ライフサイエンスコーパス: traumatic

1 EMD-MNH) in Dar Es Salaam, Tanzania with non-traumatic abdominal pain from September 2017 to October

2 ng-term outcome of vehicle-traumatic and non-traumatic AKI requiring renal replacement therapy (AKI-R

3 After propensity matching with non-traumatic AKI-RRT cases with similar demographic and cli

4 Despite severe injuries, vehicle-traumatic AKI-RRT patients had better long-term survival

5 Compared to non-traumatic AKI-RRT, vehicle-traumatic AKI-RRT patients had longer length of stay in

6 Vehicle-traumatic AKI-RRT patients had lower rates of long-term

7 ng risk models that focused on ESKD, vehicle-traumatic AKI-RRT patients were associated with lower ES

8 talization were identified, and matching non-traumatic AKI-RRT patients were identified between 2000

9 ients had better long-term survival than non-traumatic AKI-RRT patients, but a similar risk of ESKD.

10 546 vehicle-traumatic AKI-RRT patients, median age 47.6 years (inter

11 52; 95% CI, 0.325-0.937; p = 0.028) than non-traumatic AKI-RRT patients.

12 .134; 95% CI, 0.894-1.438; p = 0.301) as non-traumatic AKI-RRT patients.

13 Compared to non-traumatic AKI-RRT, vehicle-traumatic AKI-RRT patients ha

14 standing of long-term outcomes after vehicle-traumatic AKI-RRT.

15 We compared the long-term outcome of vehicle-traumatic and non-traumatic AKI requiring renal replacem

16 on the characteristic MRI features of common traumatic and pathologic conditions of the hip.

17 ging techniques, and MRI findings of various traumatic and pathologic conditions of the wrist and han

18 maging modality in the assessment of various traumatic and pathologic conditions of this region, and

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

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

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

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

23 34%) than those >=65 (ICC = 5 to 6%) and for traumatic brain injury (ICC = 5 to 13%) than other injur

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

45 Traumatic brain injury (TBI) is largely non-preventable

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 Traumatic brain injury causes monocyte functional impair

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

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

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

71 Repetitive mild traumatic brain injury in American football players has

72 Traumatic brain injury increases proinflammatory cytokin

73 Traumatic brain injury is a major risk factor for acquir

74 Traumatic brain injury is associated with elevated rates

75 Traumatic brain injury is the number one cause of death

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

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

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

79 Disparities in traumatic brain injury outcomes for ethnic minorities an

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

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

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

83 architectural disturbances were observed in traumatic brain injury patients.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 rs would improve cognitive performance after traumatic brain injury.

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

106 Consecutive patients with severe traumatic brain injury.

107 n underestimated therapeutic potential after traumatic brain injury.

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

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

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

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

112 damage during brain tissue deformation from traumatic brain injury.

113 neurological disability in individuals with traumatic brain or spinal cord injury, glaucoma and isch

114 We present here a case with traumatic cataract and corneal opacity after laser-assis

115 Sixty-seven eyes from 67 patients, with traumatic cataract severe enough to prevent slit lamp ev

116 1% had developmental cataract, and 21.3% had traumatic cataract.

117 patients with concurrent corneal opacity and traumatic cataract.

118 ient traumatic cues, partial amnesia for the traumatic context can also be observed.

119 n tumours, ischaemic stroke and haemorrhagic traumatic contusion.

120 While this hypermnesia relates to salient traumatic cues, partial amnesia for the traumatic contex

121 Of these, 91.1% had traumatic deaths, with major causes including nonhead bl

122 also plays a vital role in the diagnosis of traumatic duodenal injury by differentiating between mur

123 Duodenal wall haematoma and traumatic duodenal perforation causing pneumoretroperito

124 hip between hospital volume and survival for traumatic emergencies.

125 ms) and from Alzheimer's disease and chronic traumatic encephalopathy (CTE) (in which both 3R and 4R

126 m pathologic changes consistent with chronic traumatic encephalopathy (CTE) have been reported in ASF

127 Chronic traumatic encephalopathy (CTE) in particular is associat

128 Chronic traumatic encephalopathy (CTE) is a neurodegenerative di

129 Chronic traumatic encephalopathy (CTE) is a neurodegenerative di

130 Chronic traumatic encephalopathy (CTE) is associated with repeat

131 neurodegenerative disease, including chronic traumatic encephalopathy (CTE).

132 ly proposed diagnostic clinical criteria for traumatic encephalopathy syndrome, in particular the inc

133 ality are proposed as diagnostic features of traumatic encephalopathy syndrome, the putative clinical

134 disease, frontotemporal dementia and chronic traumatic encephalopathy(1).

135 ublic attention following reports of chronic traumatic encephalopathy, a progressive tauopathy.

136 progressive supranuclear palsy, and chronic traumatic encephalopathy.

137 e, including Alzheimer's disease and chronic traumatic encephalopathy.

138 cal extracts from donors with AD and chronic traumatic encephalopathy.

139 ve clinical syndrome associated with chronic traumatic encephalopathy.

140 ases such as Alzheimer's disease and chronic traumatic encephalopathy.

141 ly seizures and is the leading cause of post-traumatic epilepsy.

142 Those who report SDs prior to a traumatic event are at greater risk for developing PTSD;

143 Physical proximity to a traumatic event increases the severity of accompanying s

144 d from the emergency department (ED) after a traumatic event(1).

145 t observed when opioids were given after the traumatic event.

146 velop in a subset of individuals following a traumatic event.

147 People exposed to complex traumatic events are at risk of not only posttraumatic s

148 While large-scale traumatic events are known to increase psychological dis

149 Complex traumatic events associated with armed conflict, forcibl

150 known if people who have experienced complex traumatic events can benefit and tolerate these commonly

151 The Traumatic Events Inventory (TEI) and Clinician-Administe

152 Intrusive re-experiencing of traumatic events is a hallmark symptom of posttraumatic

153 interventions for people exposed to complex traumatic events is a research and clinical priority.

154 Exposure to traumatic events is common.

155 orne by the COVID-19 pandemic and other mass traumatic events that are accompanied by substantial fin

156 aw injury from any of 9 types of potentially traumatic events was determined using quarterly (3-month

157 (rg = 0.16, p = 0.026) and traits related to traumatic events, and the presence of social support (-0

158 cterized by persistent fear memory of remote traumatic events, mental re-experiencing of the trauma,

159 r PTSD symptoms in people exposed to complex traumatic events, published up to 25 October 2019.

160 D symptoms, and because they seem to precede traumatic events, we next investigated the relationship

161 health problems in people exposed to complex traumatic events.

162 s more frequent among individuals exposed to traumatic events.

163 th post-traumatic stress disorder (PTSD) and traumatic experiences, but the underlying mechanisms are

164 d to the transmission of symptoms induced by traumatic experiences.

165 muscle fibrosis in ischemia reperfusion and traumatic extremity injury.

166 drugs for neuroprotection in the setting of traumatic eye injury.

167 ive adult patients presenting with acute non-traumatic gastrointestinal symptoms, who underwent stand

168 A multiscale deep learning method for traumatic hemoperitoneum quantitative visualization had

169 terquartile range, 25-50 years; 79 men) with traumatic hemoperitoneum who underwent CT of the abdomen

170 he spinal cord of squirrel monkeys following traumatic injuries, and their relationships to function

171 cute respiratory distress syndrome following traumatic injury are substantially higher than previousl

172 and local hypoxia that occurs as a result of traumatic injury, cell transplantation, or tumor growth,

173 After surgery or traumatic injury, corneal wound healing can cause a scar

174 ths remain a major source of mortality after traumatic injury.

175 inflammatory conditions, including sepsis or traumatic injury.

176 ies of cancer or dementia, and admission for traumatic injury.

177 y injury (AKI) is a frequent complication of traumatic injury; however, long-term outcomes such as mo

178 sis for nonoperative expectant management of traumatic IT of the thoracic aorta remains weak.

179 fied by polygenic risk scores or by reported traumatic life events.

180 artment (ED) treatment in the aftermath of a traumatic life experience.

181 Secondary analyses included risks of traumatic lumbar puncture (>300 x 106 erythrocytes/L aft

182 Traumatic lumbar punctures occurred more frequently amon

183 omposite allograft recipients and victims of traumatic major limb amputation.

184 on data-driven and contextual processing of traumatic material, mechanisms proposed to be relevant f

185 -update is a promising approach to attenuate traumatic memories.

186 n which patients suffer from unwanted (e.g., traumatic) memories.

187 -beta1 is responsible for the development of traumatic muscle fibrosis, and its blockade offers a pro

188 ent dorsal horn of the spinal cord following traumatic nerve injury.

189 of potential predictors of longitudinal post-traumatic neurodegeneration and compared the variance in

190 models, diffuse axonal injury triggers post-traumatic neurodegeneration, with axonal damage leading

191 jury predicts the degree of progressive post-traumatic neurodegeneration.

192 metric T1 scans as a measure of measure post-traumatic neurodegeneration.

193 axonal injury are a strong predictor of post-traumatic neurodegeneration.

194 and late infection, indicating enhanced post-traumatic neuroinflammation.

195 cient (IFN-beta(-/-)) mice and assessed post-traumatic neuroinflammatory responses, neuropathology, a

196 immune receptor TLR4 directly regulates post-traumatic neuronal excitability.

197 multisite longitudinal study of adverse post-traumatic neuropsychiatric sequelae (APNS) among partici

198 ted knees in a rat model of established post-traumatic OA (PTOA).

199 and a mouse model of blast-induced indirect traumatic optic neuropathy (bITON) showed that PPS and P

200 The pattern indeed also was observed in traumatic or degenerative conditions.

201 ions have been reported in experimental post-traumatic osteoarthritis (PTOA) animal models and in nat

202 Post-traumatic osteoarthritis (PTOA) is associated with carti

203 artilage degradation and progression of post traumatic osteoarthritis (PTOA).

204 tions between immunogenetic factors and post-traumatic sepsis and septic shock.

205 n is associated with the development of post-traumatic sepsis and septic shock.

206 as they implicate adaptive immunity in post-traumatic sepsis.

207 tomical-functional paradox in the context of traumatic spinal cord injury (SCI) and discuss the under

208 ptibility during the chronic phase following traumatic spinal cord injury.

209 pathy represents the most common form of non-traumatic spinal cord injury.

210 Traumatic spinal tap occurred more often in patients wit

211 f patients affected by idiopathic, myopic or traumatic stage 4 MH (minimum diameter > 400 mum) treate

212 ation of an algorithm for prediction of post-traumatic stress course over 12 months using two indepen

213 CI 1.14-1.23, p < 0.001), particularly post-traumatic stress disorder (HR 9.33, 95% CI 7.96-10.94, p

214 of two clinically relevant subtypes of post-traumatic stress disorder (PTSD) and major depressive di

215 protein (CRP) have been associated with post-traumatic stress disorder (PTSD) and traumatic experienc

216 idate that has enhanced extinction in a post-traumatic stress disorder (PTSD) animal model and was re

217 ing if traumatic brain injury (TBI) and post-traumatic stress disorder (PTSD) are risk factors for Pa

218 nd are at increased risk for developing post-traumatic stress disorder (PTSD) compared with the gener

219 Post-traumatic stress disorder (PTSD) impacts many veterans a

220 Post-traumatic stress disorder (PTSD) is a common, debilitati

221 Post-traumatic stress disorder (PTSD) is a debilitating disor

222 Post-traumatic stress disorder (PTSD) is a heterogeneous cond

223 Post-traumatic stress disorder (PTSD) is characterized by emo

224 Post-traumatic stress disorder (PTSD) is characterized by per

225 rs.SIGNIFICANCE STATEMENT Patients with post-traumatic stress disorder (PTSD) show heightened amygdal

226 The increased prevalence of post-traumatic stress disorder (PTSD) that is observed in wom

227 ere calculated for depression, anxiety, post-traumatic stress disorder (PTSD), and suicidal behaviour

228 dy of the neurobiological correlates of post-traumatic stress disorder (PTSD), little is known about

229 (TBS) is a potential new treatment for post-traumatic stress disorder (PTSD).

230 ctful and commonly reported symptoms in post-traumatic stress disorder (PTSD).

231 mmon feature of panic disorder (PD) and post-traumatic stress disorder (PTSD).

232 ychiatric disorders such as phobias and post-traumatic stress disorder (PTSD).

233 order (BD), Schizophrenia, anxiety, and Post Traumatic Stress Disorder (PTSD).

234 a hallmark of emotional disorders like post-traumatic stress disorder (PTSD).

235 : presence of daily pain; screening for post-traumatic stress disorder (PTSD); new functional limitat

236 Post-traumatic stress disorder and cocaine use disorder are h

237 thus it appears that the development of post-traumatic stress disorder drives cocaine use vulnerabili

238 The onset of post-traumatic stress disorder generally occurs prior to the

239 Primary outcome was symptoms of post-traumatic stress disorder in family members 90 days afte

240 days after the ICU discharge to predict post-traumatic stress disorder symptoms at 3 months, the area

241 5 at 3 months were considered as having post-traumatic stress disorder symptoms.

242 ction of patients at risk of developing post-traumatic stress disorder symptoms.

243 01) were identified as risk factors for post-traumatic stress disorder symptoms.

244 Rates of depression, anxiety, and post-traumatic stress disorder were similar to other critical

245 e recently characterized a rat model of post-traumatic stress disorder with segregation of rats as su

246 treatments for memory disorders such as post-traumatic stress disorder(5).

247 rly symptoms of anxiety, depression, or post-traumatic stress disorder) critical illness that can be

248 n Scale; Impact of Event Scale-Revised (post-traumatic stress disorder); 6-minute walk; and/or the Eu

249 , poor sleep quality, somatic symptoms, post-traumatic stress disorder, being overweight and negative

250 logic and psychologic diagnoses such as post-traumatic stress disorder, cardiovascular disease, and d

251 ged stress, a validated rodent model of post-traumatic stress disorder, in combination with optogenet

252 otential for use in pharmacotherapy for post-traumatic stress disorder.

253 ed in depression, bipolar disorder, and post-traumatic stress disorder.

254 social stimuli in models of anxiety and post-traumatic stress disorder.

255 a model that captures features of human post-traumatic stress disorder.

256 was associated with reduced symptoms of post-traumatic stress disorder.

257 ries in disorders such as addiction and post-traumatic stress disorder.

258 ts for memory-related disorders such as post-traumatic stress disorder.

259 of many psychiatric illnesses, such as post-traumatic stress disorder.

260 ortion, and treatment of disorders like post-traumatic stress disorder.

261 tress-related memory disorders, such as post-traumatic stress disorder.

262 ted with psychiatric disorders, such as post-traumatic stress disorder.

263 as a novel treatment for depression and post-traumatic stress disorder.

264 ed in the context of the development of post-traumatic stress disorder.

265 plasticities that underlie anxiety and post-traumatic stress disorders in humans.

266 egative outcomes such as substance abuse and traumatic stress disorders.

267 been demonstrated to be useful to treat post-traumatic stress disorders.

268 logical and endocrine processes triggered by traumatic stress eventually give rise to debilitating em

269 mpassion satisfaction, burnout and secondary traumatic stress from among demographic and work-related

270 in adolescence can regulate vulnerability to traumatic stress in adulthood through region-specific ep

271 ensitization of fear learning seen following traumatic stress in mice.

272 r studies demonstrate that susceptibility to traumatic stress is associated with a cocaine use-vulner

273 Results indicate that susceptibility to traumatic stress is associated with alterations in phasi

274 ssion at these synapses blocks the effect of traumatic stress on aggression.

275 or equal to 24 hours were screened with Post-Traumatic Stress Scale 10 intensive part B after ICU dis

276 group versus control group, with a mean Post-Traumatic Stress Scale 10 intensive part B score 39 (95%

277 Sense of Coherence Scale 13 and Post-Traumatic Stress Scale 10 intensive part B were complete

278 were associated with increased level of post-traumatic stress symptoms at 12 months.

279 id not reveal any significant effect on post-traumatic stress symptoms or sense of coherence after IC

280 No differences in post-traumatic stress symptoms or sense of coherence were fou

281 Post-traumatic stress symptoms were assessed via self-report

282 egative psychological effects including post-traumatic stress symptoms, confusion, and anger.

283 mpassion satisfaction, burnout and secondary traumatic stress were 32.63+/-6.46, 27.36+/-5.29, and 26

284 on making, caregiver-related transmission of traumatic stress, and other areas may offer new targets

285 ntributes to increased aggression induced by traumatic stress, and weakening synaptic transmission at

286 and smoke exposure were related to secondary traumatic stress, explaining 9% of the variance.

287 DLINE, Published International Literature on Traumatic Stress, PsycINFO, and Science Citation Index f

288 using a mouse model of paternal exposure to traumatic stress, we identify circulating factors involv

289 gies to reduce nurses' burnout and secondary traumatic stress, while supporting compassion satisfacti

290 priming, naturally occurring aggression, and traumatic stress-induced aggression increase.

291 mpassion satisfaction, burnout and secondary traumatic stress.

292 compassion satisfaction, burnout and second traumatic stress.

293 Strikingly, FAAH inhibition during the traumatic stressor was also effective 10 d later on the

294 ental disorders can be induced by chronic or traumatic stressors.

295 ted with anxiety, perceived stress, and post-traumatic symptomatology.

296 how differences in anxiety, stress, and post-traumatic symptoms compared to non-cancer participants.

297 After minimally traumatic tooth extraction, alveolar ridge dimensions we

298 scribe the incidence, therapy and outcome of traumatic tracheobronchial injuries (TTBI) in trauma pat

299 yet strong evidence of benefit for the post-traumatic variant.

300 Active-duty Army personnel can be exposed to traumatic warzone events and are at increased risk for d