ライフサイエンスコーパス: brain injury

1 nically-relevant canine model of HCA-induced brain injury.

2 phase following moderate or severe traumatic brain injury.

3 traocular hemorrhages secondary to traumatic brain injury.

4 t cell contributes to brain inflammation and brain injury.

5 ma is a key poor prognosticator in traumatic brain injury.

6 ion of hand movements and for recovery after brain injury.

7 m neurodegenerative disease and/or traumatic brain injury.

8 mer disease, Lewy body disease, and vascular brain injury.

9 much of the synaptic damage associated with brain injury.

10 n in patients with moderate-severe traumatic brain injury.

11 traocular hemorrhages secondary to traumatic brain injury.

12 improve functional recovery after ischaemic brain injury.

13 provinces, specifically for severe traumatic brain injury.

14 al impact in a mouse model of mild traumatic brain injury.

15 cated in epileptogenesis and seizure-induced brain injury.

16 ) contribute to recovery after acute sterile brain injury.

17 and plays a central role in the response to brain injury.

18 ious complications of ischemic and traumatic brain injury.

19 lly modifiable factor to prevent CMI-related brain injury.

20 tion in patients with acute severe traumatic brain injury.

21 a pre-hospital or pitch-side test to detect brain injury.

22 rventions in infants with pre- and perinatal brain injury.

23 ncephalographic (EEG) recordings after acute brain injury.

24 in and enhance functional connectivity after brain injury.

25 ntial to ameliorate in vivo HIVgp120-induced brain injury.

26 uman immunodeficiency virus-1 (HIV-1) causes brain injury.

27 it can persist one year or more following a brain injury.

28 R compatible with ischemia or mild traumatic brain injury.

29 learning and memory outcomes after traumatic brain injury.

30 f early MRI in moderate and severe traumatic brain injury.

31 dysfunction after moderate-severe traumatic brain injury.

32 ns of athletes with sports-related traumatic brain injury.

33 fission, elongate mitochondria, and mitigate brain injury.

34 tcome predictors for patients with traumatic brain injury.

35 sport-related concussion and mild traumatic brain injury.

36 es resistant visual attention deficits after brain injury.

37 between four treatments following traumatic brain injury.

38 e brain tissue hypoxia, a measure of ongoing brain injury.

39 itions that mimic severe, moderate, and mild brain injury.

40 iable (p = 0.07) for patients with traumatic brain injury.

41 ying pathways that may aid in recovery after brain injury.

42 effects during development and in models of brain injury.

43 considered the most lethal type of traumatic brain injury.

44 ffer new insights into the nature of preterm brain injury.

45 discriminating clinical outcome in traumatic brain injury.

46 -beta1 may be a therapeutic target for acute brain injury.

47 , 4.2-16.5 months]), 95 (12.3%) had acquired brain injuries.

48 n used to attenuate the effects of traumatic brain injuries.

49 brain tissue hypoxia after severe traumatic brain injury (0.45 in intracranial pressure-only group a

50 g (1) reducing SICU care for minor traumatic brain injury, (2) optimizing postoperative airway manage

51 receptor-1 was detected in severe traumatic brain injury, absent in controls, correlated with CT-ede

52 ferrin that may limit hematoma/iron-mediated brain injury after intracerebral hemorrhage.

53 A TSPO ligand attenuates brain injury after intracerebral hemorrhage.

54 ses and cognitive impairment after traumatic brain injury, all hallmarked by the accumulation of cell

55 anesthetics can reduce ischemia-reperfusion brain injury, although the cellular mechanisms for this

56 e p75 receptor are increased, such as during brain injury, Alzheimer's disease, and epilepsy.

57 Seven (22%) moderate-severe traumatic brain injury and 0 (0%) mild traumatic brain injury pati

58 ents with isolated moderate-severe traumatic brain injury and 32 patients with isolated mild traumati

59 including 6516 (78%) after severe traumatic brain injury and 749 (9%) after severe thoracoabdominal

60 a single ventricle experience a high rate of brain injury and adverse neurodevelopmental outcome; how

61 helial cells are able to initiate the APR to brain injury and are sufficient to generate the associat

62 Thus, in addition to the acute brain injury and consequent impairment, ischemic stroke

63 epolarizations as a clinical marker of early brain injury and establish a clinically relevant model t

64 This study examined mild traumatic brain injury and genetic risk as predictors of reduced c

65 acellular vesicles (EVs) are increased after brain injury and have the potential to carry targeted in

66 ediation analysis showed that mild traumatic brain injury and high genetic risk indirectly influenced

67 s, such that individuals with mild traumatic brain injury and high genetic risk showed reduced cortic

68 measured by MRI, and produces signatures of brain injury and impaired motor function.

69 te that the TSPO ligand etifoxine attenuates brain injury and inflammation after ICH.

70 d the impact of a TSPO ligand, etifoxine, on brain injury and inflammation in 2 mouse models of ICH.

71 n cerebrospinal fluid after severe traumatic brain injury and is an informative biomarker of edema an

72 gnaling in both ischemia/reperfusion-induced brain injury and ischemic preconditioning-mediated neuro

73 ial to guide targeted therapies in traumatic brain injury and other diseases involving cerebral edema

74 and 58, many of whom carried mild traumatic brain injury and post-traumatic stress disorder diagnose

75 d that the exclusion of patients with anoxic brain injury and refractory cardiogenic shock from publi

76 n mice can facilitate mechanistic studies of brain injury and repair after ischemia, but this manipul

77 The results suggest that localized brain injury and repair, indicated by higher TSPO signal

78 following brain injuries, such as traumatic brain injury and stroke, and is often associated with ne

79 ion levels in patients with severe traumatic brain injury and the feasibility of a Phase III efficacy

80 ystems, assess the contribution of traumatic brain injury and thoracoabdominal injury to observed var

81 quantitative PLR correlates with postanoxic brain injury and, when compared to standard multimodal a

82 to those born very preterm without perinatal brain injury, and age-matched controls born at full term

83 Since adult OSA manifests MRI evidence of brain injury, and animal models lead to regional neurona

84 ion of non-vasospasm components of secondary brain injury, and is a more efficient and cost-effective

85 lthy patients with moderate-severe traumatic brain injury, and it is reversible over the first week o

86 ual and contextual factors such as diabetes, brain injury, and neighbourhood income.

87 n in mouse models of glioblastoma, traumatic brain injury, and Parkinson's disease.

88 s underlying epileptogenesis after pediatric brain injury, and provide evidence of IL-1 signaling as

89 traocular hemorrhages secondary to traumatic brain injury, and the timing of vitrectomy in relation t

90 matic epilepsy in a mouse model of pediatric brain injury, and to evaluate the role of interleukin-1

91 dramatic shift in focus from newly acquired brain injuries associated with corrective and palliative

92 asing mortality and risk for severe neonatal brain injury associated with administration-to-birth int

93 on mediated by microglia plays a key role in brain injury associated with preterm birth, but little i

94 ptiform activity per se contributes to focal brain injury, at least in the neocortical epilepsies con

95 rthermore, Rapamycin negated miR-96 mediated brain injury attenuation through inducing autophagosome

96 of inflammatory conditions such as traumatic brain injury, autoimmune disorders, and infections to ne

97 ich regulate responses to neuroinflammation, brain injury, autoimmunity and neurogenesis.

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

99 and older with moderate or severe traumatic brain injury (Barell Matrix Type 1 classification, Inter

100 t of secondary injury after severe traumatic brain injury based on brain tissue oxygenation and intra

101 y for Terson syndrome secondary to traumatic brain injury between 1997 and 2015.

102 n developed to standardize care in traumatic brain injury, between-center variation in treatment appr

103 We evaluated the expression of brain injury biomarkers on postsurgical brain tissue obt

104 A high fidelity 3D computational model of brain injury biomechanics was developed and the contours

105 recently been linked to sleep and traumatic brain injury, both of which can affect the progression o

106 nial hypertension in patients with traumatic brain injury but was associated with harm in the Eurothe

107 as markers of the severity and evolution of brain injury, but have not been widely explored in TBM.

108 xamined variation in treatment for traumatic brain injury by assessing factors influencing treatment

109 kened to the syndrome that sometimes follows brain injury called hemispatial neglect, in which patien

110 that occurs upon BBB dysfunction in various brain injuries can predispose neural circuitry to the de

111 Traumatic brain injury can lead to the neurodegenerative disease c

112 ter variation in treatment for patients with brain injury can only partly be explained by differences

113 SCIENTIFIC COMMENTARY ON THIS ARTICLE: Focal brain injury can sometimes lead to bizarre symptoms, suc

114 Right brain injury causes visual neglect - lost awareness of l

115 cation channel M4 is upregulated only after brain injury, causing edema in animal studies.

116 In severe traumatic brain injury, cerebral perfusion pressure management bas

117 brain injury group relative to those without brain injury (Cohen's d = 1.36, p=0.02) and the control

118 and 32 patients with isolated mild traumatic brain injury (comparison group) was assessed with transt

119 cardiogram within 1 day after mild traumatic brain injury (comparison group).

120 ead coil from each of 3 concussive traumatic brain injury (cTBI) patients and 4 controls twice 0 to 2

121 inopathy of prematurity; and severe neonatal brain injury, defined as an intraventricular hemorrhage

122 minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivit

123 s a measure of overall disability identified brain injury diagnosis, preinjury intelligence, motor st

124 Traumatic brain injury due to blast exposure is currently the most

125 relevant for two common clinical sequela of brain injury: edema and seizures.

126 Brain injury elicits a systemic acute-phase response (AP

127 ogic conditions, including stroke, traumatic brain injury, encephalopathy, and dementia.

128 In patients with traumatic brain injury, ESA therapy did not increase the number of

129 lycaemia is essential to avoid hypoglycaemic brain injury, especially in the vulnerable neonatal and

130 An increasing trend suggested ongoing brain injury, even though markers of inflammation declin

131 This suggests that the link between AF and brain injury extends beyond thromboembolic complications

132 major cause of delayed surgery was traumatic brain injury, followed by facial or orbital fracture, lo

133 uding significant downregulation of NLRX1 in brain injury following aneurysm.

134 use of the retina as a surrogate to evaluate brain injury following exposure to blast is also highlig

135 busive head trauma from those with traumatic brain injury from other mechanisms.

136 luded history of playing rugby and traumatic brain injury, general and mental health, life stress, co

137 children (age < 18 yr) with severe traumatic brain injury (Glasgow Coma Scale </= 8; intracranial pre

138 e patients with moderate or severe traumatic brain injury (Glasgow Coma Scale, 3-13).

139 pocampal volume was reduced in the perinatal brain injury group relative to controls (Cohen's d = 1.1

140 thesis capacity was reduced in the perinatal brain injury group relative to those without brain injur

141 Current prehospital traumatic brain injury guidelines use a systolic blood pressure th

142 and poor outcome following severe traumatic brain injury has been reported in observational studies.

143 viduals with amusia (congenitally, or from a brain injury) have difficulty humming melodies but can b

144 Among males with mild traumatic brain injury, high genetic risk for Alzheimer's disease

145 the success of endogenous neurogenesis after brain injury holds therapeutic promise.

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

147 nd Analysis of Clinical Trials in [Traumatic Brain Injury] (IMPACT) extended model sum scores to dete

148 enefits of hypothermia therapy for traumatic brain injuries in adults and children by analyzing morta

149 y a beneficial treatment following traumatic brain injuries in adults but cannot be recommended in ch

150 a common cause of morbidity after traumatic brain injury in early childhood.

151 review the suggested pathophysiology behind brain injury in HF, describe its effect on patients' out

152 sheep model that reproduces key features of brain injury in human preterm survivors.

153 and seizure susceptibility, after pediatric brain injury in mice.

154 LIP ultrasound stimulation protects against brain injury in the hippocampus and corpus callosum in r

155 Perinatal brain injuries, including hippocampal lesions, cause las

156 who had suffered a primary, closed traumatic brain injury; increased intracranial pressure; an initia

157 Management of severe traumatic brain injury informed by multimodal intracranial pressur

158 p in microglial exosomes following traumatic brain injury inhibits neuronal inflammation and contribu

159 traocular hemorrhages secondary to traumatic brain injury, irrespective of the timing of vitrectomy o

160 Traumatic brain injury is a major cause of death and disability, y

161 results provide evidence that mild traumatic brain injury is associated with greater neurodegeneratio

162 ns of altered brain physiology after diffuse brain injury is challenging.

163 Risk of brain injury is increased during neonatal cardiac surger

164 Moderate-to-severe traumatic brain injury is one of the strongest environmental risk

165 ation-directed treatment of severe traumatic brain injury is warranted.

166 stroke, intracerebral hemorrhage, traumatic brain injury, ischemia-reperfusion injury, and kidney de

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

168 ory effects of blast and potential traumatic brain injury may also exert an effect.

169 uggesting that additional damage after acute brain injury may be reflected by frequency changes in el

170 Brain injury may interrupt menstrual patterns by alterin

171 Patients with acute severe traumatic brain injury may recover consciousness before self-expre

172 tery occlusion, or neonatal hypoxic-ischemic brain injury, Mn preferentially accumulated in perilesio

173 eine (NAC) exhibits protective properties in brain injury models and has undergone a number of clinic

174 -) mice to develop spinal cord- or traumatic brain injury models for the evaluation of the regenerati

175 Results showed that mild traumatic brain injury moderated the relationship between genetic

176 te treatment of children with mild traumatic brain injury (mTBI) and intracranial injury (ICI) on com

177 s unknown the extent to which mild traumatic brain injury (mTBI) may impact these critical functions.

178 ertheless, the upregulation of signatures of brain injury observed in the Zip14 KO mice demonstrates

179 important for better understanding perinatal brain injuries, of which the most common etiologies are

180 death or major morbidity (defined as severe brain injury on postnatal ultrasonography, severe retino

181 nd have the potential to propagate secondary brain injury or generate an environment of repair and re

182 a-analysis were from patients with traumatic brain injury or subarachnoid hemorrhage.

183 lthough it is unclear whether mild traumatic brain injury, or concussion, also confers risk.

184 0.0001); 11.1% to 26.0% for severe traumatic brain injury (P < 0.0001), and 4.7% to 5.9% for thoracoa

185 age-related macular degeneration, traumatic brain injury, Parkinson's disease, and other neurodegene

186 ceptor-1 was present in all severe traumatic brain injury patients (mean = 3.54 +/- 3.39 ng/mL, peak

187 Data from 729 severe traumatic brain injury patients admitted between 1996 and 2016 wer

188 Adult traumatic brain injury patients admitted to intensive care who had

189 validation cohort comprised recent traumatic brain injury patients from San Gerardo Hospital in Monza

190 matic brain injury and 0 (0%) mild traumatic brain injury patients had systolic dysfunction within th

191 increased intracranial pressure in traumatic brain injury patients has been previously developed and

192 ng abnormalities in a cohort of 97 traumatic brain injury patients were also mapped at the grey matte

193 phic recordings) as an epilepsy biomarker in brain injury patients.

194 ure threshold management in severe traumatic brain injury patients.

195 in advance, in adult and pediatric traumatic brain injury patients.

196 One hundred nineteen severe traumatic brain injury patients.

197 ples were collected from 28 severe traumatic brain injury patients.

198 dysfunction among moderate-severe traumatic brain injury patients.

199 cently treated adult and pediatric traumatic brain injury patients.

200 Unlike other traumatic brain injury populations in children, female predominanc

201 tients who died as a result of a devastating brain injury (possible donors) in 68 hospitals during No

202 n occurs after single and repeated traumatic brain injury, possibly through sports-related concussive

203 partial seizures (CPSs) following traumatic brain injury (post-traumatic epilepsy).

204 ghly novel NLR as a significant modulator of brain injury progression.

205 phatic system has been linked with traumatic brain injury, prolonged wakefulness, and aging.

206 patients undergoing CT imaging for traumatic brain injury recruited between January and October 2015.

207 Patients with brain injury requiring invasive ICP monitoring were cons

208 Traumatic and nontraumatic brain injury results from severe disruptions in the cell

209 Vascular brain injury results in loss of structural and functiona

210 venom preconditioning (VPC) reduces surgical brain injury (SBI)-induced neuroinflammation via activat

211 e hemorrhage in the rodent model of surgical brain injury (SBI).

212 ion and Relevance: The Biomarkers for Infant Brain Injury Score, a multivariable model using 3 serum

213 e multivariable model, Biomarkers for Infant Brain Injury Score, was applied prospectively to 599 pat

214 , race/ethnicity, Injury Severity Score, and brain injury severity using the head and neck Abbreviate

215 AA and Cr (p < 005), while cerebral cortical brain injury severity was inversely associated with both

216 what opposite, roles in motor recovery after brain injury.SIGNIFICANCE STATEMENT The dorsal and ventr

217 Severe brain injury significantly influences immune responses;

218 ellence in Prehospital Injury Care Traumatic Brain Injury Study.

219 Brain injuries substantially change the entire landscape

220 devastating disorder that develops following brain injuries, such as traumatic brain injury and strok

221 rience a single moderate to severe traumatic brain injury suggest widespread persistent microglial ac

222 rophylaxis in patients with severe traumatic brain injuries (TBI).

223 itive fatigue between persons with traumatic brain injury (TBI) and healthy controls (HCs).

224 ury and determine the influence of traumatic brain injury (TBI) and massive transfusion on fibrinolys

225 Studies of the association between traumatic brain injury (TBI) and suicide attempt have yielded conf

226 re are over 2 million incidents of traumatic brain injury (TBI) and treatment options are non-existen

227 Traumatic brain injury (TBI) can have lifelong and dynamic effects

228 Traumatic brain injury (TBI) can induce cognitive dysfunction due

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

230 Traumatic brain injury (TBI) contributes to one third of injury re

231 Traumatic brain injury (TBI) increases the risk of Alzheimer's dis

232 The impact of traumatic brain injury (TBI) involves a combination of complex bio

233 Traumatic brain injury (TBI) is a common disabling condition with

234 Traumatic brain injury (TBI) is a leading cause of long-term neuro

235 Traumatic brain injury (TBI) is a leading cause of morbidity and d

236 Traumatic brain injury (TBI) is a major contributor to morbidity a

237 Traumatic brain injury (TBI) is a major public health issue, produ

238 Traumatic brain injury (TBI) is a serious public health problem, o

239 Traumatic brain injury (TBI) is a significant global public health

240 Epilepsy after pediatric traumatic brain injury (TBI) is associated with poor quality of li

241 Traumatic brain injury (TBI) is characterized by acute neurologica

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

243 Traumatic brain injury (TBI) is extremely common across the lifesp

244 Traumatic brain injury (TBI) is known to cause perturbations in th

245 Traumatic brain injury (TBI) is set to become the leading cause of

246 s after TBI.SIGNIFICANCE STATEMENT Traumatic brain injury (TBI) is the leading cause of death and dis

247 olved in the MQC in rats receiving traumatic brain injury (TBI) of different severities.

248 led cortical impact model (CCI) of traumatic brain injury (TBI) on their distribution.

249 n of pathways directly involved in traumatic brain injury (TBI) pathogenesis and have been used to in

250 f neuron-specific enolase (NSE), a traumatic brain injury (TBI) protein biomarker, in diluted blood p

251 NAs) cause neurodegeneration after traumatic brain injury (TBI) remain elusive.

252 Traumatic brain injury (TBI) results in rapid recruitment of leuko

253 E4 (ApoE4) genotype combines with traumatic brain injury (TBI) to increase the risk of developing Al

254 Blast exposure, not mild traumatic brain injury (TBI), acted as the primary military deploy

255 shown to occur in animal models of traumatic brain injury (TBI), and blocking this form of tau using

256 Brain damage due to stroke or traumatic brain injury (TBI), both leading causes of serious long-

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

258 nstay of therapy for children with traumatic brain injury (TBI), but its overall association with pat

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

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

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

262 earning, is dysregulated following traumatic brain injury (TBI), suggesting that stimulation of BDNF

263 After traumatic brain injury (TBI), the ability of cerebral vessels to a

264 o fluid shear stress in a model of traumatic brain injury (TBI), we found that shear stress induced C

265 ress, which has been implicated in traumatic brain injury (TBI).

266 lly underdiagnosed complication of traumatic brain injury (TBI).

267 following traumatic spinal cord or traumatic brain injury (TBI).

268 nic traumatic encephalopathy after traumatic brain injury (TBI).

269 ictors of outcome in patients with traumatic brain injury (TBI).

270 ersistent cognitive problems after traumatic brain injury (TBI).

271 mpact (CCI) injury murine model of traumatic brain injury (TBI).

272 this balance can be altered after traumatic brain injury (TBI).

273 people seek medical attention for traumatic brain injury (TBI).

274 rs including Alzheimer disease and traumatic brain injury (TBI).

275 l energetic metabolism arise after traumatic brain injury (TBI).

276 ckers improve outcomes after acute traumatic brain injury (TBI).

277 l brain and white matter following traumatic brain injury (TBI).

278 come measure (clinically important traumatic brain injury [TBI], need for neurological intervention,

279 term functional outcomes following traumatic brain injury(TBI).

280 g-term clinical effects of wartime traumatic brain injuries (TBIs), most of which are mild, remain in

281 n why males are more vulnerable to perinatal brain injuries than females.

282 It can develop after brain injuries that damage the hippocampus.

283 s triggered by blast-induced, mild traumatic brain injury that is commonly observed in militarized zo

284 Thus, in patients with traumatic brain injury, the concept that 90 mm Hg represents a uni

285 used in the early phase following traumatic brain injury, the prognostic utility of MRI remains unce

286 in models of stroke, infection and traumatic brain injury, though the exact role of the immunoproteas

287 volume fraction of sulcal regions exceeding brain injury thresholds were significantly larger than t

288 icipates in the response to ischemia-induced brain injury through oxidized metabolites that regulate

289 tensive care unit for acute severe traumatic brain injury to test two hypotheses: (i) in patients who

290 ts who were born very preterm with perinatal brain injury to those born very preterm without perinata

291 n altered cerebellar metabolite profiles and brain injury topography, severity of injury, and prematu

292 e first week after moderate-severe traumatic brain injury; transthoracic echocardiogram within 1 day

293 ears to be a substantial advance in treating brain injuries treated with shunts and has the potential

294 s and Decisions in Acute Pediatric Traumatic Brain Injury Trial-a comparative effectiveness study usi

295 ignificant risk reduction of severe neonatal brain injury was associated with longer administration-t

296 METHOD: Outcome after exposure to repeated brain injury was investigated in 52 retired male Scottis

297 tion of spreading depolarizations with early brain injury was then investigated in 23 patients [14 fe

298 ow Outcome Scale for patients with traumatic brain injury were the pressure reactivity index, transcr

299 The odds of discovering brain injury with adjustment for surgical stage as well

300 MRI following traumatic brain injury yields important prognostic information, wi