1 TBI and the prevalence of low TBI were compared followin
2 TBI constitutes a serious public health threat in China.
3 TBI deaths from motor vehicle crashes in children aged 0
4 TBI has been used to assess iron status in the United St
5 TBI is typically considered and treated as one pathologi
6 TBI penumbra and hippocampus had higher cellular prolife
7 TBI was associated with significantly increased risk for
8 e the first to show such changes following
a TBI, and are compatible with previous studies of the bil
9 c injury over the days and weeks following
a TBI.
10 CNS as a key mechanistic link between
acute TBI and long-term, adaptive immune responses.
11 agnostic and prognostic biomarkers for
acute TBI.
12 a proof-of-concept approach to improve
acute TBI management that may also be applicable to other neur
13 n (P-tau) in plasma from patients with
acute TBI and chronic TBI has not been investigated.
14 In adults with
acute TBI, observational studies reveal a significant mortalit
15 In 2013, age-
adjusted TBI mortality was 12.99 per 100,000 population (SE = 0.1
16 which these coagulation abnormalities
affect TBI outcomes and whether they are modifiable risk factor
17 sted ferritin and sTfR concentrations
affect TBI values and the prevalence of low TBI (<0 mg/kg) in p
18 eting microglia/macrophages activation
after TBI.
19 Acutely
after TBI there is a reduction in vascular network and vascula
20 Thirty-nine adults
after TBI (84.6% male, median age = 30.5 years, 87.2% moderate
21 pendent kinases, and blocked G1 arrest
after TBI thereby increasing the number of S phase cells in cr
22 ic release of d-serine from astrocytes
after TBI underlies much of the synaptic damage associated wit
23 Exposure to beta-blockers
after TBI was associated with a reduction of in-hospital morta
24 n may potentiate arrest in crypt cells
after TBI.
25 tic spines and rescues memory deficits
after TBI.
26 utic target to restore memory deficits
after TBI.SIGNIFICANCE STATEMENT Traumatic brain injury (TBI)
27 s attenuated by myeloid cell depletion
after TBI.
28 -1beta and IL-1 receptor were detected
after TBI.
29 king memory, and executive functioning
after TBI.
30 Growth hormone deficiency (GHD)
after TBI may impair axonal and neuropsychological recovery, a
31 Within the first 24 h
after TBI, several inflammatory response factors become upregu
32 rters were decreased as early as 2 hrs
after TBI until at least 24 hrs after TBI.
33 2 hrs after TBI until at least 24 hrs
after TBI.
34 cular astrocytic end feet was impaired
after TBI, which was most prominent in the ipsilateral brain t
35 e beneficial against memory impairment
after TBI.
36 N: WM recovery and memory improvements
after TBI were greater in patients with higher serum IGF-I at
37 interventions of neuronal inflammation
after TBI.
38 nd subsequently reduces the BDNF level
after TBI.
39 changes in pTau and PIP2/synj1 levels
after TBI, we tested if down-regulation of synj1 prevented bla
40 earlier than at 24 h in wild-type mice
after TBI.
41 ibund in Cdkn1a(p21(CIP/WAF1))-/- mice
after TBI.
42 ed nanoparticles directly to microglia
after TBI.
43 With respect to neurodegeneration
after TBI, post-mortem studies on the long-term neuropathology
44 for the accumulation of tau oligomers
after TBI, as post-TBI injection of a calpain-2 selective inhi
45 ence suggests that functional outcomes
after TBI can show improvement or deterioration up to two deca
46 hibition increased upregulation of p21
after TBI.
47 ns that have been reported in patients
after TBI.
48 1 macrophage and TH1/TH17 polarization
after TBI compared with C3H/OuJ (wild-type) mice.
49 phorylation of CREB and PSD95 proteins
after TBI.
50 ement binding protein (CREB) and PSD95
after TBI.
51 tract and neuropsychological recovery
after TBI.
52 ain and effectively improving recovery
after TBI.
53 for cell repair and survival responses
after TBI.
54 long-lasting adaptive immune responses
after TBI.
55 y can also contribute to bleeding risk
after TBI.
56 at ATM inhibition promotes GI syndrome
after TBI.
57 nal injury in white matter (WM) tracts
after TBI.
58 reduced seizure susceptibility 2 weeks
after TBI compared with vehicle, and a reduction in hippocampa
59 rovide balance between physical activity
and TBI, and guide thoughtful discourse and policy.
60 marrow iron than SF concentration alone,
and TBI can be analyzed as a continuous variable.
61 TBI without loss of consciousness [LOC],
and TBI with LOC).
62 METHODS
AND TBI patients requiring neuro-intensive care and not incl
63 ncentrations of CRP and AGP on SF, sTfR,
and TBI were generally linear, especially in PSC.
64 involving mitochondrial dysfunction, such
as TBI.
65 B-
TBI significantly reduced the levels of synaptophysin (S
66 Mild blast traumatic brain injury (
B-
TBI) induced lasting cognitive impairments in novel obje
67 and TRAIL were able to discriminate
between TBI and HV at <1 hr.
68 Blast TBI increased glycogen synthase kinase (GSK)-3beta activ
69 s in ApoE4 mice did not increase after
blast TBI.
70 rty-six of 50 patients with concussive
blast TBI (72%) had a decline in the GOS-E from the 1- to 5-ye
71 ntly worse in patients with concussive
blast TBI compared with combat-deployed controls, whereas perf
72 Service members with concussive
blast TBI experienced evolution, not resolution, of symptoms f
73 Worsening of symptoms in concussive
blast TBI was also observed on measures of posttraumatic stres
74 phosphorylation have been implicated in
both TBI and AD.
75 mpal-dependent cognitive deficits induced
by TBI in two different injury mouse models-focal contusion
76 tivity analyses were performed stratified
by TBI severity (no TBI, TBI without loss of consciousness
77 Sensitivity analyses stratified
by TBI severity produced similar results.
78 sma from patients with acute TBI and
chronic TBI has not been investigated.
79 ained elevations among patients with
chronic TBI.
80 ment Study to participate in a
comprehensive TBI survey and who either reported no prior TBI (n = 737
81 Surprisingly, ISRIB
corrected TBI-induced memory deficits when administered weeks afte
82 bination fludarabine-melphalan with low-
dose TBI after haplocord stem cell transplant assures good en
83 erebral cortex within 1 hour of
experimental TBI.
84 mplexity of the immune responses that
follow TBI.
85 Following TBI, calpain-2 activation cleaved PTPN13, activated c-Ab
86 Following TBI, endothelial activation results in a time dependent
87 s, revealed a significant decrease
following TBI.
88 piration at the location of injury
following TBI.
89 WM tracts including SPCC and PLIC
following TBI compared to controls, indicating axonal injury, with
90 trocytes in the tripartite synapse
following TBI.
91 (HRs) and 95% confidence intervals (CIs)
for TBI in a Cox regression, while adjusting for age, sex, r
92 PD, TBI, and time was primarily observed
for TBI attributed to falls.
93 Treatment strategies
for TBI are supportive, and the pathophysiology is not fully
94 e stimulation (TNS) a promising strategy
for TBI management.
95 emerges as a clinically relevant target
for TBI therapy.
96 attractive potential therapeutic target
for TBI.
97 The development of therapies
for TBI is limited by the absence of diagnostic and prognost
98 ial exosomes may provide a novel therapy
for TBI and other neurologic diseases.
99 Unfortunately, effective treatments
for TBI remain elusive.
100 d quality of life after beta-blocker use
for TBI.
101 Furthermore,
TBI represents a risk factor for a variety of neurologic
102 In comparison to TBI
group,
TBI animals with TNS treatment demonstrated significantl
103 D)-7 to -3, melphalan 140 mg/m D-2, and 2
Gy TBI D-4 and -3.
104 t cord blood transplants, we have added 4
Gy TBI to the widely used fludarabine, melphalan conditioni
105 Here, we describe
how TBI changes the metabolism of essential neurochemical co
106 uation and therapeutic intervention of
human TBI events.
107 standardised outcome of clinically
important TBI.
108 Europe, indicating the need for advances
in TBI treatment.
109 MWH or UH is the current standard of care
in TBI.
110 e direction is to validate these findings
in TBI models.
111 abolism, consistent our previous findings
in TBI patients' brains.
112 The dataset also may be incomplete
in TBI death recording or contain misclassification of mort
113 roglial exosomes on neuronal inflammation
in TBI, we focused on studying the impact of microglial exo
114 Secondary mechanisms of injury
in TBI, such as oxidative stress and inflammation, are poin
115 nterfere with oxidative stress mechanisms
in TBI and provide a proof-of-concept approach to improve a
116 ly-established biomarker for poor outcome
in TBI) and decrease in OCR.
117 f other known clinical outcome predictors
in TBI (6% and 4%, respectively).
118 me; median LY30 was lower on PTD1 to PTD3
in TBI patients compared with non-TBI patients.
119 tients with severe traumatic brain
injuries (
TBI).
120 effects of wartime traumatic brain
injuries (
TBIs), most of which are mild, remain incompletely descr
121 between persons with traumatic brain
injury (
TBI) and healthy controls (HCs).
122 ine the influence of traumatic brain
injury (
TBI) and massive transfusion on fibrinolysis status.
123 association between traumatic brain
injury (
TBI) and suicide attempt have yielded conflicting result
124 million incidents of traumatic brain
injury (
TBI) and treatment options are non-existent.
125 Traumatic brain
injury (
TBI) can have lifelong and dynamic effects on health and
126 Traumatic brain
injury (
TBI) can induce cognitive dysfunction due to the regiona
127 Traumatic brain
injury (
TBI) causes extensive neural damage, often resulting in
128 Traumatic brain
injury (
TBI) contributes to one third of injury related deaths i
129 Traumatic brain
injury (
TBI) increases the risk of Alzheimer's disease (AD).
130 The impact of traumatic brain
injury (
TBI) involves a combination of complex biochemical proce
131 Traumatic brain
injury (
TBI) is a leading cause of long-term neurological disabi
132 Traumatic brain
injury (
TBI) is a leading cause of morbidity and disability, wit
133 Traumatic brain
injury (
TBI) is a major contributor to morbidity and mortality.
134 Traumatic brain
injury (
TBI) is a major public health issue, producing significa
135 Traumatic brain
injury (
TBI) is a serious public health problem, often with deva
136 Traumatic brain
injury (
TBI) is a significant global public health problem, but
137 epsy after pediatric traumatic brain
injury (
TBI) is associated with poor quality of life.
138 Traumatic brain
injury (
TBI) is characterized by acute neurological dysfunction
139 Traumatic brain
injury (
TBI) is currently a major cause of morbidity and poor qu
140 Traumatic brain
injury (
TBI) is extremely common across the lifespan and is an e
141 Traumatic brain
injury (
TBI) is known to cause perturbations in the energy metab
142 Traumatic brain
injury (
TBI) is set to become the leading cause of neurological
143 GNIFICANCE STATEMENT Traumatic brain
injury (
TBI) is the leading cause of death and disability around
144 QC in rats receiving traumatic brain
injury (
TBI) of different severities.
145 mpact model (CCI) of traumatic brain
injury (
TBI) on their distribution.
146 directly involved in traumatic brain
injury (
TBI) pathogenesis and have been used to inform clinical
147 fic enolase (NSE), a traumatic brain
injury (
TBI) protein biomarker, in diluted blood plasma samples,
148 Traumatic brain
injury (
TBI) results in rapid recruitment of leukocytes into the
149 notype combines with traumatic brain
injury (
TBI) to increase the risk of developing Alzheimer's Dise
150 age due to stroke or traumatic brain
injury (
TBI), both leading causes of serious long-term disabilit
151 s disease (PD) after traumatic brain
injury (
TBI), but it is possible that the risk of TBI is greater
152 py for children with traumatic brain
injury (
TBI), but its overall association with patient outcome i
153 After traumatic brain
injury (
TBI), glial cells have both beneficial and deleterious r
154 been described after traumatic brain
injury (
TBI), in which it is associated with worse outcomes.
155 Following traumatic brain
injury (
TBI), ischemia and hypoxia play a major role in further
156 sregulated following traumatic brain
injury (
TBI), suggesting that stimulation of BDNF signaling path
157 After traumatic brain
injury (
TBI), the ability of cerebral vessels to appropriately r
158 stress in a model of traumatic brain
injury (
TBI), we found that shear stress induced Ca(2+) entry.
159 ite matter following traumatic brain
injury (
TBI).
160 s been implicated in traumatic brain
injury (
TBI).
161 osed complication of traumatic brain
injury (
TBI).
162 matic spinal cord or traumatic brain
injury (
TBI).
163 encephalopathy after traumatic brain
injury (
TBI).
164 tabolism arise after traumatic brain
injury (
TBI).
165 outcomes after acute traumatic brain
injury (
TBI).
166 lzheimer disease and traumatic brain
injury (
TBI).
167 clinically important traumatic brain
injury [
TBI], need for neurological intervention, and clinically
168 al outcomes following traumatic brain
injury(
TBI).
169 At 2 weeks and 3 months post-
injury,
TBI mice showed an elevated seizure response to the conv
170 Total body
iron (
TBI) that is calculated from ferritin and soluble transf
171 ferrin receptor (sTfR), and total body
iron (
TBI) were summarized in relation to infection burden (in
172 Total body
irradiation (
TBI) damages hematopoietic cells in the bone marrow and
173 rior to 9 or 9.25 Gy total body
irradiation (
TBI) reduced median time to moribund in mice to 8 days.
174 day for 2 days, and total body
irradiation (
TBI).
175 At the physiological
level,
TBI suppressed long-term potentiation in the hippocampus
176 affect TBI values and the prevalence of
low TBI (<0 mg/kg) in preschool children (PSC) (age range: 6
177 e prevalence estimates.The prevalence of
low TBI is underestimated if it is not adjusted by inflammat
178 TBI and the prevalence of
low TBI were compared following 3 adjustment approaches for
179 The
lowest TBI dose capable of achieving complete donor chimerism i
180 While
many TBI studies have focused on the brain, peripheral contri
181 and sTfR for inflammation, the adjusted
mean TBI decreased in both PSC and WRA compared with unadjust
182 1.000, respectively, for discriminating
mild TBI (Glasgow Coma Scale [GCS] score, 13-15, n = 162) fro
183 ONSD in
mild TBI, RCTS 2 and 3 were 3.3 mm (SD 0.39 mm) and 4.1 mm (0
184 measured in patients that had suffered
mild TBI (n = 10) or severe TBI (n = 10) with extra-cranial i
185 need for sequential CT in patients with
mild TBI.
186 tested our hypothesis that a focal
moderate TBI results in global decrements to structural aspects o
187 rements were performed on rats with
moderate TBI induced by controlled cortical impact on one cerebra
188 ury has been the guiding principle of
modern TBI management.
189 At 5 months,
most TBI mice exhibited spontaneous seizures during a 7 d vid
190 ere performed stratified by TBI severity (
no TBI, TBI without loss of consciousness [LOC], and TBI wi
191 D1 to PTD3 in TBI patients compared with
non-
TBI patients.
192 ; of those, 88 (78%) died from
nonsurvivable TBI or brain death.
193 1.07, 1.46), with 83% of the association
of TBI with attempted suicide mediated by co-occurring psyc
194 els were used to examine the associations
of TBI mortality with location, sex, and age group.
195 analysis was performed by external cause
of TBI.
196 ashes and falls were the 2 leading causes
of TBI mortality between 2006 and 2013.
197 tSAH may reflect an underrated component
of TBI pathophysiology.
198 ng awareness of the lifelong consequences
of TBI, substantial gaps in research exist.
199 S survey procedures to plot distributions
of TBI and produce prevalence estimates of ID and IDA for e
200 -invasive method for studying the effects
of TBI on energy metabolism.
201 s reduces or delays pathological features
of TBI.
202 n is a feature of several different forms
of TBI in humans, and that administration of cis P-tau targ
203 Adults with a history
of TBI at least 4 months before study enrollment with eithe
204 elling non-demented older adults, history
of TBI is common but may not preferentially impact cognitiv
205 ne subjects (4 controls, 3 with a history
of TBI, 2 with mild cognitive impairment due to suspected A
206 of reliable biomarkers for the management
of TBI would improve clinical interventions.
207 derstanding pathophysiological mechanisms
of TBI could change current management in the intensive car
208 g inhibitory interneurons, in a rat model
of TBI as well as in brains of human epileptic patients.
209 matic activation of JNK in a rodent model
of TBI.
210 cells, were assessed in an in vitro model
of TBI.
211 to differences in the course and outcome
of TBI.
212 ROS may improve the pathological outcomes
of TBI.
213 r nonclassical monocytes in the pathology
of TBI in mice, including important clinical outcomes assoc
214 racts from the acute to the chronic phase
of TBI to treat cultured BV2 microglia in vitro The microgl
215 re, CBF and PbrO2 at the hyperacute phase
of TBI.
216 y (TBI), but it is possible that the risk
of TBI is greater in the prodromal period of PD.
217 he reasons for the particularly high risk
of TBI mortality among particular populations, as well as t
218 Risk
of TBI was greater in PD patients in their prodromal period
219 rkers exist to help diagnose the severity
of TBI to identify patients who are at risk of developing s
220 ture, there is a need for a clear summary
of TBI neuroimmunology.
221 gies and their implications for survivors
of TBI, which could inform long-term health management in t
222 suffering from the long-lasting symptoms
of TBI.
223 Treatment
of TBI patients with beta-blockers offers a potentially ben
224 ablished cutoffs for iron repletion based
on TBI.
225 Rats (naive, sham-
operated,
TBI) underwent a moderate controlled cortical impact.
226 f AD pathology after repeated concussions
or TBI.
227 equences emphasises that, for many
patients,
TBI should be conceptualised as a chronic health conditi
228 The interaction between
PD,
TBI, and time was primarily observed for TBI attributed
229 th Revision codes, partially mediated the
PD-
TBI association.
230 In the setting of non-
penetrating TBI, sterile brain inflammatory responses are associated
231 ion to label the entire cortex at 1 day
post TBI followed by whole brain axial and coronal images usi
232 mulation of tau oligomers after TBI, as
post-
TBI injection of a calpain-2 selective inhibitor inhibit
233 neuroimaging can be used to investigate
post-
TBI changes in neurometabolism.
234 vasive detection of cerebral metabolism
post-
TBI, providing a new tool to monitor the effect of thera
235 arization of macrophages for up to 3 wk
post-
TBI.
236 Moreover, RhoA-ROCK inhibition
prevents TBI-induced spine remodeling and mature spine loss.
237 TBI survey and who either reported no
prior TBI (n = 737) or prior symptomatic TBI resulting in trea
238 the cognitive profile associated with
prior TBI exposure among community-dwelling older adults witho
239 rowing population of older adults with
prior TBI who do not have a diagnosis of dementia, however, ha
240 er adults without dementia, those with
prior TBI with LOC were more likely to report subjective memor
241 We used a repetitive (
r)
TBI mouse model and harvested the injured brain extracts
242 a strong association between PD and a
recent TBI in the prodromal period of PD.
243 the associations between deployment-
related TBI, psychiatric diagnoses, and attempted suicide among
244 Severe TBI was produced using controlled cortical impact (CCI)
245 Mean ONSD in moderate and
severe TBI (RCTS score 4 and above) was 4.83 mm and above, SD 0
246 ups included massively transfused and
severe TBI patients.
247 bserved in patients with moderate and
severe TBI, correlating with admission RCTS of 4 and above.
248 e study including patients with blunt
severe TBI (AIS >/= 3), those that received LMWH or UH VTE prop
249 LMWH prophylaxis in
severe TBI is associated with better survival and lower thrombo
250 e a substantial impact on outcomes in
severe TBI.
251 Twenty-two participants with moderate-
severe TBI and 20 HCs performed four blocks of a difficult work
252 Fourteen patients with acute moderate/
severe TBI underwent baseline DTI and following one hour of 80%
253 were higher in individuals with more
severe TBI (GCS, </=12 vs 13-15).
254 hat had suffered mild TBI (n = 10) or
severe TBI (n = 10) with extra-cranial injury or extracranial i
255 Moderate to
severe TBI elicits neuroinflammation and c-Jun-N-terminal kinas
256 CST5 identified patients with
severe TBI from all other cohorts and importantly was able to d
257 functional survival of children with
severe TBI.
258 rs, 87.2% moderate-severe, median time
since TBI = 16.3 months, n = 4 with GHD) were scanned twice, 1
259 NHANES has used the total body iron
stores (
TBI) model, in which the log ratio of sTfR to SF is asse
260 no prior TBI (n = 737) or prior
symptomatic TBI resulting in treatment in a hospital (n = 247).
261 erformed stratified by TBI severity (no
TBI,
TBI without loss of consciousness [LOC], and TBI with LO
262 ppocampal neurons - that are targeted by
ten TBI-altered miRNAs.
263 These data argue
that TBI elicits pathological spine remodeling that contribut
264 he hippocampal CA1 subfield demonstrate
that TBI inhibits the expression of long-term potentiation (L
265 We found
that TBI impairs both motor and cognitive performance and inh
266 We hypothesized
that TBI would alter hepatic function, including bile acid sy
267 Here, we show
that TBI persistently activates the integrated stress respons
268 The TBI group had lower incidence of relapse at 1 year (15%
269 The TBI model better predicts the absence of bone marrow iro
270 In comparison
to TBI group, TBI animals with TNS treatment demonstrated s
271 ATR kinase inhibition using AZD6738 prior
to TBI did not reduce median time to moribund.
272 ding associated with ATM inhibition prior
to TBI was increased crypt loss within the intestine epithe
273 hatic system and it has obvious relevance
to TBI.
274 rain phospholipid homeostasis in response
to TBI and that the ApoE4 isoform is dysfunctional in this
275 rovascular network and its acute response
to TBI is poorly defined and emerging evidence suggests tha
276 e galectin-3 knockout animals in response
to TBI.
277 We aimed to examine the time-
to-
TBI in PD patients in their prodromal period compared to
278 suggest that it could be repurposed to
treat TBI.
279 We compared outcomes between the
two TBI groups using regression models adjusting for demogra
280 of Defense definition of mild,
uncomplicated TBI.
281 9 included studies encompassing 2005
unique TBI patients with beta-blocker treatment and 6240 unique
282 This may explain
why TBI patients are more vulnerable to cognitive dysfunctio
283 ing of metabolic impairments associated
with TBI pathogenesis.
284 e chronic cognitive deficits associated
with TBI remain unknown.
285 in the various symptomology associated
with TBI.
286 S AND Five hundred and fifteen patients
with TBI admitted in Addenbrooke's Hospital, United Kingdom (
287 tau ratio weakly distinguished patients
with TBI who had good outcomes (Glasgow Outcome Scale-Extende
288 and uniformity in the care of patients
with TBI, and ensuring timely detection or exclusion of PTHP
289 icians involved in the care of patients
with TBI, including neurosurgeons, neurologists, neurointensi
290 ening and detection of PTHP in patients
with TBI, with practice likely varying significantly between
291 nt an increasing proportion of patients
with TBI-as preinjury comorbidities and their therapies deman
292 pituitary dysfunction in adult patients
with TBI.
293 wPRx with PRx in the cohort of patients
with TBI.
294 d onto the cortex of brain injured rats
with TBI.
295 Respondents
with TBI did not perform significantly differently from respo
296 nt was increased only among respondents
with TBI with LOC and not among those with TBI without LOC.
297 s with TBI with LOC and not among those
with TBI without LOC.
298 Veterans
with TBI (16%) were more likely to attempt suicide than those
299 icantly differently from respondents
without TBI on any measure of objective cognitive function in ei
300 memory impairment compared to those
without TBI even after adjustment for demographics, medical como