ライフサイエンスコーパス: brain injury

1 imated therapeutic potential after traumatic brain injury.

2 ve physical outcome 6 months after traumatic brain injury.

3 lleviate the cognitive deficits arising from brain injury.

4 Recovery Scale-Revised) 3 months after acute brain injury.

5 ation during normal physiology and following brain injury.

6 cer itself, but rather occurs in response to brain injury.

7 l role in the management of severe traumatic brain injury.

8 for hypoglycemia, with a goal of preventing brain injury.

9 cannulation method carries a higher risk of brain injury.

10 ane oxygenation nonsurvivors developed acute brain injury.

11 verity of cognitive deficits after traumatic brain injury.

12 with subsequent DOC after a severe traumatic brain injury.

13 cing recovery from stroke and other types of brain injury.

14 schemia respectively, mimicking events after brain injury.

15 mpal dentate gyrus and epileptogenesis after brain injury.

16 ion, and functional recovery after perinatal brain injury.

17 data on the frequency of different types of brain injury.

18 y, both of which are vulnerable to traumatic brain injury.

19 ts in long-term potentiation after traumatic brain injury.

20 ase scenario of a patient with a devastating brain injury.

21 is involved in the pathogenesis of ischemic brain injury.

22 ic impairment were not associated with acute brain injury.

23 nd the most common type was hypoxic-ischemic brain injury.

24 s highly upregulated in astrocytes following brain injury.

25 ality of life up to 10 years after traumatic brain injury.

26 id (AMPA) receptor (CP-AMPAR) currents after brain injury.

27 ons in cerebral autoregulation, and acquired brain injury.

28 d utility for motor rehabilitation following brain injury.

29 patients, particularly after focal/lesional brain injury.

30 tal care programmes for paediatric traumatic brain injury.

31 fliximab) for 4 weeks, before undergoing I/R brain injury.

32 have a mutual promoting effect to secondary brain injury.

33 72 h after the diagnosis of severe traumatic brain injury.

34 a consecutive series of patients with acute brain injury.

35 ring brain tissue deformation from traumatic brain injury.

36 poreal membrane oxygenation causes secondary brain injury.

37 s aberrant complement activation, leading to brain injury.

38 6 ideal heart donors, 24 (66.7%) with anoxic brain injury.

39 in the case of a patient with a devastating brain injury.

40 pathophysiological concentration range after brain injury.

41 y to enhance functional rehabilitation after brain injury.

42 mprove cognitive performance after traumatic brain injury.

43 or younger patients and those with traumatic brain injury.

44 Consecutive patients with severe traumatic brain injury.

45 to determine consciousness in patients with brain injuries.

46 ders of consciousness (DoC) caused by severe brain injuries.

47 consciousness and recovery in patients with brain injuries.

48 ents in subjects who have had mild traumatic brain injuries.

49 unt importance for functional recovery after brain injuries.

50 microglia to phagocytose and migrate toward brain injuries.

51 and plays a protective role in ZIKV-mediated brain injuries.

52 ted as mediating neuronal damage in vascular brain injuries.

53 oke (10% vs 1%; p < 0.001), hypoxic-ischemic brain injury (13% vs 1%; p < 0.001), and brain death (11

54 ard ratio, 0.98; 95% CI [0.96-0.99]), anoxic brain injury (3.55 [1.2-10.5]), aspiration (2.29 [1.22-4

55 oncerned about "recovery after a devastating brain injury" (34%), and that "doctors would not try as

56 the state of consciousness in patients with brain injuries(4,5).

57 mmon acute brain injury was hypoxic-ischemic brain injury (44%), followed by intracranial hemorrhage

58 n, 23% (95% CI, 0.14-0.32%) hypoxic-ischemic brain injury, 6% (95% CI, 0.02-0.11%) ischemic stroke, 6

59 oke (10% vs 1%; p < 0.001), hypoxic-ischemic brain injury (7% vs 1%; p = 0.02), and brain death (9% v

60 ynapse loss resulting from diffuse traumatic brain injury, a highly prevalent connectional disorder.

61 of these, hemorrhage, sepsis, and traumatic brain injury accounted for 73.3%.

62 eriventricular leukomalacia, a major form of brain injury affecting premature infants.

63 One in four patients developed acute brain injury after extracorporeal cardiopulmonary resusc

64 Only eight patients (32%) were without acute brain injury after extracorporeal membrane oxygenation.

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

66 chemic stroke, hemorrhagic stroke, traumatic brain injury, Alzheimer's disease, and multiple sclerosi

67 repeatedly over time in patients with severe brain injuries and found that sniff responses significan

68 f reactions leading to primary and secondary brain injuries and permanent neurological deficits.

69 hronic phase after moderate-severe traumatic brain injury and 19 healthy control subjects.

70 aimed to measure this integrity in traumatic brain injury and anoxo-ischemic (cardiac arrest) coma pa

71 ohort of very preterm infants without severe brain injury and born before 32 weeks gestational age.

72 potential drug target against atopic asthma, brain injury and central nervous system disorders, as we

73 orty patients with moderate-severe traumatic brain injury and cognitive impairments completed a rando

74 ere immunosuppressed acutely after traumatic brain injury and could not produce interleukin-1beta, tu

75 ent a finite element model of post-traumatic brain injury and decompressive craniectomy that incorpor

76 learance, but diverge in their mechanisms of brain injury and disease presentation.

77 ttenuated cognitive deficits after traumatic brain injury and enhanced synaptic plasticity in hippoca

78 cessary to make predictions in patients with brain injury and hypothesize dissociations.

79 hophysiology of mild blast-induced traumatic brain injury and identifying the physical forces associa

80 Brain injury and inflammatory proteins show promise as o

81 the evolution of an important form of human brain injury and is a viable therapeutic target.

82 m, timing, and effective monitoring of acute brain injury and its management is necessary.

83 gy of chronic cerebral hypoperfusion-induced brain injury and may therefore represent a promising the

84 atment for spasticity by millions of stroke, brain injury and multiple sclerosis patients, many of wh

85 bed as a treatment for spasticity in stroke, brain injury and multiple sclerosis patients, who are of

86 hod should be useful to study other types of brain injury and neurodegeneration and cellular response

87 s or proteins are likely useful for treating brain injury and neurogenerative diseases.

88 ific microvascular pathology after traumatic brain injury and other brain pathologies.

89 Patients with nonpenetrating traumatic brain injury and postresuscitation Glasgow Coma Scale sc

90 We hypothesized that acute regional brain injury and recovery associate with differences in

91 seizures after moderate-to-severe traumatic brain injury and to correlate continuous electroencephal

92 ess (DOC) are a common consequence of severe brain injuries, and clinical evaluation is critical to p

93 diabetic peripheral neuropathies, traumatic brain injury, and amyotrophic lateral sclerosis.

94 of CO poisoning include cardiac dysfunction, brain injury, and death.

95 slices were prepared 1 week after traumatic brain injury, and long-term potentiation was studied usi

96 l conditions, including infection, traumatic brain injury, and neurodegenerative diseases, has become

97 ive effect in preclinical models of neonatal brain injury, and phase 2 trials have suggested possible

98 mine its alteration in response to traumatic brain injury, and test potential therapeutic treatments

99 igodendroglial-specific responses to hypoxic brain injury, and uncovered molecular mechanisms involve

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

101 arsenic and cadmium exposures with vascular brain injury are consistent with established literature.

102 The functional consequences of focal brain injury are thought to be contingent on neuronal al

103 ury suggesting that patients sustained acute brain injury as a consequence of cardiogenic shock and c

104 rench, Spanish, or Portuguese with traumatic brain injury as the base trauma, clearly formulated ques

105 We compared the prevalence of brain injury between patients undergoing venoarterial an

106 erence was seen in the rate of overall acute brain injury between venoarterial extracorporeal membran

107 circulation and associations with structural brain injury, brain volumetry, and postnatal clinical fa

108 ommonly seen after moderate/severe traumatic brain injury but has been of uncertain aetiology.

109 drugs can enhance cognition after traumatic brain injury, but individual responses are highly variab

110 sociated with worse outcomes following acute brain injury, but their effect on long-term clinical out

111 ore likely to arrive with more severe anoxic brain injury, but this does not account for all the disp

112 ocal brain inflammation aggravates secondary brain injury by exacerbating blood-brain barrier damage,

113 Severe brain injuries can lead to long-lasting disorders of con

114 s that a single moderate or severe traumatic brain injury can also induce progressive neuropathologic

115 Brain injuries caused by an explosive blast or blunt for

116 rity of human TBIs also present with diffuse brain injury caused by acceleration-deceleration forces

117 Traumatic brain injury causes monocyte functional impairments that

118 mbrane oxygenation patients had more overall brain injury compared with venovenous extracorporeal mem

119 ive deficits, resembling delirium, and acute brain injury contributing to long-term cognitive impairm

120 pairments in these abilities after traumatic brain injury correlate in a dissociable manner with the

121 apy is associated with white matter-specific brain injury, cortical volume loss, mineralization, micr

122 he ICU stay in comatose patients with severe brain injury could enlarge the pool of actual lung donor

123 In several models of brain injury, drugs that inhibit alpha5 subunit-containi

124 lets interact with neutrophils to exacerbate brain injury during ischemic stroke.

125 Reported acute brain injury during venoarterial extracorporeal membrane

126 spring, but how it interplays with perinatal brain injury (especially birth asphyxia or hypoxia ische

127 zheimer's disease, and people with traumatic brain injury exert less cognitive control during retriev

128 In patients at risk of hypoxic ischemic brain injury following cardiac arrest, we sought to: 1)

129 Traumatic brain injury generated by blast may induce long-term neu

130 Patients with hypoxic-ischemic brain injury had more hypertension (8 vs 4; p = 0.047),

131 hUCBCs in a mouse model of hypoxic-ischaemic brain injury (HI).

132 those >=65 (ICC = 5 to 6%) and for traumatic brain injury (ICC = 5 to 13%) than other injuries (ICC =

133 fections in the postacute phase of traumatic brain injury impede optimal recovery and contribute subs

134 l properties of the tissue surrounding focal brain injuries in humans.

135 Falls resulted in the majority of traumatic brain injuries in the total population, however, undocum

136 ts and improved spastic gait disorders after brain injury in a disease model.

137 izing behavior independent of supratentorial brain injury in a dose-dependent fashion.

138 reciprocal escalation of immune and neonatal brain injury in a subset of ASD that may benefit from mo

139 Repetitive mild traumatic brain injury in American football players has garnered i

140 ival time of newborns, and reduces perinatal brain injury in cases of intrauterine inflammation.

141 the types, timing, and risk factors of acute brain injury in extracorporeal membrane oxygenation.

142 in the SVZ niche following distant cortical brain injury in mice.

143 B signaling, pro-inflammatory responses, and brain injury in offspring.

144 Despite the common occurrence of brain injury in patients undergoing extracorporeal membr

145 s debate over the presence and prevalence of brain injury in patients with celiac disease.

146 lack information on characteristics of acute brain injury in patients with extracorporeal membrane ox

147 g is necessary to define the timing of acute brain injury in patients with extracorporeal membrane ox

148 he S1P(1) receptor substantially exacerbates brain injury in permanent and transient models of ischem

149 espite a decrease in the prevalence of acute brain injury in recent years, mortality rates remain hig

150 nd mood impairment, indicating potential for brain injury in regions that control these functions.

151 rall effect of microglial phagocytosis after brain injury in vivo is neuroprotective or neurotoxic is

152 f the mechanisms regulating cell death after brain injury in vivo We show that mechanical injury to t

153 The risk factors for acute brain injury included hypertension history (11 vs 1; p =

154 Traumatic brain injury increased the time required to solve diffic

155 Traumatic brain injury increases proinflammatory cytokines, which

156 g for promoting neuronal recovery.IMPORTANCE Brain injury induced by acute simian (or human) immunode

157 Brain injury-induced changes at somatic junctions trigge

158 hanisms underlying repetitive mild traumatic brain injury-induced neurodegeneration are unknown and a

159 ets for pharmacologic treatment of traumatic brain injury-induced persistent cognitive deficits.

160 were matched for age, hypotension, traumatic brain injury, injury mechanism, and need for emergent su

161 Traumatic brain injury is a leading cause of hospital visits for c

162 Traumatic brain injury is a major risk factor for acquired epileps

163 Traumatic brain injury is associated with elevated rates of neurod

164 Although acute brain injury is common in patients receiving extracorpor

165 eal cardiopulmonary resuscitation-associated brain injury is necessary.

166 Traumatic brain injury is the number one cause of death in childre

167 After severe brain injury, it can be difficult to determine the state

168 iratory infections even late after traumatic brain injury may pose a more serious threat than is curr

169 tural counterpart provides information about brain injury mechanisms.

170 ost-injury, S. pneumoniae-infected traumatic brain injury mice (TBI + Sp) had a 25% mortality rate, i

171 problem solving and memory in the traumatic brain injury mice.

172 oducibility for the potential application in brain injury monitoring.

173 Mild traumatic brain injury (mTBI) in a murine model increases survival

174 d without a recent history of mild traumatic brain injury (mTBI) on deployment were evaluated within

175 e impairments associated with mild traumatic brain injury (mTBI).

176 of persistent symptoms after mild traumatic brain injury (mTBI).

177 tal results which show that a mild traumatic brain injury (mTBI, often referred to as concussion) cau

178 ons most frequently evaluated were traumatic brain injury (n = 96), general pediatric critical illnes

179 n a greater understanding of p75NTR in acute brain injuries, neurodegenerative diseases and general r

180 ammation-induced acute dysfunction and acute brain injury occur by overlapping or discrete mechanisms

181 Brain injury occurs within days in simian immunodeficien

182 e patients with chronic focal and multifocal brain injuries of ischaemic, haemorrhagic and traumatic

183 hypothesized that neonates with more severe brain injury on magnetic resonance imaging (MRI) would e

184 l perspective regarding the effects of early brain injury on the development of cognitive and behavio

185 netic resonance imaging findings of vascular brain injury or cerebral atrophy in adult American India

186 c changes of microglia in the absence of any brain injury or disease.

187 th the ultimate goal of aiding recovery from brain injury or disease.

188 pedes functional recovery later in life from brain injury or disease.

189 During brain injury or infection, bone-marrow derived macrophag

190 ognition of their potential as biomarkers of brain injury or neurodegeneration in CSF and blood.

191 up of school-aged EPT children with no known brain injury or neurological deficits.

192 hronic stress, protein misfolding, traumatic brain injury or other pathological mechanisms may explai

193 onducted in rats subject to fluid percussion brain injury or sham injury.

194 as risk factors for disparities in traumatic brain injury outcomes between undocumented immigrants an

195 Disparities in traumatic brain injury outcomes for ethnic minorities and the unin

196 tomy patients up to 10 years after traumatic brain injury (p = 0.004).

197 The data were collected from 379 traumatic brain injury patients admitted to Addenbrooke's Hospital

198 that early tracheostomy in severe traumatic brain injury patients contributes to a lower exposure to

199 Initially, mild classified traumatic brain injury patients had a median Quality of Life after

200 Overall, traumatic brain injury patients showed slow information processing

201 ressure (ABP) measurements from 34 traumatic brain injury patients were applied to create artificial

202 on limitation physiology in hypoxic-ischemic brain injury patients with brain hypoxia, as defined by

203 In hypoxic-ischemic brain injury patients with brain hypoxia, there is an el

204 decompressive craniectomy affects traumatic brain injury patients' quality of life in the long term.

205 in a cohort of 92 moderate-severe traumatic brain injury patients.

206 ural disturbances were observed in traumatic brain injury patients.

207 However, it remains unclear if structural brain injury plays a role in these outcomes and whether

208 tual disability, degenerative brain disease, brain injury, psychiatric disorders, functional disorder

209 locking TLR4 signaling in vivo shortly after brain injury reduced dentate network excitability and se

210 Traumatic brain injury reduced long-term potentiation in the hippo

211 In addition, because traumatic brain injury reduces long-term potentiation in the hippo

212 t chronic cognitive problems after traumatic brain injury relate to diffuse axonal injury and the con

213 ain pathologies such as stroke and traumatic brain injury remains an elusive goal.

214 s for uninsured children following traumatic brain injury requires a greater understanding of the fac

215 ty and mortality are compounded by traumatic brain injury resulting from blunt trauma, blast exposure

216 Brain injury resulting from repeated mild traumatic insu

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

218 myelitis and likely play a role in traumatic brain injury, seizure, and stroke.

219 mol:mol were equally predictive of perinatal brain injury (sensitivity 100%, specificity 93.3%, posit

220 esized their appearance would correlate with brain injury severity early after cardiac arrest and ret

221 ctomy was necessary in all initial traumatic brain injury severity groups.

222 the Mayo Classification System for Traumatic Brain Injury Severity.

223 cing recovery from stroke and other types of brain injury.SIGNIFICANCE STATEMENT An improved understa

224 sis in the various etiologies of devastating brain injury, some common themes emerge.

225 n important diagnostic tool to detect subtle brain injury specifically in mild TBI patients.

226 as homeostatic regulators, especially after brain injuries, such as stroke.

227 (CTE) is associated with repeated traumatic brain injuries (TBI) and is characterized by cognitive d

228 ent was higher in patients without traumatic brain injury (TBI) (35%, N = 679) compared to those with

229 01) from unintentional trauma, and traumatic brain injury (TBI) (OR = 5.77, p < 0.001) and mortality

230 activation occurs following severe traumatic brain injury (TBI) and is believed to contribute to subs

231 ion of MMPs have been described in traumatic brain injury (TBI) and may contribute to additional tiss

232 Determining if traumatic brain injury (TBI) and post-traumatic stress disorder (P

233 Traumatic brain injury (TBI) and rapid eye movement sleep behaviou

234 re required to better characterise traumatic brain injury (TBI) and to identify the most effective tr

235 is a key cause of disability after traumatic brain injury (TBI) but relationships with overall functi

236 Traumatic brain injury (TBI) can result in excitation: inhibition

237 Traumatic brain injury (TBI) causes brain edema that induces incre

238 Traumatic brain injury (TBI) causes early seizures and is the lead

239 Traumatic brain injury (TBI) has been designated as a signature in

240 brain degeneration associated with traumatic brain injury (TBI) has been modeled in Drosophila using

241 l part of the management of severe traumatic brain injury (TBI) in children.

242 nt priority, yet current models of traumatic brain injury (TBI) inadequately recapitulate the human i

243 Traumatic brain injury (TBI) is a common reason for pediatric emer

244 ve deficits.SIGNIFICANCE STATEMENT Traumatic brain injury (TBI) is a debilitating neurological disord

245 Traumatic brain injury (TBI) is a leading cause of injury-related

246 Traumatic brain injury (TBI) is a leading global cause of death an

247 neurodegeneration in survivors of traumatic brain injury (TBI) is a major cause of morbidity, with n

248 Traumatic brain injury (TBI) is a pervasive problem in the United

249 Traumatic brain injury (TBI) is a risk factor for neurodegenerativ

250 Traumatic brain injury (TBI) is a risk factor for the later develo

251 Traumatic brain injury (TBI) is a serious global health problem, m

252 Traumatic brain injury (TBI) is a significant medical problem with

253 Traumatic brain injury (TBI) is largely non-preventable and often

254 Traumatic brain injury (TBI) is often accompanied by gastrointesti

255 Traumatic brain injury (TBI) is often characterized by alterations

256 Traumatic brain injury (TBI) is the leading cause of death and dis

257 Traumatic brain injury (TBI) is the most common cause of death on

258 Traumatic brain injury (TBI) is the strongest environmental risk f

259 for the point-of-care diagnosis of traumatic brain injury (TBI) lack sensitivity, require specialist

260 neration, including that caused by traumatic brain injury (TBI) often leads to severe bladder dysfunc

261 Traumatic brain injury (TBI) results in a cascade of cellular resp

262 (C) systems in the pathogenesis of traumatic brain injury (TBI) was investigated by quantifying Cprot

263 universal pathological hallmark of traumatic brain injury (TBI) with molecular markers of angiogenesi

264 s, e.g., in Parkinson's disease or traumatic brain injury (TBI), and hence it will be useful to the w

265 tion of blood flow to a limb after traumatic brain injury (TBI), can modify levels of pathology-assoc

266 After traumatic brain injury (TBI), plasma concentration of glial fibril

267 After traumatic brain injury (TBI), some people have worse recovery than

268 proportion of patients with severe traumatic brain injury (TBI), yet clinical trials and outcome stud

269 eactive microglia are hallmarks of traumatic brain injury (TBI), yet whether these cells contribute t

270 ve disease-modifying therapies for traumatic brain injury (TBI).

271 for evaluating patients following traumatic brain injury (TBI).

272 te to inflammatory responses after traumatic brain injury (TBI).

273 that is associated with repetitive traumatic brain injury (TBI).

274 et for clinical intervention after traumatic brain injury (TBI).

275 rising intracranial pressure after traumatic brain injury (TBI).

276 equent neuroinflammation following traumatic brain injury (TBI); however, the underlying mechanism re

277 are glioblastoma multiforme (GBM), traumatic brain injuries (TBIs), multiple sclerosis (MS), intracer

278 ; excepting cases with evidence of perinatal brain injury) than in those with combined (19 [19%] of 9

279 to evaluation of therapeutics for traumatic brain injury, this hybrid microlens imaging method shoul

280 anding modifiable factors that contribute to brain injury to optimize neurocognitive function is para

281 quality of life with a Quality of Life after Brain Injury total score greater than or equal to 60 com

282 patients had a median Quality of Life after Brain Injury total score of 83 (decompressive craniectom

283 ld reflected by median Quality of Life after Brain Injury total scores of 62 (no decompressive cranie

284 insured pediatric patients with a traumatic brain injury, uninsured patients were in worse condition

285 fuse axonal injury (DAI) caused by traumatic brain injury, using two different therapeutic windows, a

286 neurofibrillary tangles (NFTs), and vascular brain injury (VBI).

287 derived E2 is neuroprotective after ischemic brain injury via a mechanism that involves suppression o

288 ommon involved location for hypoxic-ischemic brain injury was cerebral cortices (82%) and cerebellum

289 Isolated traumatic brain injury was defined as patients with a head Abbrevi

290 The most common acute brain injury was hypoxic-ischemic brain injury (44%), fo

291 Brain injury was more common in venoarterial extracorpor

292 While ischemic brain injury was more common in venoarterial extracorpor

293 Structural brain injury was present in the entire Fontan cohort; th

294 Hypoxic-ischemic brain injury was the most common type of injury suggesti

295 nterfaces across all severities of traumatic brain injury, we combined computational, analytical, and

296 Undocumented immigrants with traumatic brain injuries were more likely to be younger, have shor

297 18 yr old) with a severe isolated traumatic brain injury were identified in the National Trauma Data

298 nt spatially biased attention after acquired brain injury, were randomly assigned to the experimental

299 nesthetized mice were subjected to traumatic brain injury with a closed-head, free-weight drop method

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