ライフサイエンスコーパス: TBI

1 TBI + Sp mice infected 60 days post-injury had a 60% mor

2 TBI increased expression of DNA sensors cyclic GMP-AMP s

3 TBI increased expression of proinflammatory mediators in

4 TBI was used in 660 patients (46%).

5 TBI-induced activation of microglia and peripherally-der

6 TBI-induced secondary injury processes including persist

7 The study included 33 TBI patients with ventricular CSF serially sampled, and

8 108 participants (43 TBI, 26 PD, 8 RBD, 31 controls) were assessed.

9 uid (CSF) concentrations of MMPs after acute TBI and in relation to clinical outcomes, with patients

10 tected mice from BBB degradation after acute TBI.

11 itors may be useful therapeutically in acute TBI and post-concussion syndrome.

12 tion of these cells into brain acutely after TBI would attenuate secondary damage and preserve anatom

13 nuated and improved cognitive function after TBI.

14 y-based analysis of rat microglia 24 h after TBI using the controlled cortical impact model, validate

15 e role of IFN-beta in secondary injury after TBI using a controlled cortical impact model in adult ma

16 ial activation and white matter injury after TBI.

17 in any of the subsets of interneurons after TBI.

18 deficits, and limited tissue loss long after TBI.

19 ion of chronically activated microglia after TBI led to widespread changes in the cortical transcript

20 phase removal of neurotoxic microglia after TBI using CSF1R inhibitors markedly reduce chronic neuro

21 patients arrived alive at military MTF after TBI.

22 nisms behind chronic neurodegeneration after TBI, along with a putative treatment strategy.

23 to these cells to enhance neurogenesis after TBI.

24 lso upregulated early and persistently after TBI.

25 aminergic abnormalities are often seen after TBI, but patients usually lack parkinsonian features.

26 ociated with the emergence of seizures after TBI.

27 s increased the likelihood of survival after TBI.

28 iately from the central nervous system after TBI.

29 es, known agents of clinical worsening after TBI.

30 ered before or after irradiation, alleviated TBI and PBI-BM5-induced TJ disruption, barrier dysfuncti

31 rainage function in aged mice can ameliorate TBI-induced gliosis.

32 ylic cranioplasty restoring cranial anatomy (TBI Closed Skull Group).

33 d by miRNA-seq analysis of human control and TBI (acute and chronic) serum samples.

34 ased in TBI compared to both sham groups and TBI RIC.

35 ative PD risk in veterans with TBI(mild) and TBI(non-mild) versus those without TBI when PTSD was pre

36 results show that patients with early PD and TBI have distinct patterns of striatal dopamine abnormal

37 Patients with PD and TBI showed distinct patterns of DaT reduction, with pati

38 identified in 40% of samples from PTLDS and TBI patients (categories 2 and 3 above, n = 59/148).

39 subjects with sports-related TBI (sTBI) and TBI in military veterans (mtTBI) without cognitive impai

40 imulus that upset marrow homeostasis such as TBI.

41 Because TBI increases the risks of other forms of neurodegenerat

42 at pre-existing lymphatic dysfunction before TBI leads to increased neuroinflammation and negative co

43 impairments were decreased in IFN-beta(-/-) TBI mice compared with their injured WT counterparts; im

44 The association between TBI and subsequent breast cancer, especially among those

45 ards models assessed the association between TBI and subsequent breast cancer.

46 Both TBI and PTSD were significantly associated with PD in si

47 study was the first to demonstrate that both TBI and PTSD are independently associated with increased

48 he humanized mouse, marrow aplasia caused by TBI could be alleviated by cell therapy with human bone

49 y, and elevated plasma LPS; TJ disruption by TBI was more severe in Lpar2(-/-) mice compared to wild-

50 Trauma Effectiveness Research in TBI (CENTER-TBI) China registry is a prospective, multicentre, longi

51 nd neurological function in both CCI and CHI TBI models in mice.

52 iffusion imaging network analysis on chronic TBI patients, with different injury severities and healt

53 nergistic excess risk in those with comorbid TBI/PTSD.

54 CI, rats received either a hemi-craniectomy (TBI Open Skull Group) or an immediate acrylic cranioplas

55 ve long-term functional recovery or decrease TBI neuropathology at 28 d post-injury.

56 and metabolite levels at 24 h after diffuse TBI.

57 to identify acute, chronic, focal or diffuse TBI and potentially, presence of neurodegenerative seque

58 Adult male C57BL/6 mice received diffuse TBI by midline fluid percussion or were sham-injured.

59 The Drosophila TBI (dTBI) device inflicts mild, moderate, or severe bra

60 ction, calibration and use of the Drosophila TBI (dTBI) device, a platform that employs a piezoelectr

61 nd female rats at 48 h after an experimental TBI, and how these changes related to neuromotor functio

62 following 2 different models of experimental TBI, controlled cortical impact (CCI), and closed head i

63 Following TBI, the repopulated microglia displayed a ramified morp

64 95% CI, < 0.01 to 0.05; P = .0269) following TBI and 0.33 (95% CI, 0.25 to 0.40) and 0.09 (95% CI, 0.

65 ion in microglia due to activation following TBI.

66 xiety and depressive-like behavior following TBI.SIGNIFICANCE STATEMENT A recent clinical study showe

67 onset of many pathological events following TBI, leading to blood brain barrier (BBB) dysfunction, n

68 ival (OS) was significantly higher following TBI (0.91; 95% CI, 0.86 to 0.95; P < .0001) versus chemo

69 aracterize neurological impairment following TBI in rats with an unrepaired craniectomy versus rats w

70 d lower relapse risk were observed following TBI plus etoposide compared with chemoconditioning.

71 erent roles in the pathophysiology following TBI, and are in turn associated with clinical outcomes.

72 ted in rats with unrepaired skulls following TBI suggests this model may be beneficial for testing ne

73 3.67-3.97), and 2.71 (95% CI: 2.66-2.77) for TBI(mild) , TBI(non-mild) , and PTSD, respectively).

74 resent a tunable, head-specific approach for TBI in Drosophila that recapitulates mammalian injury ph

75 the most effective treatment approaches for TBI.

76 nd proteins provide potential biomarkers for TBI and therapeutic RIC in order to monitor disease prog

77 f picomolar concentrations of biomarkers for TBI in biofluids.

78 e present a strong therapeutic candidate for TBI, immunomodulatory nanoparticles (IMPs), which ablate

79 inically translatable acute intervention for TBI with a well-defined mechanism of action and benefici

80 is, twenty-four putative protein markers for TBI and RIC were identified.

81 The overall study cohort prevalence for TBI(mild) , TBI(non-mild) , and PTSD was 0.65%, 0.69%, a

82 ta may be a potential therapeutic target for TBI.

83 ta may be a potential therapeutic target for TBI.SIGNIFICANCE STATEMENT TBI frequently causes long-te

84 will aid in evaluation of new treatments for TBI and help target specific neuronal subtypes as a func

85 Because current treatments for TBI merely ameliorate secondary effects of the initial i

86 new concepts that the therapeutic window for TBI may be far longer than traditionally believed if chr

87 rast, after delayed infection monocytes from TBI + Sp mice had higher levels of interleukin-1beta, tu

88 This study strongly supports future TBI development by providing a rational method to compar

89 erate or severe TBI, n = 4) from the Glasgow TBI Archive and Penn Neurodegenerative Disease Brain Ban

90 old) in mouse serum on day 1 after 0.5-10 Gy TBI.

91 blative conditioning with fractionated 12 Gy TBI and etoposide versus fludarabine, thiotepa, and eith

92 sed 30-day survival of CD2F1 mice after 9 Gy TBI 12.5-25% compared with the vehicle control treated g

93 90% survival at 50 mg/kg against lethal 9-Gy TBI.

94 However, how TBI affects different interneurons, and how this relates

95 However, it was not understood how TBI leads to an increase in IFNbeta and whether inductio

96 Rat miRNA profiles identified TBI across all acute and chronic intervals.

97 Human miRNA profiles identified TBI across all acute and chronic time points and, at 24

98 This study sought to identify TBI-induced molecular alterations in plasma and whether

99 clinical suspicion of tick-borne illnesses (TBI).

100 nd for improving the efficacy of the drug in TBI.

101 uences of meningeal lymphatic dysfunction in TBI and suggest that therapeutics targeting the meningea

102 sm underlying impaired lymphatic function in TBI, we examined how increased intracranial pressure (IC

103 ury, reversed early cognitive impairments in TBI mice and led to transient improvements in motor func

104 ) was found to be significantly increased in TBI compared to both sham groups and TBI RIC.

105 of MMP-1, MMP-3 and MMP-10 were increased in TBI patients (at baseline) compared with the iNPH group

106 herapy for attenuating early inflammation in TBI.

107 s) was found in the controls but was lost in TBI patients.

108 d to the cognitive impairments manifested in TBI patients.

109 rimary reason for morbidity and mortality in TBI.

110 ay potentially influence clinical outcome in TBI patients.

111 ropean NeuroTrauma Effectiveness Research in TBI (CENTER-TBI) China registry is a prospective, multic

112 type I IFN mechanisms to address its role in TBI pathophysiology.

113 Our aim was to compare the incidence, TBI and treatment in US and UK-led military MTF to ascer

114 artially explained by age, sex, and incident TBI.

115 osis-exposed controls (13 developed incident TBI without subsequent active tuberculosis).

116 ies, sputum TB bacteriologies, TB infection (TBI) testing (tuberculin skin test [TST] and interferon

117 hildren and incident tuberculosis infection (TBI) exist.

118 ated with repeated traumatic brain injuries (TBI) and is characterized by cognitive decline and the p

119 multiforme (GBM), traumatic brain injuries (TBIs), multiple sclerosis (MS), intracerebral hemorrhage

120 in patients without traumatic brain injury (TBI) (35%, N = 679) compared to those with TBI (28%, N =

121 urs following severe traumatic brain injury (TBI) and is believed to contribute to subsequent neurode

122 ve been described in traumatic brain injury (TBI) and may contribute to additional tissue injury and

123 Determining if traumatic brain injury (TBI) and post-traumatic stress disorder (PTSD) are risk

124 Traumatic brain injury (TBI) and rapid eye movement sleep behavioural disorder (

125 better characterise traumatic brain injury (TBI) and to identify the most effective treatment approa

126 of disability after traumatic brain injury (TBI) but relationships with overall functioning in daily

127 Traumatic brain injury (TBI) can result in excitation: inhibition imbalance, as

128 Traumatic brain injury (TBI) causes brain edema that induces increased intracran

129 Traumatic brain injury (TBI) causes early seizures and is the leading cause of p

130 Traumatic brain injury (TBI) has been designated as a signature injury of modern

131 tion associated with traumatic brain injury (TBI) has been modeled in Drosophila using devices that i

132 et current models of traumatic brain injury (TBI) inadequately recapitulate the human immune response

133 Traumatic brain injury (TBI) is a common reason for pediatric emergency room vis

134 GNIFICANCE STATEMENT Traumatic brain injury (TBI) is a debilitating neurological disorder that can se

135 Traumatic brain injury (TBI) is a leading global cause of death and disability.

136 tion in survivors of traumatic brain injury (TBI) is a major cause of morbidity, with no effective th

137 Traumatic brain injury (TBI) is a risk factor for neurodegenerative disease, inc

138 Traumatic brain injury (TBI) is a risk factor for the later development of neuro

139 Traumatic brain injury (TBI) is a serious global health problem, many individual

140 Traumatic brain injury (TBI) is a significant medical problem with limited treat

141 Traumatic brain injury (TBI) is largely non-preventable and often kills or perma

142 Traumatic brain injury (TBI) is often accompanied by gastrointestinal and metabo

143 Traumatic brain injury (TBI) is often characterized by alterations in brain conn

144 Traumatic brain injury (TBI) is the leading cause of death and disability due to

145 Traumatic brain injury (TBI) is the most common cause of death on the modern bat

146 Traumatic brain injury (TBI) is the strongest environmental risk factor for the

147 of-care diagnosis of traumatic brain injury (TBI) lack sensitivity, require specialist handling or in

148 Traumatic brain injury (TBI) results in a cascade of cellular responses, which p

149 the pathogenesis of traumatic brain injury (TBI) was investigated by quantifying Cproteins in plasma

150 ological hallmark of traumatic brain injury (TBI) with molecular markers of angiogenesis and endothel

151 rkinson's disease or traumatic brain injury (TBI), and hence it will be useful to the wider neuroscie

152 flow to a limb after traumatic brain injury (TBI), can modify levels of pathology-associated circulat

153 After traumatic brain injury (TBI), some people have worse recovery than others.

154 patients with severe traumatic brain injury (TBI), yet clinical trials and outcome studies contain re

155 lia are hallmarks of traumatic brain injury (TBI), yet whether these cells contribute to cognitive de

156 ifying therapies for traumatic brain injury (TBI).

157 g patients following traumatic brain injury (TBI).

158 tory responses after traumatic brain injury (TBI).

159 ated with repetitive traumatic brain injury (TBI).

160 l intervention after traumatic brain injury (TBI).

161 anial pressure after traumatic brain injury (TBI).

162 flammation following traumatic brain injury (TBI); however, the underlying mechanism remains elusive.

163 icacy of transmission-blocking intervention (TBI) candidates against Plasmodium falciparum and vivax.

164 mild blast-related TBI (bTBI) to investigate TBI-induced changes within the cortex and hippocampus.

165 Total body irradiation (TBI) before allogeneic hematopoietic stem cell transplan

166 subjected to either total body irradiation (TBI) or partial body irradiation (PBI-BM5).

167 ore or after 4 Gy of total-body irradiation (TBI) promoted rapid and complete hematopoietic recovery,

168 Lethal total body irradiation (TBI) triggers multifactorial health issues in a potentia

169 D45-SAP plus 2 Gy of total body irradiation (TBI), 2 Gy of TBI, 8 Gy of TBI, or no conditioning and t

170 posed to Co-60 gamma total body irradiation (TBI).

171 -suppressive effects of sublethal and lethal TBI in mice.

172 n as the overarching host response to lethal TBI.

173 PLX5622 treatment limited TBI-associated neuropathological changes at 3 months pos

174 display features characteristic of mammalian TBI, including severity-dependent ataxia, life span redu

175 moniae-infected traumatic brain injury mice (TBI + Sp) had a 25% mortality rate, in contrast to no mo

176 In mice, TBI and PBI-BM5 disrupted colonic epithelial tight junct

177 d had a history of persistent PTH after mild TBI for at least 12 months.

178 Though most TBIs are mild, even mild TBI can induce long term effects, including cognitive an

179 d in children <2 years old attended for mild TBI in the emergency room of our tertiary hospital over

180 Surgical intervention for mild TBI is rarely necessary in children aged <2 years, but t

181 ect subtle brain injury specifically in mild TBI patients.

182 eplacement (TR) mice following repeated mild TBI (rmTBI) using a lateral fluid percussion injury mode

183 articular is associated with repetitive mild TBI (mTBI) and is characterized pathologically by aggreg

184 s important to determine if repetitive, mild TBI (rmTBI) will also disrupt the gut microbiota.

185 rall study cohort prevalence for TBI(mild) , TBI(non-mild) , and PTSD was 0.65%, 0.69%, and 5.5%, res

186 and 2.71 (95% CI: 2.66-2.77) for TBI(mild) , TBI(non-mild) , and PTSD, respectively).

187 e ability of the stress response to mitigate TBI-induced brain degeneration.

188 Though most TBIs are mild, even mild TBI can induce long term effect

189 iated by polymeric gene carriers in a murine TBI model and investigate the anatomical parameters that

190 lood-brain barrier (BBB), 12 mo after murine TBI, is associated with arrested axonal neurodegeneratio

191 st damaging excitability in the aftermath of TBI and that treatment of edema has the potential to rev

192 A lack of biomarkers of TBI has impeded medication development.

193 ese changes were accompanied by cessation of TBI-induced chronic axonal degeneration.

194 ould improve diagnosis and classification of TBI subgroups.

195 ion of pro-inflammatory markers in cortex of TBI + Sp compared with TBI + PBS mice after both early a

196 ted to hospital with a clinical diagnosis of TBI and an indication for CT.

197 ults, 18-64 years, with primary diagnosis of TBI from 2004-2014 Nationwide Inpatient Samples, latent

198 Gy of total body irradiation (TBI), 2 Gy of TBI, 8 Gy of TBI, or no conditioning and treated by usin

199 body irradiation (TBI), 2 Gy of TBI, 8 Gy of TBI, or no conditioning and treated by using transplanta

200 , with treatment initiated within 2 hours of TBI: out-of-hospital tranexamic acid (1 g) bolus and in-

201 order to comprehend the immediate impacts of TBI.

202 In addition, monocytes from lungs of TBI + Sp mice were immunosuppressed acutely after trauma

203 den and pathology was also found in lungs of TBI + Sp mice.

204 (miRNAs) may serve as noninvasive markers of TBI, we performed miRNA-seq to study TBI-induced changes

205 nderstand the neuropathological mechanism of TBI-related disorders, we conducted transcriptome sequen

206 he first description of a humanized model of TBI and show that TBI places significant stress on the b

207 emonstrate in an experimental mouse model of TBI that mild forms of brain trauma cause severe deficit

208 cellular vesicle proteins in a mild model of TBI with parallels to concussive head injury.

209 he effects of a mixed diffuse-focal model of TBI, the lateral fluid percussion injury (LFPI), on inte

210 nces in serum miRNAs using two rat models of TBI (controlled cortical impact [CCI] and fluid percussi

211 se brain has little effect on the outcome of TBI, but inducing the turnover of these cells through ei

212 ion of microglia during the chronic phase of TBI followed by repopulation results in long-term improv

213 electron microscopy revealed full repair of TBI-induced breaks in cortical and hippocampal BBB endot

214 Hence, early signatures of TBI would be of great clinical value.

215 nology might eventually help the triaging of TBI patients and assist clinical decision making at poin

216 PD, TBI, and PTSD were ascertained by validated Internationa

217 dministration in a rabbit model of pediatric TBI, D-Sino conjugates specifically targeted activated m

218 sed during the Early phase (day 0 and 1 post-TBI).

219 time points, namely, days 1, 3, 7 and 9 post-TBI.

220 These results suggest that acute post-TBI cerebrovascular function is worse in males, and that

221 t-TBI) or double doses (48 h and 5 days post-TBI) subcutaneous (SC) injection increased 30-day surviv

222 (within 1 week) and late (up to 90 days post-TBI).

223 ain connectivity and cognitive deficits post-TBI.

224 (1.5 mg/kg) with single (24, 48 or 72 h post-TBI) or double doses (48 h and 5 days post-TBI) subcutan

225 ma metabolites were significantly lower post-TBI (six amino acids, two acylcarnitines, one carnosine)

226 ghts into the cerebral microvasculature post-TBI.

227 n understanding and predicting outcomes post-TBI.

228 rences in the neurovasculature response post-TBI may contribute to the differences seen in how males

229 eversal learning in the water maze task post-TBI.

230 elated to neuromotor function at 1-week post-TBI.

231 injury (LFPI), on interneurons, 8 weeks post-TBI in rats.

232 tive interaction observed with comorbid PTSD/TBI in dual-risk factor analyses, with significant 2.69-

233 ed, 417 were randomly assigned, 212 received TBI, and 201 received chemoconditioning.

234 We therefore recommend TBI plus etoposide for patients > 4 years old with high-

235 utilized a mouse model of mild blast-related TBI (bTBI) to investigate TBI-induced changes within the

236 s/military Servicemembers with blast-related TBI, we found marked Purkinje cell dendritic arbor struc

237 somes (ADEs) of subjects with sports-related TBI (sTBI) and TBI in military veterans (mtTBI) without

238 ative combination chemotherapy could replace TBI in such patients.

239 ery of righting reflex: sham, TBI, sham RIC, TBI RIC.

240 ed neuroinflammation is induced after severe TBI and contributes to neurological deficits and on-goin

241 mine functional status 6 months after severe TBI in older adults, changes in this status over 2 years

242 r age groups (P = 0.017).Conclusions: Severe TBI in older adults is a condition with very high mortal

243 Patients with early PD and moderate/severe TBI showed similar reductions in caudate DaT binding, bu

244 udy to measure DaT levels in moderate/severe TBI, healthy controls, patients with early PD and RBD.

245 rvival in casualties with moderate or severe TBI (p<0.0001, OR 2.71, 95% CI 2.34 to 4.73).

246 0; long-term survivors of moderate or severe TBI, n = 4) from the Glasgow TBI Archive and Penn Neurod

247 Although gut dysbiosis after single, severe TBI has been documented, the majority of head injuries a

248 Among patients with moderate to severe TBI, out-of-hospital tranexamic acid administration with

249 1554 patients with mild-to-severe TBI were assessed at 6 months post injury on the Glasgow

250 were more likely to have moderate-to-severe TBI, to be admitted on weekends, to urban, medium-to-lar

251 of 96 patients surviving moderate-to-severe TBI, we performed shape analysis of local volume deficit

252 adults who had been hospitalized with severe TBI over the 10-year period; 428 (79%) patients died in

253 Australia, between 2007 and 2016 with severe TBI.

254 ed, including 552 (20%) patients with severe TBI.

255 1 h after recovery of righting reflex: sham, TBI, sham RIC, TBI RIC.

256 peutic target for TBI.SIGNIFICANCE STATEMENT TBI frequently causes long-term neurological and psychia

257 Registry datasets were adapted to stratify TBI using the Mayo Classification System for Traumatic B

258 In both studies, TBI + Sp mice had poorer motor function recovery compare

259 kers of TBI, we performed miRNA-seq to study TBI-induced changes in rat hippocampal miRNAs up to one

260 In summary, TBI induces a robust neuroinflammatory response that is

261 The present study demonstrates that TBI is followed by robust activation of type I IFN pathw

262 on of a humanized model of TBI and show that TBI places significant stress on the bone marrow.

263 The TBI Closed Skull Group continued to perform better than

264 The TBI prevalence (defined as either TST or IGRA positivity

265 Three weeks after the CCI injury, the TBI Closed Skull Group demonstrated improved motor perfo

266 Recent discoveries regarding the TBI-responsive migratory behavior and differentiation po

267 l Group continued to perform better than the TBI Open Skull Group throughout weeks 4, 8, 12 and 16.

268 come to make up a significant portion of the TBIs which are sustained in warzones.

269 In addition to TBI induced changes, we found that female rats had great

270 ly characterized a head-specific approach to TBI in Drosophila, a powerful genetic system that shares

271 rated improved motor performance compared to TBI Open Skull Group.

272 ure and a mitigator in CD2F1 mice exposed to TBI.

273 that in the general population, exposure to TBI at age < 30 years was associated with a 4.4-fold hig

274 ivariable analysis revealed that exposure to TBI was associated with an increased risk of subsequent

275 ch there was no known history of exposure to TBI was selected as non-injured controls (n = 32).

276 g patients who develop seizures secondary to TBI from patients who do not.

277 mphatic system may offer strategies to treat TBI.

278 ntary neurobehavioral tests, PLX5622-treated TBI mice also had improved long-term motor and cognitive

279 d mice, whereas microglia in vehicle-treated TBI mice showed the typical chronic posttraumatic hypert

280 aseline were associated with an unfavourable TBI outcome (p = 0.002-0.02).

281 r HIV or had an unknown HIV status, and were TBI positive.

282 We test whether TBI, PD and RBD have distinct striatal dopamine abnormal

283 ed coma for many indications associated with TBI, where acute inflammation plays a critical role in d

284 markers in cortex of TBI + Sp compared with TBI + PBS mice after both early and late infection, indi

285 poorer motor function recovery compared with TBI + PBS mice.

286 bly similar to those observed in humans with TBI.

287 l health problem, many individuals live with TBI-related neurological dysfunction.

288 1280) included out-of-hospital patients with TBI aged 15 years or older with Glasgow Coma Scale score

289 Patients with TBI and PD had reduced DaT levels in the caudate (12.2%

290 describe the existing care for patients with TBI and the outcomes in China.

291 otor signs are absent in these patients with TBI because of relatively intact putaminal dopamine leve

292 , 2014, to Aug 1, 2017, 13 627 patients with TBI from 56 centres were enrolled in the registry.

293 sh two classes of hospitalized patients with TBI with divergent healthcare needs, informing the plann

294 inger-prick blood samples from patients with TBI, and that the biomarker is released immediately from

295 of tranexamic acid may benefit patients with TBI.

296 ssociated with survival in all patients with TBI.

297 (TBI) (35%, N = 679) compared to those with TBI (28%, N = 84) (P = 0.017).

298 old excess relative PD risk in veterans with TBI(mild) and TBI(non-mild) versus those without TBI whe

299 ustified for all children aged <2 years with TBI and low/intermediate risk of intracranial lesions, e

300 mild) and TBI(non-mild) versus those without TBI when PTSD was present versus 2.17-fold and 2.80-fold