injures the esophagus and elicits symptoms.

272 n reactive nitrogen species damages axons by injuring their mitochondria and inducing demyelination.

273 When skin is injured, there is a massive increase of heat shock prote

274 designed to selectively release morphine in injured tissue and to prevent blood-brain barrier permea

275 and confirmed that DRP1 has a vital role in injured tissue regeneration.

276 fferentiation of stem cells, responsible for injured tissue repair, and simultaneously discourage bac

277 ing on skin and mucosa, but poised to invade injured tissue to cause local infections.

278 large baseline ischemic cores (irreversibly injured tissue).

279 transcriptional profiles were obtained from injured tissue.

280 ir native environment or conditions found in injured tissue.

281 ed in serum, cerebrospinal fluid, and in the injured tissue.

282 the chemokine receptor CCR2 to gain entry to injured tissues from the bloodstream, are purportedly ne

283 important for T cells to access inflamed or injured tissues with abrupt topographical changes.

284 usively intracellular (except in diseased or injured tissues), our data show that schistosomes displa

285 EMS) technicians arriving with intentionally injured trauma patients from January 1 to December 31, 2

286 This report of a severely injured trilobite from the Middle Ordovician ( 465 Ma) a

287 C motif ligand 8 (CXCL8)/CXCL1 expression by injured tubular cells.

288 nd perform the critical tasks of dismantling injured vessels and creating channels for new vascular r

289 d factor (VWF) mediates platelet adhesion to injured vessels by sequestering platelets from blood flo

290 sis by forming aggregates that plug holes in injured vessels.

291 gration of transplanted converted cells into injured vessels.

292 However, in the corneas injured via DM stripping, most of the cells in the poste

293 l degeneration or axonal regrowth within the injured visual system.

294 expression levels are upregulated in balloon-injured vs. uninjured VSMCs.

295 and interaction of all SOC components in the injured VSMCs, where Homer1 interacts with Orai1 and var

296 tion when the concerned spinal segments were injured was studied in 384 patients with clinically comp

297 ointimal hyperplasia compared with similarly injured wild-type controls.

298 accumulation of the apoptosis probes at the injured xiphoid cartilage site.

299 number of apoptotic chondrocytes within the injured xiphoid cartilage, which was confirmed by TUNEL

300 proportionately sampled group of non-assault-injured youth enrolled from September 2009 through Decem