ライフサイエンスコーパス: traumatic brain injury

1 Canadian provinces, specifically for severe traumatic brain injury.

2 y mechanical impact in a mouse model of mild traumatic brain injury.

3 ma are serious complications of ischemic and traumatic brain injury.

4 tical function in patients with acute severe traumatic brain injury.

5 uces an SIR compatible with ischemia or mild traumatic brain injury.

6 11A-31 on learning and memory outcomes after traumatic brain injury.

7 tic role of early MRI in moderate and severe traumatic brain injury.

8 f systolic dysfunction after moderate-severe traumatic brain injury.

9 ty in brains of athletes with sports-related traumatic brain injury.

10 he best outcome predictors for patients with traumatic brain injury.

11 ions about sport-related concussion and mild traumatic brain injury.

12 flammatory cytokine expression in a model of traumatic brain injury.

13 o, we evaluated the outcome in two models of traumatic brain injury.

14 h for preserving neurological function after traumatic brain injury.

15 e compared to controls immediately following traumatic brain injury.

16 d, and there is no efficacious treatment for traumatic brain injury.

17 iscrete phenomenon in the pathophysiology of traumatic brain injury.

18 n in a unique sample of combat veterans with traumatic brain injury.

19 vivo needle prick model to mimic sequelae of traumatic brain injury.

20 teractions between four treatments following traumatic brain injury.

21 and has a beneficial effect on outcome after traumatic brain injury.

22 cohort consisted of 817 subjects with severe traumatic brain injury.

23 Sedated patients with severe traumatic brain injury.

24 e lesions are comparable with impact-induced traumatic brain injury.

25 tic amnesia is very common immediately after traumatic brain injury.

26 rologic disorders as diverse as migraine and traumatic brain injury.

27 ng that axonal integrity is maintained after traumatic brain injury.

28 odel in which pathology arises from a single traumatic brain injury.

29 the subsequent outcome in 2 mouse models of traumatic brain injury.

30 the main causes of ongoing disability after traumatic brain injury.

31 inuous variable (p = 0.07) for patients with traumatic brain injury.

32 terns for discriminating clinical outcome in traumatic brain injury.

33 are still considered the most lethal type of traumatic brain injury.

34 the acute phase following moderate or severe traumatic brain injury.

35 omy for intraocular hemorrhages secondary to traumatic brain injury.

36 rebral edema is a key poor prognosticator in traumatic brain injury.

37 rising from neurodegenerative disease and/or traumatic brain injury.

38 dysfunction in patients with moderate-severe traumatic brain injury.

39 omy for intraocular hemorrhages secondary to traumatic brain injury.

40 ia has been used to attenuate the effects of traumatic brain injuries.

41 s-related concussion and other types of mild traumatic brain injuries.

42 at associated with impact-induced, non-blast traumatic brain injuries.

43 time with brain tissue hypoxia after severe traumatic brain injury (0.45 in intracranial pressure-on

44 , including (1) reducing SICU care for minor traumatic brain injury, (2) optimizing postoperative air

45 lfonylurea receptor-1 was detected in severe traumatic brain injury, absent in controls, correlated w

46 tive diseases and cognitive impairment after traumatic brain injury, all hallmarked by the accumulati

47 luding cases with and without chronic impact traumatic brain injuries and cases with chronic exposure

48 Increased aggression is common after traumatic brain injuries and may persist after cognitive

49 Seven (22%) moderate-severe traumatic brain injury and 0 (0%) mild traumatic brain i

50 in 32 patients with isolated moderate-severe traumatic brain injury and 32 patients with isolated mil

51 n hospital including 6516 (78%) after severe traumatic brain injury and 749 (9%) after severe thoraco

52 This study examined mild traumatic brain injury and genetic risk as predictors of

53 oderated mediation analysis showed that mild traumatic brain injury and high genetic risk indirectly

54 l thickness, such that individuals with mild traumatic brain injury and high genetic risk showed redu

55 ory neurotransmitter systems is common after traumatic brain injury and is an important cause of cogn

56 le in human cerebrospinal fluid after severe traumatic brain injury and is an informative biomarker o

57 its potential to guide targeted therapies in traumatic brain injury and other diseases involving cere

58 ages of 19 and 58, many of whom carried mild traumatic brain injury and post-traumatic stress disorde

59 ed 408 patients, 10 to 65 years of age, with traumatic brain injury and refractory elevated intracran

60 , decompressive craniectomy in patients with traumatic brain injury and refractory intracranial hyper

61 t develops following brain injuries, such as traumatic brain injury and stroke, and is often associat

62 egenerative pathway promotes pathogenesis in traumatic brain injury and suggest that anti-SARM1 thera

63 e oxygenation levels in patients with severe traumatic brain injury and the feasibility of a Phase II

64 n trauma systems, assess the contribution of traumatic brain injury and thoracoabdominal injury to ob

65 iously healthy patients with moderate-severe traumatic brain injury, and it is reversible over the fi

66 o the brain in mouse models of glioblastoma, traumatic brain injury, and Parkinson's disease.

67 us neurological disorders, including stroke, traumatic brain injury, and subarachnoid hemorrhage.

68 omy for intraocular hemorrhages secondary to traumatic brain injury, and the timing of vitrectomy in

69 rtex connectivity in the chronic phase after traumatic brain injury, and this abnormality was also ob

70 the United States over 1.7 million cases of traumatic brain injury are reported yearly, but predicti

71 egates in axons of the corpus callosum after traumatic brain injury as compared to Sarm1(+/+) mice.

72 degeneration, demonstrate multiple improved traumatic brain injury-associated phenotypes after injur

73 tribution of inflammatory conditions such as traumatic brain injury, autoimmune disorders, and infect

74 Mild blast traumatic brain injury (B-TBI) induced lasting cognitive

75 ) 10 years and older with moderate or severe traumatic brain injury (Barell Matrix Type 1 classificat

76 Treatment of secondary injury after severe traumatic brain injury based on brain tissue oxygenation

77 vitrectomy for Terson syndrome secondary to traumatic brain injury between 1997 and 2015.

78 s have been developed to standardize care in traumatic brain injury, between-center variation in trea

79 brain, has recently been linked to sleep and traumatic brain injury, both of which can affect the pro

80 Injury severity in blast induced Traumatic Brain Injury (bTBI) increases with blast overp

81 f the pathophysiology of mild, blast-induced traumatic brain injury (bTBI) the exposure of dissociate

82 s intracranial hypertension in patients with traumatic brain injury but was associated with harm in t

83 It has been consistently observed after traumatic brain injury, but whether axon degeneration is

84 We examined variation in treatment for traumatic brain injury by assessing factors influencing

85 Mice subjected to sham or traumatic brain injury by controlled cortical impact rec

86 Traumatic brain injury can lead to the neurodegenerative

87 In severe traumatic brain injury, cerebral perfusion pressure mana

88 in injury and 32 patients with isolated mild traumatic brain injury (comparison group) was assessed w

89 racic echocardiogram within 1 day after mild traumatic brain injury (comparison group).

90 e classified into post-traumatic amnesia and traumatic brain injury control groups, based on their pe

91 -channel head coil from each of 3 concussive traumatic brain injury (cTBI) patients and 4 controls tw

92 Long-term diffuse traumatic brain injury (dTBI) causes neuronal hyperexcit

93 Traumatic brain injury due to blast exposure is currentl

94 her neurologic conditions, including stroke, traumatic brain injury, encephalopathy, and dementia.

95 In patients with traumatic brain injury, ESA therapy did not increase the

96 ction with previous studies with axotomy and traumatic brain injury, establish SARM1 as the central d

97 ast exposure, five cases with chronic impact traumatic brain injury, five cases with exposure to opia

98 The major cause of delayed surgery was traumatic brain injury, followed by facial or orbital fr

99 ren with abusive head trauma from those with traumatic brain injury from other mechanisms.

100 ssment included history of playing rugby and traumatic brain injury, general and mental health, life

101 nsecutive children (age < 18 yr) with severe traumatic brain injury (Glasgow Coma Scale </= 8; intrac

102 ndred three patients with moderate or severe traumatic brain injury (Glasgow Coma Scale, 3-13).

103 Current prehospital traumatic brain injury guidelines use a systolic blood p

104 Autonomic impairment after acute traumatic brain injury has been associated independently

105 xygenation and poor outcome following severe traumatic brain injury has been reported in observationa

106 n injury, or to a single, moderate or severe traumatic brain injury, has led to an awareness that it

107 lecular pathways underlying the pathology of traumatic brain injury have not been defined, and there

108 Among males with mild traumatic brain injury, high genetic risk for Alzheimer'

109 Diagnosed with traumatic brain injury (HR = 4.09, 95% CI: 2.08, 8.05),

110 rognosis and Analysis of Clinical Trials in [Traumatic Brain Injury] (IMPACT) extended model sum scor

111 quantify benefits of hypothermia therapy for traumatic brain injuries in adults and children by analy

112 a is likely a beneficial treatment following traumatic brain injuries in adults but cannot be recomme

113 ophin receptor expression after experimental traumatic brain injury in adult mice.

114 pilepsy is a common cause of morbidity after traumatic brain injury in early childhood.

115 his platform to study metabolic responses to traumatic brain injury in hippocampal slice cultures, an

116 Propofol sedation at 24 hours after traumatic brain injury increased lesion volume, enhanced

117 sive care who had suffered a primary, closed traumatic brain injury; increased intracranial pressure;

118 Management of severe traumatic brain injury informed by multimodal intracrani

119 miR-124-3p in microglial exosomes following traumatic brain injury inhibits neuronal inflammation an

120 ls with intraocular hemorrhages secondary to traumatic brain injury, irrespective of the timing of vi

121 Traumatic brain injury is a major cause of death and dis

122 Traumatic brain injury is a major global public health p

123 impact (CCI) procedure in rats, we show that traumatic brain injury is associated with an increase in

124 These results provide evidence that mild traumatic brain injury is associated with greater neurod

125 ong-term mortality after head trauma without traumatic brain injury is elevated.

126 Clearly differentiating concussion from traumatic brain injury is essential to achieve reliable

127 Moderate-to-severe traumatic brain injury is one of the strongest environme

128 sue oxygenation-directed treatment of severe traumatic brain injury is warranted.

129 nogenesis, stroke, intracerebral hemorrhage, traumatic brain injury, ischemia-reperfusion injury, and

130 is the first-line imaging technique for all traumatic brain injury, it is incapable of providing lon

131 Prior studies have suggested that traumatic brain injury may affect cardiac function.

132 non-auditory effects of blast and potential traumatic brain injury may also exert an effect.

133 ity in the neuromonitoring setting of severe traumatic brain injury may carry novel pathophysiologica

134 Patients with acute severe traumatic brain injury may recover consciousness before

135 henotypes after injury in a closed-head mild traumatic brain injury model.

136 lgals-1(-/-) mice to develop spinal cord- or traumatic brain injury models for the evaluation of the

137 Results showed that mild traumatic brain injury moderated the relationship betwee

138 Repeated mild traumatic brain injuries (mTBI) may lead to serious neur

139 appropriate treatment of children with mild traumatic brain injury (mTBI) and intracranial injury (I

140 Evidence is accumulating that repeated mild traumatic brain injury (mTBI) incidents can lead to pers

141 Mild traumatic brain injury (mTBI) is an emerging risk for ch

142 Non-penetrating or mild traumatic brain injury (mTBI) is commonly experienced in

143 it remains unknown the extent to which mild traumatic brain injury (mTBI) may impact these critical

144 ) as a diagnostic tool in patients with mild traumatic brain injury (mTBI) with posttraumatic migrain

145 Mild traumatic brain injury (mTBI), also commonly referred to

146 ask (n = 35; phase 2b) and a brain MRI after traumatic brain injury (n = 23; phase 2c).

147 y of the neurodegeneration that occurs after traumatic brain injury, now termed chronic traumatic enc

148 l/glial DNA was identified in patients after traumatic brain injury or cardiac arrest; and exocrine p

149 olarization in the cerebral cortex following traumatic brain injury or cerebral ischemia, significant

150 oprotection in damaged tissue resulting from traumatic brain injury or cerebral ischemia.

151 le for meta-analysis were from patients with traumatic brain injury or subarachnoid hemorrhage.

152 disease, although it is unclear whether mild traumatic brain injury, or concussion, also confers risk

153 nboxers who were exposed to repetitive, mild traumatic brain injury, or to a single, moderate or seve

154 y, introducing a new variable of interest in traumatic brain injury outcome research.

155 nces (P < 0.0001); 11.1% to 26.0% for severe traumatic brain injury (P < 0.0001), and 4.7% to 5.9% fo

156 troke, AD, age-related macular degeneration, traumatic brain injury, Parkinson's disease, and other n

157 directed treatment of most blast-associated traumatic brain injuries, partly because the underlying

158 nylurea receptor-1 was present in all severe traumatic brain injury patients (mean = 3.54 +/- 3.39 ng

159 Data from 729 severe traumatic brain injury patients admitted between 1996 an

160 Adult traumatic brain injury patients admitted to intensive ca

161 The adult validation cohort comprised recent traumatic brain injury patients from San Gerardo Hospita

162 evere traumatic brain injury and 0 (0%) mild traumatic brain injury patients had systolic dysfunction

163 isodes of increased intracranial pressure in traumatic brain injury patients has been previously deve

164 nsor imaging abnormalities in a cohort of 97 traumatic brain injury patients were also mapped at the

165 rough standard behavioral assessments in 181 traumatic brain injury patients who had lost the ability

166 0 minutes in advance, in adult and pediatric traumatic brain injury patients.

167 One hundred nineteen severe traumatic brain injury patients.

168 fluid samples were collected from 28 severe traumatic brain injury patients.

169 f systolic dysfunction among moderate-severe traumatic brain injury patients.

170 orts of recently treated adult and pediatric traumatic brain injury patients.

171 sion pressure threshold management in severe traumatic brain injury patients.

172 Unlike other traumatic brain injury populations in children, female p

173 activation occurs after single and repeated traumatic brain injury, possibly through sports-related

174 of complex partial seizures (CPSs) following traumatic brain injury (post-traumatic epilepsy).

175 neuropathology; ibuprofen was preferred for traumatic brain injury, postcraniotomy, and thromboembol

176 ribed glymphatic system has been linked with traumatic brain injury, prolonged wakefulness, and aging

177 However, acute brain lesions, such as traumatic brain injury, reactivate developmental-like pr

178 tial Glasgow Coma Scale score for predicting traumatic brain injury recovery, but it takes days/weeks

179 mant as posttraumatic amnesia for predicting traumatic brain injury recovery, introducing a new varia

180 ssion could be used as an early predictor of traumatic brain injury recovery.

181 nsecutive patients undergoing CT imaging for traumatic brain injury recruited between January and Oct

182 but whether axon degeneration is a driver of traumatic brain injury remains unclear.

183 vidence that memory impairment acutely after traumatic brain injury results from altered parahippocam

184 Repetitive mild traumatic brain injury (rmTBI), resulting from insults c

185 of the Excellence in Prehospital Injury Care Traumatic Brain Injury Study.

186 duals experience a single moderate to severe traumatic brain injury suggest widespread persistent mic

187 ures of several brain pathologies, including traumatic brain injuries (TBI).

188 sm (VTE) prophylaxis in patients with severe traumatic brain injuries (TBI).

189 the blood-brain barrier (BBB) in response to traumatic brain injury (TBI) allows for the accumulation

190 is an important pathoanatomical subgroup of traumatic brain injury (TBI) and a major driver of morta

191 promise for clinical usefulness in suspected traumatic brain injury (TBI) and concussion.

192 with cognitive fatigue between persons with traumatic brain injury (TBI) and healthy controls (HCs).

193 Concomitant traumatic brain injury (TBI) and long bone fracture are

194 after injury and determine the influence of traumatic brain injury (TBI) and massive transfusion on

195 Objective reliable markers to assess traumatic brain injury (TBI) and predict outcome soon af

196 Studies of the association between traumatic brain injury (TBI) and suicide attempt have yi

197 ually, there are over 2 million incidents of traumatic brain injury (TBI) and treatment options are n

198 f veterans who sustained combat-related mild traumatic brain injury (TBI) are associated with scalar

199 The late effects of traumatic brain injury (TBI) are of great interest, but

200 Traumatic brain injury (TBI) can have lifelong and dynam

201 Traumatic brain injury (TBI) can induce cognitive dysfun

202 Traumatic brain injury (TBI) causes extensive neural dam

203 Traumatic brain injury (TBI) contributes to one third of

204 Traumatic brain injury (TBI) elicits an inflammatory res

205 cells in suppressing neuroinflammation after traumatic brain injury (TBI) in mice.

206 on individuals living with disabilities from traumatic brain injury (TBI) in the United States, and 8

207 Traumatic brain injury (TBI) increases the risk of Alzhe

208 The impact of traumatic brain injury (TBI) involves a combination of c

209 Traumatic brain injury (TBI) is a candidate for selectiv

210 Traumatic brain injury (TBI) is a clinically important e

211 Traumatic brain injury (TBI) is a common disabling condi

212 Traumatic brain injury (TBI) is a leading cause of death

213 Traumatic brain injury (TBI) is a leading cause of long-

214 Traumatic brain injury (TBI) is a leading cause of morbi

215 Traumatic brain injury (TBI) is a major cause of death a

216 Traumatic brain injury (TBI) is a major cause of morbidi

217 Traumatic brain injury (TBI) is a major cause of mortali

218 Traumatic brain injury (TBI) is a major contributor to m

219 Traumatic brain injury (TBI) is a major health and socio

220 Traumatic brain injury (TBI) is a major human health con

221 Traumatic brain injury (TBI) is a major public health is

222 Traumatic brain injury (TBI) is a serious public health

223 Traumatic brain injury (TBI) is a significant global pub

224 etrospectively examined whether a history of traumatic brain injury (TBI) is associated with an earli

225 Epilepsy after pediatric traumatic brain injury (TBI) is associated with poor qua

226 Traumatic brain injury (TBI) is characterized by acute n

227 Traumatic brain injury (TBI) is currently a major cause

228 Severe traumatic brain injury (TBI) is currently managed in the

229 Traumatic brain injury (TBI) is extremely common across

230 Traumatic brain injury (TBI) is known to cause perturbat

231 Traumatic brain injury (TBI) is set to become the leadin

232 ry deficits after TBI.SIGNIFICANCE STATEMENT Traumatic brain injury (TBI) is the leading cause of dea

233 ession involved in the MQC in rats receiving traumatic brain injury (TBI) of different severities.

234 a controlled cortical impact model (CCI) of traumatic brain injury (TBI) on their distribution.

235 sregulation of pathways directly involved in traumatic brain injury (TBI) pathogenesis and have been

236 Traumatic brain injury (TBI) promotes neural stem/progen

237 etection of neuron-specific enolase (NSE), a traumatic brain injury (TBI) protein biomarker, in dilut

238 oRNAs (miRNAs) cause neurodegeneration after traumatic brain injury (TBI) remain elusive.

239 Traumatic brain injury (TBI) results in a host of pathol

240 Traumatic brain injury (TBI) results in persistent disru

241 Traumatic brain injury (TBI) results in rapid recruitmen

242 Head trauma with or without traumatic brain injury (TBI) shortened mean life expecta

243 earning and memory impairments are common in traumatic brain injury (TBI) survivors.

244 ipoprotein E4 (ApoE4) genotype combines with traumatic brain injury (TBI) to increase the risk of dev

245 major role in the etiology of mouse model of traumatic brain injury (TBI), a condition associated wit

246 Animals were subjected to moderate traumatic brain injury (TBI), a condition characterized

247 Blast exposure, not mild traumatic brain injury (TBI), acted as the primary milit

248 usly been shown to occur in animal models of traumatic brain injury (TBI), and blocking this form of

249 Brain damage due to stroke or traumatic brain injury (TBI), both leading causes of ser

250 eater risk of Parkinson's disease (PD) after traumatic brain injury (TBI), but it is possible that th

251 g is a mainstay of therapy for children with traumatic brain injury (TBI), but its overall associatio

252 tive disease, cerebral ischemia (stroke) and traumatic brain injury (TBI), drives spreading neurotoxi

253 After traumatic brain injury (TBI), glial cells have both bene

254 PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated

255 Following traumatic brain injury (TBI), ischemia and hypoxia play

256 After traumatic brain injury (TBI), neurons surviving the init

257 ngth and learning, is dysregulated following traumatic brain injury (TBI), suggesting that stimulatio

258 After traumatic brain injury (TBI), the ability of cerebral ve

259 trocytes to fluid shear stress in a model of traumatic brain injury (TBI), we found that shear stress

260 t potentially underdiagnosed complication of traumatic brain injury (TBI).

261 l changes following traumatic spinal cord or traumatic brain injury (TBI).

262 t and chronic traumatic encephalopathy after traumatic brain injury (TBI).

263 ndent predictors of outcome in patients with traumatic brain injury (TBI).

264 treating persistent cognitive problems after traumatic brain injury (TBI).

265 cortical impact (CCI) injury murine model of traumatic brain injury (TBI).

266 bosis, and this balance can be altered after traumatic brain injury (TBI).

267 .5 million people seek medical attention for traumatic brain injury (TBI).

268 diffusion gradients in hypoxic regions after traumatic brain injury (TBI).

269 assess the effects of CO in a mouse model of traumatic brain injury (TBI).

270 ic disorders including Alzheimer disease and traumatic brain injury (TBI).

271 ng (MTI) can detect diffuse axonal injury in traumatic brain injury (TBI).

272 logical disorders as diverse as migraine and traumatic brain injury (TBI).

273 in cerebral energetic metabolism arise after traumatic brain injury (TBI).

274 ses of death after trauma are hemorrhage and traumatic brain injury (TBI).

275 source of distress and disability following traumatic brain injury (TBI).

276 (beta)-blockers improve outcomes after acute traumatic brain injury (TBI).

277 or determinant of adverse outcomes following traumatic brain injury (TBI).

278 ri-lesional brain and white matter following traumatic brain injury (TBI).

279 r of ER stress, which has been implicated in traumatic brain injury (TBI).

280 ecific outcome measure (clinically important traumatic brain injury [TBI], need for neurological inte

281 rove long term functional outcomes following traumatic brain injury(TBI).

282 The long-term clinical effects of wartime traumatic brain injuries (TBIs), most of which are mild,

283 s led to an awareness that it is exposure to traumatic brain injury that carries with it a risk of th

284 dary events triggered by blast-induced, mild traumatic brain injury that is commonly observed in mili

285 ion and those affected by various degrees of traumatic brain injury), the identification of reliable

286 Thus, in patients with traumatic brain injury, the concept that 90 mm Hg repres

287 creasingly used in the early phase following traumatic brain injury, the prognostic utility of MRI re

288 functionality essential to the treatment of traumatic brain injury; the measurement performance of o

289 microglia in models of stroke, infection and traumatic brain injury, though the exact role of the imm

290 to the intensive care unit for acute severe traumatic brain injury to test two hypotheses: (i) in pa

291 nd over the first week after moderate-severe traumatic brain injury; transthoracic echocardiogram wit

292 Approaches and Decisions in Acute Pediatric Traumatic Brain Injury Trial-a comparative effectiveness

293 improve outcomes in an experimental model of traumatic brain injury, TSG-6 expression has not been ex

294 series, we investigated several features of traumatic brain injuries, using clinical histopathology

295 Nineteen patients with traumatic brain injury were classified into post-traumat

296 y or Glasgow Outcome Scale for patients with traumatic brain injury were the pressure reactivity inde

297 of dairy products, history of melanoma, and traumatic brain injury, whereas a reduced risk has been

298 lthy civilians, and from civilians with mild traumatic brain injury, which is commonly comorbid with

299 tion that can decrease ischemic injury after traumatic brain injury without increasing bleeding tende

300 MRI following traumatic brain injury yields important prognostic infor