ライフサイエンスコーパス: injury

1 tivity to ischemia- and reperfusion- induced injury).

2 and contribute to alcohol-induced hepatocyte injury.

3 ial development, maturation, and response to injury.

4 mals that fully regenerates even after major injury.

5 increased cardiomyocyte proliferation after injury.

6 ce to generate neurons from MG after retinal injury.

7 ntestinal epithelial cell (IEC) responses to injury.

8 minating clinical outcome in traumatic brain injury.

9 estricted in distribution to sites of tissue injury.

10 ietic vascular niches after myelosuppressive injury.

11 3 of 60 patients (5%) who had an orthopedic injury.

12 and make a modest contribution to glomerular injury.

13 regulatory T cell after ischemia-reperfusion injury.

14 erful approach to monitoring post-transplant injury.

15 ces, specifically for severe traumatic brain injury.

16 n the ER, contributes to apoptosis and organ injury.

17 d by autoreactive T cells that contribute to injury.

18 phagy has a protective effect on acute liver injury.

19 neuroprotective properties in models of CNS injury.

20 platelet accumulation at the site of vessel injury.

21 ive capabilities against myocardial ischemic injury.

22 (for which there was no recorded adversity) injury.

23 neural stem cell numbers in areas of tissue injury.

24 erate and generate new endothelium following injury.

25 lays a central role in the response to brain injury.

26 se abnormalities persisted to 120 days after injury.

27 entially incorporated into clots after laser injury.

28 -hospital or pitch-side test to detect brain injury.

29 arker and pathway discovery after myocardial injury.

30 rostatin-1 during renal ischemia-reperfusion injury.

31 he optic nerve (ON) head at 9 hours after ON injury.

32 ating hematopoietic reconstitution following injury.

33 s, contributing to the development of kidney injury.

34 epithelial cells during ischemia-reperfusion injury.

35 cted lupus-prone MRL/Lpr mice from end-organ injury.

36 lean tissue recovery following a severe burn injury.

37 d against ischemia-reperfusion-induced renal injury.

38 duced in the lesion site up to 2 weeks after injury.

39 a/reactive oxygen species (ROS)-induced lung injury.

40 the regenerative response to skeletal muscle injury.

41 c significance of phagocytosis during tissue injury.

42 , mechanically ventilated pigs, without lung injury.

43 stase (NE) expression induced by obstructive injury.

44 istent with the absence of progressive graft injury.

45 female mice, neither before nor after nerve injury.

46 cate 20% as a threshold of more severe liver injury.

47 chanisms that restore tissue integrity after injury.

48 involved in recovery of hand function after injury.

49 PAI-1 also regulates fibrosis during cardiac injury.

50 s restoration of tissue that has suffered an injury.

51 isplayed preserved axons up to 4 weeks after injury.

52 icial in the setting of critical illness and injury.

53 ic shear stress on RBC-induced microvascular injury.

54 in the pathogenesis of this form of hepatic injury.

55 r work functioning were not found late after injury.

56 rleukin-17 and interleukin-22 by day 5 after injury.

57 arette smoke, silica, or sepsis-induced lung injury.

58 ay be therapeutic in settings of acute liver injury.

59 ld or to recover basic movement after neural injuries.

60 onment was the most common location for most injuries.

61 ated adverse events included musculoskeletal injuries.

62 d January 1, 2015, with blunt or penetrating injuries.

63 nal ligaments (P = .412), or disk (P = .665) injuries.

64 he need for CT imaging in children with head injuries.

65 t-years), including the rate of acute kidney injury (7.1 and 6.2 events per 1000 patient-years, respe

66 frequent (23 cases), followed by open globe injuries (8 cases).

67 gth of stay, lower incidence of acute kidney injury, acute respiratory distress syndrome, and need fo

68 cal, and immunological components of retinal injury after alkali burn and explored a novel neuroprote

69 ance of neurovascular disease and subsequent injury after ischemic events, fundamental knowledge in t

70 d impacts inter-individual susceptibility to injury after preterm birth.Inflammation mediated by micr

71 Treatment of secondary injury after severe traumatic brain injury based on brai

72 ty increased in individuals with spinal cord injury after the I-wave protocol.

73 Patients with severe extracranial injuries (AIS >/= 3), death within 72 hours, or hospital

74 Acute kidney injury (AKI) in children is associated with poor short-t

75 One year after injury, AKI was associated with development of chronic k

76 t features in the pathogenesis of acute lung injury (ALI).

77 y between different types of self-harm: self-injury alone pound753 (SD 2061), self-poisoning alone po

78 ears, seeking ED care for an assault-related injury and a proportionately sampled group of non-assaul

79 wn program of liver regeneration after acute injury and allow for exploration of latent regenerative

80 aspects of metabolic alterations after burn injury and as a novel potential molecular target to impr

81 cate that the evolution of grey/white matter injury and blood-brain barrier disruption after ICH can

82 Interestingly, both the renal injury and dysfunction in wild-type mice undergoing iAKI

83 de that chronic cutaneous injury can lead to injury and dysfunction of the most distal part of small

84 othermia by DHC on long-term ischemic stroke injury and functional outcome.

85 More recently, the presence of epithelial injury and inflammation in the airways of athletes was d

86 Its overuse provokes liver injury and it is the second most common cause of liver f

87 scle stem cells, is altered following a burn injury and likely hinders regrowth of muscle.

88 le immune pathways responsible for allograft injury and loss.

89 etection methods, as well as mechanism(s) of injury and mitigation in patients after radiotherapy or

90 ooming is a common practice that can lead to injury and morbidity.

91 d energy against the accompanying dangers of injury and predation.

92 functional outcomes by both reducing tissue injury and promoting the development of reparative macro

93 p < 0.05) decreased acute necrotic/apoptotic injury and significantly (p < 0.05) improved function an

94 psychological disorders, cancer, organismal injury and skeletal and muscular disorders, as well as n

95 platelets to thrombosis at sites of arterial injury and that platelets contribute to venous thrombosi

96 ification (HO) after blast-related extremity injury and traumatic injuries, respectively.

97 ent with right ankle pain after an inversion injury and underwent plain radiography.

98 CD6 plays any role in intestinal I/R-induced injury and, if so, the underlying mechanisms, remain unk

99 r than 20 (n = 10) at days 1, 3, and 5 after injury, and age- and gender-matched controls.

100 min excretion, segmental sclerosis, podocyte injury, and apoptosis.

101 iates reversible and irreversible myocardial injury, and it is a strong predictor of left ventricular

102 traumatic brain injury, ischemia-reperfusion injury, and kidney degeneration in mammals and is also i

103 nctionally regenerate their retina following injury, and Muller glia (MG) are the source of regenerat

104 les and brain injury topography, severity of injury, and prematurity-related clinical complications.

105 hage, hemorrhagic transformation of ischemic injury, and presumed perinatal hemorrhagic stroke.

106 rlying epileptogenesis after pediatric brain injury, and provide evidence of IL-1 signaling as a medi

107 s, including in a mouse model of optic nerve injury, and show that the same pathway is active in huma

108 in JG cells of adult mice results in kidney injury, and suggest that JG cells are critically involve

109 ent of hyperchloremic acidosis, acute kidney injury, and survival among those with higher and lower c

110 nts with important injuries, while excluding injury, and the need for imaging in many patients.

111 egenerative and regenerative processes after injury are still controversial and insufficiently charac

112 death in the everolimus group (acute kidney injury associated with diarrhoea), and two deaths in the

113 iated by microglia plays a key role in brain injury associated with preterm birth, but little is know

114 rd injury (cervical level 4, American Spinal Injury Association Impairment Scale category A).

115 nvasively image kidney dysfunction and local injuries at the anatomical level.

116 eved in part by reducing macrophage-mediated injury at the lesion epicenter.

117 reperfusion leads to local and remote organ injury attributed to inflammatory response during the re

118 Mild blast traumatic brain injury (B-TBI) induced lasting cognitive impairments in

119 econdary injury after severe traumatic brain injury based on brain tissue oxygenation and intracrania

120 in breakdown products, SBDPs) and glial cell injury biomarker, glial fibrillary acidic protein (GFAP)

121 Proteolytic neuronal injury biomarkers (alphaII-spectrin breakdown products,

122 We evaluated the expression of brain injury biomarkers on postsurgical brain tissue obtained

123 ated with PLC (P < .001) and arch (P = .006) injuries but not with body (P = .056), longitudinal liga

124 the protection against H/R-induced myocytes injury by AS-1.

125 mary response gene 88), or after superficial injury by blotting with tissue paper.

126 ts were identified as having sustained minor injury by the combination of three standard criteria inc

127 We conclude that chronic cutaneous injury can lead to injury and dysfunction of the most di

128 ant was a 53-year-old man with a spinal cord injury (cervical level 4, American Spinal Injury Associa

129 lidated in an independent planned myocardial injury cohort (n=15; P<1.33E-04, 1-way repeated measures

130 The major mechanism of skin injury common to these exposures is radiation-induced ox

131 Severe acute kidney injury conferred an increased risk of death by day 28 af

132 s suggest that signals from diverse modes of injury converge on p38alpha mitogen-activated protein ki

133 n these results, the Children's Intracranial Injury Decision Aid score is a potentially novel tool to

134 of a physical injury, evidence of anatomical injury defined as minor by an injury severity score betw

135 ptides, we determined that thrombin-mediated injury depended upon interactions between protease-activ

136 In the immature lung, inflammation and injury disrupt the epithelial-mesenchymal interactions r

137 sion tensor imaging (DTI) to identify axonal injury distant from contusions.

138 Although secondary ocular blast injuries due to flying debris are more common, primary o

139 of extracellular histones in that pulmonary injury during influenza was exacerbated.

140 cules into the brain contributes to neuronal injury during stroke and other cerebrovascular diseases.

141 or preterm infants with diffuse white matter injury (DWMI) caused by hypoxia.

142 Following peripheral axon injury, dysregulation of non-coding microRNAs (miRs) occ

143 All cases of drug-induced liver injury enrolled into a prospective database over a 10-ye

144 roximately 30% of myelinated spinal axons at injury epicenter 3 months after SCI, demonstrating that

145 nderscore the importance of documenting head injuries even within the mild range as they may interact

146 nt for medical care within 24h of a physical injury, evidence of anatomical injury defined as minor b

147 e dentistry aims to heal dental tissue after injury, existing polymeric restorative materials, or fil

148 suggests that the link between AF and brain injury extends beyond thromboembolic complications to in

149 e-related increases in proteinuria, podocyte injury, fibronectin accumulation, TGF-beta expression, a

150 ion of Hif1alpha developed less-severe liver injury following administration of ethanol, injection of

151 apacity that could be used as a biomarker of injury for outcome prediction or target for rehabilitati

152 Following cartilage injury, Gdf5-lineage cells underpin synovial hyperplasia

153 erular damage due to glycerol-induced kidney-injury had strongest impact on DY-654 elimination.

154 oor outcome following severe traumatic brain injury has been reported in observational studies.

155 ischemia contributes to ischemia/reperfusion injury has not been thoroughly studied.

156 iled ventilator liberation, and acute kidney injury +/- hemodialysis requirement.

157 How McSCs respond to injury, however, remains largely unknown.

158 ynthesizing enzyme serine racemase after CCI injury improved synaptic plasticity, brain oscillations,

159 h turning compliance and preventing pressure injuries in acutely ill patients.

160 alence to measure the burden of diseases and injuries in Japan and in the 47 Japanese prefectures fro

161 t protects mice from ventilator-induced lung injury in a manner independent of neutrophil recruitment

162 ibitor significantly reduced renal allograft injury in a model of severe antibody-mediated damage in

163 the strongest association with acute kidney injury in a replication patient population containing 20

164 drug-related or alcohol-related and violent injury in adolescence.

165 We report that, after spinal cord contusion injury in adult female mice, the biosynthesis of SPM is

166 In this study, we performed optic nerve injury in adult naked mole-rats, the longest living rode

167 blockade decreases IRI and subsequent tissue injury in DCD renal allografts in a large animal transpl

168 mon cause of morbidity after traumatic brain injury in early childhood.

169 causes complement-dependent endothelial cell injury in kidney transplants, as assessed by expression

170 es recovery after traumatic spinal contusion injury in mice, a benefit achieved in part by reducing m

171 e regeneration following cardiotoxin-induced injury in mice.

172 g for the treatment of chronic demyelinating injury in multiple sclerosis.

173 ventilation is used to prevent further lung injury in patients on invasive mechanical ventilation.

174 Furthermore, renal injury in preeclampsia associated with an elevated urina

175 ine externalization immediately after axonal injury in purified retinal ganglion cells.

176 er unilateral sciatic nerve entrapment (SNE) injury in rats.

177 accumulation occurs and contributes to renal injury in SLE.

178 clear attenuation of ventilator-induced lung injury in terms of respiratory mechanics, blood gases, a

179 ltrasound stimulation protects against brain injury in the hippocampus and corpus callosum in rats wi

180 downstream of BMP antagonism for response to injury in the neonatal brain.

181 uate the histologic characteristics of graft injury in the presence of anti-angiotensin II type 1 rec

182 ization of bleeding after a severe tail clip injury in these mice.

183 nd the mechanism of recovery following nerve injury in this species we investigated the process of ax

184 ected cortical neurons from slow excitotoxic injury in vitro, without influencing NMDA-induced intrac

185 s and 79 risk factors of death, disease, and injury incidence and prevalence to measure the burden of

186 of these compounds on retinal neurovascular injury induced by hyperglycemia.

187 (DRG) neurons, which may contribute to nerve injury-induced neuropathic pain.

188 neuron, significantly attenuated ultraviolet injury-induced sensitization.

189 We conclude that dysferlin prevents injury-induced SR Ca(2+) leak.

190 Nerve injury induces changes in gene transcription in dorsal r

191 Since injury induces loss of this interaction, we hypothesized

192 ulation in the kidney and renal dysfunction, injury, inflammation, and fibrosis.

193 rt a model in which acute inflammation after injury initiates important regenerative signals in part

194 in) protected mice from ischemia-reperfusion injury (IRI).

195 itment to damaged tissues upon acute sterile injuries is necessary for clearance of necrotic debris a

196 hepatic stellate cells (HSCs) in response to injury is a key step in hepatic fibrosis, and is charact

197 To examine whether acute kidney injury is associated with delirium and coma in criticall

198 Acute kidney injury is associated with high mortality, especially in

199 Acute kidney injury is common and is associated with poor outcomes, i

200 Risk of brain injury is increased during neonatal cardiac surgery, whe

201 Reperfusion injury is largely attributed to excess mitochondrial pro

202 preventing contrast-associated acute kidney injury is marginal, if any.

203 Subcortical white matter injury is often accompanied by orofacial motor dysfuncti

204 nd diversity and the magnitude of myocardial injury is responsible for the resolving and nonresolving

205 t mammalian cardiomyocyte regeneration after injury is thought to be minimal.

206 edicaid expansion with hospitalization after injury is vital in the disposition planning for these pa

207 e, intracerebral hemorrhage, traumatic brain injury, ischemia-reperfusion injury, and kidney degenera

208 Before injury, leukocytes are near the vascular region, that is

209 ells in rats with renal ischemia-reperfusion injury, mainly by mitogenic, angiogenic, and anti-inflam

210 Cellular injury markers lactate dehydrogenase and aspartate amino

211 ity promotes hyperlipidemia and hypothalamic injury, MC4R agonists are nevertheless more effective to

212 ion, 39% (574 of 1461) had signs of thoracic injuries (men, 74.0% [425 of 574]; mean age, 46.6 years;

213 cclusion, or neonatal hypoxic-ischemic brain injury, Mn preferentially accumulated in perilesional ti

214 d stem cells in a renal ischemia-reperfusion injury model.

215 adiponectin, apolipoprotein C-I, and kidney injury molecule-1).

216 37.8%; p < 0.001) and varied by type of CNS injury; mortality was 79.6% in patients with intracrania

217 ogical disorders such as stroke, spinal cord injury, multiple sclerosis, amyotrophic lateral sclerosi

218 s had respiratory conditions (n = 387; 18%), injuries (n = 289; 13%), nonspecific signs and symptoms,

219 admission (n = 1388) and at 12 months after injury (n = 852).

220 ous system pathologies with prominent myelin injury, namely, progressive multifocal leukoencephalopat

221 at is similar to the ventilator-induced lung injury observed in mechanically ventilated patients.

222 Injury of CNS nerve tracts remodels circuitry through de

223 Modulation of cathepsin activity may prevent injury of organs exposed to ischemia.

224 diers is adversely affected by the death and injury of other unit members, but whether risk of suicid

225 Neuronal injury often leads to devastating consequences such as l

226 Injury or disease to the CNS results in multifaceted cel

227 d organs to assist in their maintenance upon injury or stress.

228 drug-related or alcohol-related, or violent injury) or accident-related (for which there was no reco

229 patients (2.5%) without severe acute kidney injury (P<0.001).

230 before injury versus 12.5+/-0.2 microm after injury; P<0.001).

231 ormalities in a cohort of 97 traumatic brain injury patients were also mapped at the grey matter-whit

232 nction among moderate-severe traumatic brain injury patients.

233 pound806 (SD 1568), self-poisoning and self-injury pound987 (SD 1823; p<0.0001).

234 ote safe work practices for patient handling injury prevention.

235 define the nature and extent of soft tissue injuries prior to physical therapy.

236 l outcomes associated with mortality in this injury process.

237 le in controlling OB-ISCs in homeostasis and injury repair, which is likely to be crucial in preventi

238 during ordinary tissue turnover or following injury represents a central biological problem.

239 blast-related extremity injury and traumatic injuries, respectively.

240 gement of platelet GPIbalpha is required for injury responses in diverse disease models.

241 life span exceeding 30 years, and found that injury responses in this species are quite distinct from

242 e transcriptional programs uncovered several injury-responsive genes across regenerative and nonregen

243 Spasms after spinal cord injury (SCI) are debilitating involuntary muscle contrac

244 Also, in rat T9-T10 hemisection spinal cord injury (SCI), we demonstrated that the tailored scaffold

245 nge in CaN expression and localization after injury, SCI induced upregulation of the native regulator

246 sis (King's Outcome Scale for Childhood Head Injury score < 5a) in the development cohort.

247 On multivariate regression controlling for injury severity and demographic variables, the differenc

248 uman blunt trauma patients (n = 472, average injury severity score [ISS] = 20.2) exhibited elevations

249 of anatomical injury defined as minor by an injury severity score between 2 and 8 and normal physiol

250 PATIENTS OR Trauma patients with injury severity scores greater than 20 (n = 10) at days

251 or demographics, mechanism, vital signs, and injury severity.

252 to reduce risks of harm after self-inflicted injury should be extended to drug-related or alcohol-rel

253 pposite, roles in motor recovery after brain injury.SIGNIFICANCE STATEMENT The dorsal and ventral pre

254 ation or axonal regeneration after acute CNS injury.SIGNIFICANCE STATEMENT The roles of microglia, th

255 at local adenosine generated by cells at the injury site is critical for protection from IRI through

256 tion of these tasks, they neither die at the injury site nor are phagocytosed.

257 myelin and Remak Schwann cells distal to the injury site reorganize and modify their properties to fo

258 is, approximately 100-300 mum away from the injury site.

259 Upon injury, stem cells increase proliferation, followed by l

260 lar ATP and UTP molecules released following injury/stress.

261 s study was to determine the types of ocular injuries sustained in the earthquake in Nepal and its ma

262 axis in patients with severe traumatic brain injuries (TBI).

263 Traumatic brain injury (TBI) causes extensive neural damage, often resul

264 Traumatic brain injury (TBI) is a serious public health problem, often w

265 Traumatic brain injury (TBI) is extremely common across the lifespan and

266 Traumatic brain injury (TBI) is known to cause perturbations in the ener

267 on-specific enolase (NSE), a traumatic brain injury (TBI) protein biomarker, in diluted blood plasma

268 inantly been described after traumatic brain injury (TBI), in which it is associated with worse outco

269 g, is dysregulated following traumatic brain injury (TBI), suggesting that stimulation of BDNF signal

270 luding Alzheimer disease and traumatic brain injury (TBI).

271 lence, 25.6%), with more women sustaining an injury than men (868 [27.1%] vs 562 [23.7%]; P = .01).

272 , hemolytic anemia, schistocytes, and tissue injury that characterize TTP.

273 suggest that these patients may develop lung injury that is similar to the ventilator-induced lung in

274 PFOS was found to induce Sertoli cell injury through disruptive effects on actin microfilament

275 opment to refine neuronal connections, after injury to clear damaged neurons, or pathologically durin

276 impair hepatocyte proliferation during liver injury to evaluate the contribution of non-hepatocytes t

277 myloidosis and neurodegeneration or neuronal injury to more fully characterise the heterogeneous path

278 er regeneration.SIGNIFICANCE STATEMENT After injury to peripheral nerves, the myelin and Remak Schwan

279 cipation in sports has resulted in increased injury tolls due to shifts toward participation in compe

280 red cerebellar metabolite profiles and brain injury topography, severity of injury, and prematurity-r

281 n rodents following photothrombotic cortical injury, transient middle cerebral artery occlusion, or n

282 ion that affects how patients with traumatic injury (trauma patients) interact with locoregional heal

283 43 patients (11.0%) with severe acute kidney injury versus 105 of the 4140 patients (2.5%) without se

284 ter AKI (mean+/-SEM: 3.3+/-0.1 microm before injury versus 12.5+/-0.2 microm after injury; P<0.001).

285 d into a rat model of radiation-induced lung injury via endotracheal (ET) or intravascular (IV) admin

286 reatment mitigates cold IRI-associated renal injury via mitochondrial actions and could represent a n

287 Contrast-associated acute kidney injury was a secondary end point.

288 Acute tubular and glomerular renal injury was accompanied by nonheme iron deposition and hy

289 Severe acute kidney injury was associated with increased use of mechanical v

290 Closed globe injury was most frequent (23 cases), followed by open gl

291 mon carotid artery (CCA) balloon angioplasty injury was performed in rats.

292 Grooming-related injury was reported by 1430 groomers (weighted prevalenc

293 ed to determine variables predicting whether injuries were reported.

294 Only 566 (66%) of 850 injuries were reported.

295 vels and ErbB2 receptor expression after PNS injury were disrupted in the absence of alphaBC.

296 lls without CD4(+) cells mediated glomerular injury when MPO was planted in glomeruli.

297 All causes of renal allograft injury, when severe and/or sustained, can result in chro

298 an reliably identify patients with important injuries, while excluding injury, and the need for imagi

299 odontoblastic processes 2 wk following tooth injury without pulp exposure, whereas EphB2 was expresse

300 nse against pathogen exposure and epithelial injury, yet little is known about how enteropathogens ma