ライフサイエンスコーパス: traumatic brain injury

1 ype and severity of cognitive deficits after traumatic brain injury.

2 ted deficits in long-term potentiation after traumatic brain injury.

3 related quality of life up to 10 years after traumatic brain injury.

4 d in-hospital care programmes for paediatric traumatic brain injury.

5 m Hg) for 72 h after the diagnosis of severe traumatic brain injury.

6 e cohort of patients with moderate-to-severe traumatic brain injury.

7 s and in asymptomatic men with no history of traumatic brain injury.

8 c evaluation in critically ill patients with traumatic brain injury.

9 smolar therapy is often used to treat severe traumatic brain injury.

10 type-specific responses in a mouse model of traumatic brain injury.

11 Cognitive impairment is common following traumatic brain injury.

12 tted to the emergency department with severe traumatic brain injury.

13 se controlled cortical impact (CCI) model of traumatic brain injury.

14 rognosis in patients with moderate or severe traumatic brain injury.

15 lzheimer's disease, Parkinson's disease, and traumatic brain injury.

16 that might occur in EDS patients after mild traumatic brain injury.

17 damage during brain tissue deformation from traumatic brain injury.

18 might be a valuable therapeutic target after traumatic brain injury.

19 ubjects and 35 patients with moderate/severe traumatic brain injury.

20 compliance with goal-directed therapy after traumatic brain injury.

21 pairment, posttraumatic stress disorder, and traumatic brain injury.

22 over 30 to 60 days, before and after induced traumatic brain injury.

23 matic brain injury and six (3%) had moderate traumatic brain injury.

24 rs of ferroptotic death were increased after traumatic brain injury.

25 (PEGASUS) programme in children with severe traumatic brain injury.

26 proteins characterize acute and chronic mild traumatic brain injury.

27 a 27% improvement in the slowing produced by traumatic brain injury.

28 terns for discriminating clinical outcome in traumatic brain injury.

29 Canadian provinces, specifically for severe traumatic brain injury.

30 teractions between four treatments following traumatic brain injury.

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

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

33 observed for younger patients and those with traumatic brain injury.

34 rs would improve cognitive performance after traumatic brain injury.

35 Consecutive patients with severe traumatic brain injury.

36 n underestimated therapeutic potential after traumatic brain injury.

37 arly improve physical outcome 6 months after traumatic brain injury.

38 a critical role in the management of severe traumatic brain injury.

39 oped coma with subsequent DOC after a severe traumatic brain injury.

40 ive ability, both of which are vulnerable to traumatic brain injury.

41 ce impairments in subjects who have had mild traumatic brain injuries.

42 ute neurological diseases such as stroke and traumatic brain injuries.

43 te deaths are now split between those due to traumatic brain injury (52%) and multiple organ dysfunct

44 cortical synapse loss resulting from diffuse traumatic brain injury, a highly prevalent connectional

45 were P/PP; of these, hemorrhage, sepsis, and traumatic brain injury accounted for 73.3%.

46 6 yr within 1 wk after a sports-related mild traumatic brain injury (acute mTBI) ( n = 18), 3 mo or l

47 This includes traumatic brain injury, Alexander's disease, Alzheimer's

48 and one of the most common sequelae of mild traumatic brain injury, also known as concussion.

49 cluding ischemic stroke, hemorrhagic stroke, traumatic brain injury, Alzheimer's disease, and multipl

50 s in the chronic phase after moderate-severe traumatic brain injury and 19 healthy control subjects.

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

52 We aimed to measure this integrity in traumatic brain injury and anoxo-ischemic (cardiac arres

53 Forty patients with moderate-severe traumatic brain injury and cognitive impairments complet

54 Sp mice were immunosuppressed acutely after traumatic brain injury and could not produce interleukin

55 k, we present a finite element model of post-traumatic brain injury and decompressive craniectomy tha

56 eceptors attenuated cognitive deficits after traumatic brain injury and enhanced synaptic plasticity

57 e critically injured with a preponderance of traumatic brain injury and had a 7-fold higher DD level

58 ng the pathophysiology of mild blast-induced traumatic brain injury and identifying the physical forc

59 riety of conditions, such as stroke, sepsis, traumatic brain injury and neurodegenerative diseases.

60 gnose specific microvascular pathology after traumatic brain injury and other brain pathologies.

61 ir and improvement of recovery after stroke, traumatic brain injury and other diseases in which neuro

62 Patients with nonpenetrating traumatic brain injury and postresuscitation Glasgow Com

63 ual to four patients with moderate or severe traumatic brain injury and reporting glial fibrillary ac

64 ion in models of stroke, multiple sclerosis, traumatic brain injury and seizure, each having profound

65 ASUS programme, of whom 193 (97%) had severe traumatic brain injury and six (3%) had moderate traumat

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

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

68 trographic seizures after moderate-to-severe traumatic brain injury and to correlate continuous elect

69 nduced and diabetic peripheral neuropathies, traumatic brain injury, and amyotrophic lateral sclerosi

70 nd related parkinsonisms, Alzheimer disease, traumatic brain injury, and even in normal aging.

71 ippocampal slices were prepared 1 week after traumatic brain injury, and long-term potentiation was s

72 eurological conditions, including infection, traumatic brain injury, and neurodegenerative diseases,

73 BBE, determine its alteration in response to traumatic brain injury, and test potential therapeutic t

74 to the pathogenesis of in vitro and in vivo traumatic brain injury, and whether inhibition of 15-lip

75 Cognitive deficits after traumatic brain injury are a leading cause of disability

76 An enigma of mild traumatic brain injury are observations of substantial b

77 seven patients with subclinical EDS and mild traumatic brain injury are presented.

78 English, French, Spanish, or Portuguese with traumatic brain injury as the base trauma, clearly formu

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

80 ) 10 years and older with moderate or severe traumatic brain injury (Barell Matrix Type 1 classificat

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

82 Blast-induced traumatic brain injury (bTBI) has been recognized as the

83 that is commonly seen after moderate/severe traumatic brain injury but has been of uncertain aetiolo

84 ic predictors following a moderate or severe traumatic brain injury but their prognostic accuracy is

85 paminergic drugs can enhance cognition after traumatic brain injury, but individual responses are hig

86 mprove clinical outcomes in pediatric severe traumatic brain injury, but the evidence is extremely fr

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

88 ce suggests that a single moderate or severe traumatic brain injury can also induce progressive neuro

89 patients with a hypodopaminergic state after traumatic brain injury can help stratify the choice of c

90 Traumatic brain injury causes monocyte functional impair

91 ithin 4 hours of injury after nonpenetrating traumatic brain injury characterized by Glasgow Coma Sca

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

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

94 After traumatic brain injury, continuous electroencephalograph

95 ically, impairments in these abilities after traumatic brain injury correlate in a dissociable manner

96 ma exposure, comorbid depression, history of traumatic brain injury, current alcohol abuse or depende

97 iety of neuropsychiatric disorders including traumatic brain injury, demyelinating disease, Alzheimer

98 Traumatic brain injury due to blast exposure is currentl

99 In traumatic brain injury, dysregulation of fibrinolysis ma

100 ts with Alzheimer's disease, and people with traumatic brain injury exert less cognitive control duri

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

102 tion into the hippocampus of adult mice with traumatic brain injury, functionally integrate as mature

103 Traumatic brain injury generated by blast may induce lon

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

105 y useful for the diagnosis and management of traumatic brain injury, glaucoma and hypertension, respe

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

107 34%) than those >=65 (ICC = 5 to 6%) and for traumatic brain injury (ICC = 5 to 13%) than other injur

108 traumatic microbleeds in patients with acute traumatic brain injury; (ii) determine whether appearanc

109 The Progesterone for the Treatment of Traumatic Brain Injury III clinical trial rigorously mon

110 nrolled in Progesterone for the Treatment of Traumatic Brain Injury III, mortality was 12.5%.

111 ipating in Progesterone for the Treatment of Traumatic Brain Injury III.

112 iratory infections in the postacute phase of traumatic brain injury impede optimal recovery and contr

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

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

115 Falls resulted in the majority of traumatic brain injuries in the total population, howeve

116 Repetitive mild traumatic brain injury in American football players has

117 asonable animal-on-a-chip model for inducing traumatic brain injury in an animal, producing significa

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

119 Traumatic brain injury increased the time required to so

120 Traumatic brain injury increases proinflammatory cytokin

121 le the mechanisms underlying repetitive mild traumatic brain injury-induced neurodegeneration are unk

122 novel targets for pharmacologic treatment of traumatic brain injury-induced persistent cognitive defi

123 Cohorts were matched for age, hypotension, traumatic brain injury, injury mechanism, and need for e

124 Traumatic brain injury is a leading cause of death and d

125 Traumatic brain injury is a leading cause of hospital vi

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

127 Traumatic brain injury is a major risk factor for acquir

128 Mild traumatic brain injury is an all-too-common outcome from

129 Traumatic brain injury is associated with elevated rates

130 cranial direct current stimulation following traumatic brain injury is dependent on white matter dama

131 Continuous assessment of physiology after traumatic brain injury is essential to prevent secondary

132 Traumatic brain injury is the number one cause of death

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

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

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

136 that respiratory infections even late after traumatic brain injury may pose a more serious threat th

137 gest that effective goal-directed therapy in traumatic brain injury may provide an opportunity to imp

138 t 3 days post-injury, S. pneumoniae-infected traumatic brain injury mice (TBI + Sp) had a 25% mortali

139 roved both problem solving and memory in the traumatic brain injury mice.

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

141 The diffuse nature of mild traumatic brain injury (mTBI) impacts brain white-matter

142 Mild traumatic brain injury (mTBI) in a murine model increase

143 rs with and without a recent history of mild traumatic brain injury (mTBI) on deployment were evaluat

144 showed previously in C57BL/6J mice that mild traumatic brain injury (mTBI) transiently induced bone f

145 A single mild traumatic brain injury (mTBI) typically causes only tran

146 tle balance impairments associated with mild traumatic brain injury (mTBI).

147 n investigated as a diagnostic tool for mild traumatic brain injury (mTBI).

148 he setting of persistent symptoms after mild traumatic brain injury (mTBI).

149 experimental results which show that a mild traumatic brain injury (mTBI, often referred to as concu

150 Populations most frequently evaluated were traumatic brain injury (n = 96), general pediatric criti

151 such as chronic stress, protein misfolding, traumatic brain injury or other pathological mechanisms

152 eatment potential for patients on Earth with traumatic brain injury or other pathology leading to int

153 us served as risk factors for disparities in traumatic brain injury outcomes between undocumented imm

154 Disparities in traumatic brain injury outcomes for ethnic minorities an

155 ve craniectomy patients up to 10 years after traumatic brain injury (p = 0.004).

156 time consistent with typical timescales for traumatic brain injury pathogenesis.

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

158 The data were collected from 379 traumatic brain injury patients admitted to Addenbrooke'

159 is suggest that early tracheostomy in severe traumatic brain injury patients contributes to a lower e

160 Initially, mild classified traumatic brain injury patients had a median Quality of

161 Overall, traumatic brain injury patients showed slow information

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

163 al blood pressure (ABP) measurements from 34 traumatic brain injury patients were applied to create a

164 nalyzed if decompressive craniectomy affects traumatic brain injury patients' quality of life in the

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

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

167 architectural disturbances were observed in traumatic brain injury patients.

168 same tasks in a cohort of 92 moderate-severe traumatic brain injury patients.

169 sed learning to multidimensional time-series traumatic brain injury physiology.

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

171 Prognosis and Analysis of Clinical Trials in Traumatic Brain Injury (r = 0.51; p = 0.01) and Injury S

172 Traumatic brain injury reduced long-term potentiation in

173 In addition, because traumatic brain injury reduces long-term potentiation in

174 lished that chronic cognitive problems after traumatic brain injury relate to diffuse axonal injury a

175 mmatory brain pathologies such as stroke and traumatic brain injury remains an elusive goal.

176 ng outcomes for uninsured children following traumatic brain injury requires a greater understanding

177 co-morbidity and mortality are compounded by traumatic brain injury resulting from blunt trauma, blas

178 urogenesis in a mouse model of repeated mild traumatic brain injury (rmTBI).

179 in animal models of alcoholism, depression, traumatic brain injury, schizophrenia, multiple sclerosi

180 encephalomyelitis and likely play a role in traumatic brain injury, seizure, and stroke.

181 ive craniectomy was necessary in all initial traumatic brain injury severity groups.

182 TBI using the Mayo Classification System for Traumatic Brain Injury Severity.

183 ruitment of macrophages and microglia to the traumatic brain injury site.

184 acerebral hemorrhage, acute ischemic stroke, traumatic brain injury, subarachnoid hemorrhage, and pos

185 phalopathy (CTE) is associated with repeated traumatic brain injuries (TBI) and is characterized by c

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

187 ve management was higher in patients without traumatic brain injury (TBI) (35%, N = 679) compared to

188 5, p < 0.001) from unintentional trauma, and traumatic brain injury (TBI) (OR = 5.77, p < 0.001) and

189 Traumatic brain injury (TBI) affects millions of people

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

191 icroglial activation occurs following severe traumatic brain injury (TBI) and is believed to contribu

192 ed expression of MMPs have been described in traumatic brain injury (TBI) and may contribute to addit

193 Determining if traumatic brain injury (TBI) and post-traumatic stress d

194 Traumatic brain injury (TBI) and rapid eye movement slee

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

196 studies are required to better characterise traumatic brain injury (TBI) and to identify the most ef

197 mpairment is a key cause of disability after traumatic brain injury (TBI) but relationships with over

198 Traumatic brain injury (TBI) can result in excitation: i

199 Traumatic brain injury (TBI) causes brain edema that ind

200 Traumatic brain injury (TBI) causes early seizures and i

201 Traumatic brain injury (TBI) causes extensive neural dam

202 Moderate or severe traumatic brain injury (TBI) causes widespread neuronal

203 vulnerable to poor long-term outcomes after traumatic brain injury (TBI) compared to adults.

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

205 Traumatic brain injury (TBI) has been designated as a si

206 Repetitive traumatic brain injury (TBI) has been linked to late lif

207 The brain degeneration associated with traumatic brain injury (TBI) has been modeled in Drosoph

208 an integral part of the management of severe traumatic brain injury (TBI) in children.

209 tivity disorder (ADHD) is a major sequela of traumatic brain injury (TBI) in youths.

210 is an urgent priority, yet current models of traumatic brain injury (TBI) inadequately recapitulate t

211 Focal traumatic brain injury (TBI) induces astrogliosis, a pro

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

213 Traumatic brain injury (TBI) is a common reason for pedi

214 nd cognitive deficits.SIGNIFICANCE STATEMENT Traumatic brain injury (TBI) is a debilitating neurologi

215 Traumatic brain injury (TBI) is a global health problem

216 sis after diffuse TBI.SIGNIFICANCE STATEMENT Traumatic brain injury (TBI) is a leading cause of acqui

217 Traumatic brain injury (TBI) is a leading cause of injur

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

219 Traumatic brain injury (TBI) is a leading global cause o

220 Chronic neurodegeneration in survivors of traumatic brain injury (TBI) is a major cause of morbidi

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

222 Traumatic brain injury (TBI) is a pervasive problem in t

223 Traumatic brain injury (TBI) is a risk factor for Alzhei

224 Traumatic brain injury (TBI) is a risk factor for neurod

225 Traumatic brain injury (TBI) is a risk factor for the la

226 Traumatic brain injury (TBI) is a serious global health

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

228 Traumatic brain injury (TBI) is a significant medical pr

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 largely non-preventable

232 Identifying new lipid markers linked to traumatic brain injury (TBI) is of major importance in c

233 Traumatic brain injury (TBI) is often accompanied by gas

234 Traumatic brain injury (TBI) is often characterized by a

235 Traumatic brain injury (TBI) is one of the most common i

236 Traumatic brain injury (TBI) is one the most common huma

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

238 Cerebral autoregulatory dysfunction after traumatic brain injury (TBI) is strongly linked to poor

239 Traumatic brain injury (TBI) is the leading cause of dea

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

241 Traumatic brain injury (TBI) is the most common cause of

242 Traumatic brain injury (TBI) is the strongest environmen

243 hnologies for the point-of-care diagnosis of traumatic brain injury (TBI) lack sensitivity, require s

244 Traumatic brain injury (TBI) leads to increased rates of

245 Brain degeneration, including that caused by traumatic brain injury (TBI) often leads to severe bladd

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

247 of physical activity are common features in traumatic brain injury (TBI) patients that may contribut

248 The burden of traumatic brain injury (TBI) poses a large public health

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

250 Traumatic brain injury (TBI) results in a cascade of cel

251 omplement (C) systems in the pathogenesis of traumatic brain injury (TBI) was investigated by quantif

252 osed as a universal pathological hallmark of traumatic brain injury (TBI) with molecular markers of a

253 nd injuries, e.g., in Parkinson's disease or traumatic brain injury (TBI), and hence it will be usefu

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

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

256 f acute and chronic pain are associated with traumatic brain injury (TBI), but mechanisms responsible

257 recirculation of blood flow to a limb after traumatic brain injury (TBI), can modify levels of patho

258 njuries, specifically long bone fracture and traumatic brain injury (TBI), frequently occur together.

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

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

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

262 After traumatic brain injury (TBI), plasma concentration of gl

263 After traumatic brain injury (TBI), some people have worse rec

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

265 ncreasing proportion of patients with severe traumatic brain injury (TBI), yet clinical trials and ou

266 tion and reactive microglia are hallmarks of traumatic brain injury (TBI), yet whether these cells co

267 ) contribute to inflammatory responses after traumatic brain injury (TBI).

268 e disease that is associated with repetitive traumatic brain injury (TBI).

269 rtant target for clinical intervention after traumatic brain injury (TBI).

270 ture of neurodegenerative disorder following traumatic brain injury (TBI).

271 lator of the pathophysiology associated with traumatic brain injury (TBI).

272 to manage rising intracranial pressure after traumatic brain injury (TBI).

273 viated Injury Scale score >=3 defined severe traumatic brain injury (TBI).

274 g, for its role in recovery after stroke and traumatic brain injury (TBI).

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

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

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

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

279 o definitive disease-modifying therapies for traumatic brain injury (TBI).

280 sing tools for evaluating patients following traumatic brain injury (TBI).

281 s and subsequent neuroinflammation following traumatic brain injury (TBI); however, the underlying me

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

283 thologies are glioblastoma multiforme (GBM), traumatic brain injuries (TBIs), multiple sclerosis (MS)

284 n addition to evaluation of therapeutics for traumatic brain injury, this hybrid microlens imaging me

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

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

287 We included children (aged <18 years) with traumatic brain injury (trauma mechanism and image findi

288 Traumatic brain injury triggers multiple cell death path

289 pared with insured pediatric patients with a traumatic brain injury, uninsured patients were in worse

290 treat diffuse axonal injury (DAI) caused by traumatic brain injury, using two different therapeutic

291 Isolated traumatic brain injury was defined as patients with a he

292 anatomic interfaces across all severities of traumatic brain injury, we combined computational, analy

293 Undocumented immigrants with traumatic brain injuries were more likely to be younger,

294 optic nerve ultrasonography in patients with traumatic brain injury were 97% (95% CI, 92% to 99%), 86

295 atients (< 18 yr old) with a severe isolated traumatic brain injury were identified in the National T

296 ar therapy in pediatric patients with severe traumatic brain injury were included.

297 e cognitive effects of methylphenidate after traumatic brain injury were only seen in patients with l

298 This is a particular challenge for traumatic brain injury, where patterns of damage and the

299 Anesthetized mice were subjected to traumatic brain injury with a closed-head, free-weight d

300 A history of traumatic brain injury with loss of consciousness (LOC)