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1 r cancer is highly stressful and potentially traumatic.
2 t ICH events were spontaneous (71.7%) versus traumatic (28.3%).
3 inflammatory mediators and inhibits the post-traumatic activation of JNK in a rodent model of TBI.
4                                        Using traumatic and vincristine-induced injury models in neuro
5 ence of IL-1 signaling as a mediator of post-traumatic astrogliosis and seizure susceptibility.SIGNIF
6 y MHC-II on Schwann cells thus promotes post-traumatic axonal loss and neuropathic pain.
7 noncalcium (VNCa) technique for detection of traumatic bone marrow edema in patients with vertebral c
8 ts interpreted virtual noncalcium images for traumatic bone marrow edema.
9 sm (VTE) prophylaxis in patients with severe traumatic brain injuries (TBI).
10    The long-term clinical effects of wartime traumatic brain injuries (TBIs), most of which are mild,
11 quantify benefits of hypothermia therapy for traumatic brain injuries in adults and children by analy
12 a is likely a beneficial treatment following traumatic brain injuries in adults but cannot be recomme
13  time with brain tissue hypoxia after severe traumatic brain injury (0.45 in intracranial pressure-on
14                                   Mild blast traumatic brain injury (B-TBI) induced lasting cognitive
15 ) 10 years and older with moderate or severe traumatic brain injury (Barell Matrix Type 1 classificat
16 in injury and 32 patients with isolated mild traumatic brain injury (comparison group) was assessed w
17 racic echocardiogram within 1 day after mild traumatic brain injury (comparison group).
18 -channel head coil from each of 3 concussive traumatic brain injury (cTBI) patients and 4 controls tw
19 nsecutive children (age < 18 yr) with severe traumatic brain injury (Glasgow Coma Scale </= 8; intrac
20 ndred three patients with moderate or severe traumatic brain injury (Glasgow Coma Scale, 3-13).
21  appropriate treatment of children with mild traumatic brain injury (mTBI) and intracranial injury (I
22  it remains unknown the extent to which mild traumatic brain injury (mTBI) may impact these critical
23 nces (P < 0.0001); 11.1% to 26.0% for severe traumatic brain injury (P < 0.0001), and 4.7% to 5.9% fo
24 of complex partial seizures (CPSs) following traumatic brain injury (post-traumatic epilepsy).
25  with cognitive fatigue between persons with traumatic brain injury (TBI) and healthy controls (HCs).
26  after injury and determine the influence of traumatic brain injury (TBI) and massive transfusion on
27           Studies of the association between traumatic brain injury (TBI) and suicide attempt have yi
28 ually, there are over 2 million incidents of traumatic brain injury (TBI) and treatment options are n
29                                              Traumatic brain injury (TBI) can have lifelong and dynam
30                                              Traumatic brain injury (TBI) can induce cognitive dysfun
31                                              Traumatic brain injury (TBI) causes extensive neural dam
32                                              Traumatic brain injury (TBI) contributes to one third of
33                                              Traumatic brain injury (TBI) increases the risk of Alzhe
34                                The impact of traumatic brain injury (TBI) involves a combination of c
35                                              Traumatic brain injury (TBI) is a leading cause of long-
36                                              Traumatic brain injury (TBI) is a leading cause of morbi
37                                              Traumatic brain injury (TBI) is a major contributor to m
38                                              Traumatic brain injury (TBI) is a major public health is
39                                              Traumatic brain injury (TBI) is a serious public health
40                                              Traumatic brain injury (TBI) is a significant global pub
41                     Epilepsy after pediatric traumatic brain injury (TBI) is associated with poor qua
42                                              Traumatic brain injury (TBI) is characterized by acute n
43                                              Traumatic brain injury (TBI) is currently a major cause
44                                              Traumatic brain injury (TBI) is extremely common across
45                                              Traumatic brain injury (TBI) is known to cause perturbat
46                                              Traumatic brain injury (TBI) is set to become the leadin
47 ry deficits after TBI.SIGNIFICANCE STATEMENT Traumatic brain injury (TBI) is the leading cause of dea
48 ession involved in the MQC in rats receiving traumatic brain injury (TBI) of different severities.
49  a controlled cortical impact model (CCI) of traumatic brain injury (TBI) on their distribution.
50 sregulation of pathways directly involved in traumatic brain injury (TBI) pathogenesis and have been
51 etection of neuron-specific enolase (NSE), a traumatic brain injury (TBI) protein biomarker, in dilut
52                                              Traumatic brain injury (TBI) results in rapid recruitmen
53 ipoprotein E4 (ApoE4) genotype combines with traumatic brain injury (TBI) to increase the risk of dev
54 usly been shown to occur in animal models of traumatic brain injury (TBI), and blocking this form of
55                Brain damage due to stroke or traumatic brain injury (TBI), both leading causes of ser
56 eater risk of Parkinson's disease (PD) after traumatic brain injury (TBI), but it is possible that th
57 g is a mainstay of therapy for children with traumatic brain injury (TBI), but its overall associatio
58                                        After traumatic brain injury (TBI), glial cells have both bene
59   PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated
60                                    Following traumatic brain injury (TBI), ischemia and hypoxia play
61 ngth and learning, is dysregulated following traumatic brain injury (TBI), suggesting that stimulatio
62                                        After traumatic brain injury (TBI), the ability of cerebral ve
63 trocytes to fluid shear stress in a model of traumatic brain injury (TBI), we found that shear stress
64 ri-lesional brain and white matter following traumatic brain injury (TBI).
65 r of ER stress, which has been implicated in traumatic brain injury (TBI).
66 t potentially underdiagnosed complication of traumatic brain injury (TBI).
67 l changes following traumatic spinal cord or traumatic brain injury (TBI).
68 t and chronic traumatic encephalopathy after traumatic brain injury (TBI).
69 in cerebral energetic metabolism arise after traumatic brain injury (TBI).
70 (beta)-blockers improve outcomes after acute traumatic brain injury (TBI).
71 ic disorders including Alzheimer disease and traumatic brain injury (TBI).
72 ecific outcome measure (clinically important traumatic brain injury [TBI], need for neurological inte
73                  Seven (22%) moderate-severe traumatic brain injury and 0 (0%) mild traumatic brain i
74 in 32 patients with isolated moderate-severe traumatic brain injury and 32 patients with isolated mil
75 n hospital including 6516 (78%) after severe traumatic brain injury and 749 (9%) after severe thoraco
76                     This study examined mild traumatic brain injury and genetic risk as predictors of
77 oderated mediation analysis showed that mild traumatic brain injury and high genetic risk indirectly
78 l thickness, such that individuals with mild traumatic brain injury and high genetic risk showed redu
79 le in human cerebrospinal fluid after severe traumatic brain injury and is an informative biomarker o
80 its potential to guide targeted therapies in traumatic brain injury and other diseases involving cere
81 ages of 19 and 58, many of whom carried mild traumatic brain injury and post-traumatic stress disorde
82 t develops following brain injuries, such as traumatic brain injury and stroke, and is often associat
83 e oxygenation levels in patients with severe traumatic brain injury and the feasibility of a Phase II
84 n trauma systems, assess the contribution of traumatic brain injury and thoracoabdominal injury to ob
85   Treatment of secondary injury after severe traumatic brain injury based on brain tissue oxygenation
86  vitrectomy for Terson syndrome secondary to traumatic brain injury between 1997 and 2015.
87 s intracranial hypertension in patients with traumatic brain injury but was associated with harm in t
88       We examined variation in treatment for traumatic brain injury by assessing factors influencing
89                                              Traumatic brain injury due to blast exposure is currentl
90 ren with abusive head trauma from those with traumatic brain injury from other mechanisms.
91                          Current prehospital traumatic brain injury guidelines use a systolic blood p
92 xygenation and poor outcome following severe traumatic brain injury has been reported in observationa
93 pilepsy is a common cause of morbidity after traumatic brain injury in early childhood.
94                         Management of severe traumatic brain injury informed by multimodal intracrani
95                                              Traumatic brain injury is a major cause of death and dis
96     These results provide evidence that mild traumatic brain injury is associated with greater neurod
97 sue oxygenation-directed treatment of severe traumatic brain injury is warranted.
98            Prior studies have suggested that traumatic brain injury may affect cardiac function.
99  non-auditory effects of blast and potential traumatic brain injury may also exert an effect.
100                   Patients with acute severe traumatic brain injury may recover consciousness before
101 lgals-1(-/-) mice to develop spinal cord- or traumatic brain injury models for the evaluation of the
102                     Results showed that mild traumatic brain injury moderated the relationship betwee
103 le for meta-analysis were from patients with traumatic brain injury or subarachnoid hemorrhage.
104 nylurea receptor-1 was present in all severe traumatic brain injury patients (mean = 3.54 +/- 3.39 ng
105                         Data from 729 severe traumatic brain injury patients admitted between 1996 an
106                                        Adult traumatic brain injury patients admitted to intensive ca
107 evere traumatic brain injury and 0 (0%) mild traumatic brain injury patients had systolic dysfunction
108 nsor imaging abnormalities in a cohort of 97 traumatic brain injury patients were also mapped at the
109 orts of recently treated adult and pediatric traumatic brain injury patients.
110 sion pressure threshold management in severe traumatic brain injury patients.
111 0 minutes in advance, in adult and pediatric traumatic brain injury patients.
112                  One hundred nineteen severe traumatic brain injury patients.
113  fluid samples were collected from 28 severe traumatic brain injury patients.
114 f systolic dysfunction among moderate-severe traumatic brain injury patients.
115                                 Unlike other traumatic brain injury populations in children, female p
116 nsecutive patients undergoing CT imaging for traumatic brain injury recruited between January and Oct
117  to the intensive care unit for acute severe traumatic brain injury to test two hypotheses: (i) in pa
118  Approaches and Decisions in Acute Pediatric Traumatic Brain Injury Trial-a comparative effectiveness
119 y or Glasgow Outcome Scale for patients with traumatic brain injury were the pressure reactivity inde
120                                MRI following traumatic brain injury yields important prognostic infor
121 rove long term functional outcomes following traumatic brain injury(TBI).
122 , including (1) reducing SICU care for minor traumatic brain injury, (2) optimizing postoperative air
123 tive diseases and cognitive impairment after traumatic brain injury, all hallmarked by the accumulati
124 iously healthy patients with moderate-severe traumatic brain injury, and it is reversible over the fi
125 o the brain in mouse models of glioblastoma, traumatic brain injury, and Parkinson's disease.
126 brain, has recently been linked to sleep and traumatic brain injury, both of which can affect the pro
127                             In patients with traumatic brain injury, ESA therapy did not increase the
128       The major cause of delayed surgery was traumatic brain injury, followed by facial or orbital fr
129 ssment included history of playing rugby and traumatic brain injury, general and mental health, life
130                        Among males with mild traumatic brain injury, high genetic risk for Alzheimer'
131 nogenesis, stroke, intracerebral hemorrhage, traumatic brain injury, ischemia-reperfusion injury, and
132 troke, AD, age-related macular degeneration, traumatic brain injury, Parkinson's disease, and other n
133 ribed glymphatic system has been linked with traumatic brain injury, prolonged wakefulness, and aging
134                       Thus, in patients with traumatic brain injury, the concept that 90 mm Hg repres
135 creasingly used in the early phase following traumatic brain injury, the prognostic utility of MRI re
136 microglia in models of stroke, infection and traumatic brain injury, though the exact role of the imm
137 are still considered the most lethal type of traumatic brain injury.
138 terns for discriminating clinical outcome in traumatic brain injury.
139 the acute phase following moderate or severe traumatic brain injury.
140 omy for intraocular hemorrhages secondary to traumatic brain injury.
141 rebral edema is a key poor prognosticator in traumatic brain injury.
142 rising from neurodegenerative disease and/or traumatic brain injury.
143 dysfunction in patients with moderate-severe traumatic brain injury.
144 omy for intraocular hemorrhages secondary to traumatic brain injury.
145 y mechanical impact in a mouse model of mild traumatic brain injury.
146  Canadian provinces, specifically for severe traumatic brain injury.
147 ma are serious complications of ischemic and traumatic brain injury.
148 tical function in patients with acute severe traumatic brain injury.
149 teractions between four treatments following traumatic brain injury.
150 inuous variable (p = 0.07) for patients with traumatic brain injury.
151 sive care who had suffered a primary, closed traumatic brain injury; increased intracranial pressure;
152 nd over the first week after moderate-severe traumatic brain injury; transthoracic echocardiogram wit
153 rognosis and Analysis of Clinical Trials in [Traumatic Brain Injury] (IMPACT) extended model sum scor
154  plays key roles in the repair process after traumatic brain lesions.
155       To determine whether delayed repair of traumatic canalicular laceration affects the final outco
156 ecords of 334 patients who underwent primary traumatic canalicular laceration repair were retrospecti
157 al rates remain low after hemorrhage-induced traumatic cardiac arrest (TCA).
158 his large animal model of hemorrhage-induced traumatic cardiac arrest with NCTH.
159 dsagittal tissue bridges at the epicenter of traumatic cervical spinal cord lesions in 24 subacute te
160 onscious state with language (n = 4) or post-traumatic confusional state (n = 4).
161                                        After traumatic cutaneous inoculation, several fungi can cause
162 ion of the spinal cord and formation of post-traumatic cysts.
163 , as were 24 cases with a clear diagnosis of traumatic death before investigation; 210 cases were inc
164               Ophthalmoplegia secondary to a traumatic dissecting aneurysm in the cavernous segment o
165 d associated with the development of chronic traumatic encephalopathy (CTE) and Alzheimer's disease.
166 ade with the more recently described chronic traumatic encephalopathy (CTE).
167 eurological conditions, particularly chronic traumatic encephalopathy (CTE).
168 e of acute neurologic impairment and chronic traumatic encephalopathy after traumatic brain injury (T
169                                      Chronic traumatic encephalopathy can occur after sporting injuri
170 cations, where pathology in cases of chronic traumatic encephalopathy is observed.
171 o central to Alzheimer's disease and chronic traumatic encephalopathy, a successful tau therapeutic f
172 ase, progressive supranuclear palsy, chronic traumatic encephalopathy, and other tauopathies.
173 europathology is prominently seen in chronic traumatic encephalopathy, and whether human neuroimaging
174 alsy, corticobasal degeneration, and chronic traumatic encephalopathy, but did not label nonpathologi
175 isk of the neurodegenerative disease chronic traumatic encephalopathy.
176 bed as polypathology, which includes chronic traumatic encephalopathy.
177 are common causes of post-operative and post-traumatic endophthalmitis.
178        This study aimed to characterize post-traumatic epilepsy in a mouse model of pediatric brain i
179 ays model heritable absence epilepsy or post-traumatic epilepsy in humans, and may instead reflect ty
180 CPSs) following traumatic brain injury (post-traumatic epilepsy).
181 as to whether biological sex and the type of traumatic event influence shared or distinct biological
182 traumatic stress disorder (PTSD) following a traumatic event.
183 ssociation between pre-migration potentially traumatic events and mental health after controlling for
184                    Pre-migration potentially traumatic events and post-migration stressors related to
185                    Pre-migration potentially traumatic events and post-migration stressors were posit
186 pre-migration and post-migration potentially traumatic events and stressors and mental health, and as
187 eory offer a framework for understanding how traumatic events can lead to a range of behaviors associ
188                The natural aging process and traumatic events such as lower-limb loss can alter the h
189 The mean number of pre-migration potentially traumatic events was 2.1 (SD 1.4).
190                    Considering the effect of traumatic experience on post-traumatic stress disorder (
191 del certain behavioral traits resulting from traumatic experiences in humans.
192           Individuals respond differently to traumatic experiences, including their propensity to dev
193 ling) reduces emotional distress after other traumatic experiences.
194 isms underlying depression and anxiety after traumatic experiences.
195 We report the findings of an individual with traumatic high-cervical spinal cord injury who coordinat
196 al-energy CT for suspicion of a nondisplaced traumatic hip fracture.
197 ensitivity for the detection of nondisplaced traumatic hip fractures and improved diagnostic confiden
198                                              Traumatic implantation of contaminated plant material is
199 frica and South and Central America, follows traumatic implantation of saprophytic fungi and frequent
200 ed fracture healing because of systemic post-traumatic inflammation.
201                             Widely different traumatic injuries evoke surprisingly similar gene expre
202 ransplantation strategies in a wide range of traumatic injuries for which therapeutic intervention is
203 ansplantation strategies for a wide range of traumatic injuries is the determination of a suitable ti
204 taneously or after provoking events, such as traumatic injuries to the pelvis, upper and lower exterm
205 death caused by demyelinating, ischemic, and traumatic injuries, implying its involvement in a wide s
206 HO) after blast-related extremity injury and traumatic injuries, respectively.
207 damage and can be reversible in ischemic and traumatic injuries.
208 juries and contusion or occult fracture) for traumatic injuries.
209 sed interventions to regenerate large scale, traumatic injuries.
210 evel decision that affects how patients with traumatic injury (trauma patients) interact with locoreg
211  [SD, 16.2]; men, 197 [61%]; had experienced traumatic injury after a fall, 223 [69%]), 258 completed
212 entral nervous system axons, associated with traumatic injury and demyelinating diseases such as mult
213 inical research on cellular therapeutics for traumatic injury and its sequelae and discuss prospects
214 nrolled 1138 patients recently admitted with traumatic injury to 1 of 4 major trauma hospitals across
215 , we first demonstrate that a mouse model of traumatic injury to the pediatric brain reproduces many
216                        The moderate and mild traumatic injury was inflicted by focal laser lesion and
217 al interventions can now be applied to treat traumatic injury, David J Lockey calls for research to d
218 ndrome and delirium tremens in patients with traumatic injury.
219 munocompromised patients or individuals with traumatic injury.
220  also detect "danger" signals (pathogenic or traumatic insult), become activated, produce proinflamma
221  in the intensive care unit with stable, non-traumatic intracerebral haemorrhage volume less than 30
222 diologically confirmed single spontaneous or traumatic intracranial hemorrhage, of whom 39 (83%) had
223 usal radiologically confirmed spontaneous or traumatic intracranial hemorrhage, of whom none had hear
224 ce and investigated how this influenced post-traumatic intraneural inflammation and neuropathic pain
225 embolization was successful in patients with traumatic leak and PLPS and, thus, should be considered
226                                Patients with traumatic leak and PLPS were combined into 1 group of 16
227 ologies of chylothorax: 2 patients (8%) with traumatic leak from a thoracic duct (TD) branch, 14 pati
228 perimental housing conditions did not induce traumatic levels of chronic stress.
229                                              Traumatic life experiences are associated with alcohol u
230 stress with fear conditioning to precipitate traumatic-like memories.
231 target for treating disorders that stem from traumatic memories, yet little is known about how this p
232 ments (EMs) while simultaneously recalling a traumatic memory, which renders the memory less vivid an
233 f anesthesia, hypothermia, cardioplegia, and traumatic myocardial injury.
234 maging may provide early markers of onset of traumatic neurodegenerative disease.
235 ese cells attenuated the development of post-traumatic OA, reduced pain and increased cartilage devel
236                                              Traumatic optic neuropathy (TON) is a devastating cause
237                                              Traumatic optic neuropathy (TON) is an acute injury of t
238 e spectrum of lesions characteristic of post-traumatic osteoarthritis (PTOA) across the knee joint in
239 tients were evaluated for basketball-related traumatic retinal detachment.
240 ractalkine receptor, promotes recovery after traumatic spinal contusion injury in mice, a benefit ach
241                                              Traumatic spinal cord injury (SCI) causes a cascade of d
242  chemokine receptor, promotes recovery after traumatic spinal cord injury in mice, a benefit achieved
243 ontributes to pathological changes following traumatic spinal cord or traumatic brain injury (TBI).
244 omote resilience to adverse effects of acute traumatic stress and facilitate adaptation to repeated s
245 ty Disorder [GAD]-2 anxiety scale), and post-traumatic stress disorder (measured by the Post-Traumati
246 ontrol subjects (n = 20), patients with post-traumatic stress disorder (n = 25) demonstrated intrinsi
247           Part of the symptomatology of post-traumatic stress disorder (PTSD) are alterations in arou
248               KEY POINTS: Patients with post-traumatic stress disorder (PTSD) are at a significantly
249 in to elucidate the mechanisms by which post-traumatic stress disorder (PTSD) at a young age contribu
250 men are at increased risk of developing post-traumatic stress disorder (PTSD) following a traumatic e
251                               ABSTRACT: Post-traumatic stress disorder (PTSD) is associated with incr
252                                         Post-traumatic stress disorder (PTSD) is characterized by exa
253 ctors, and correlates of cancer-related post-traumatic stress disorder (PTSD) symptoms and diagnoses.
254             We assessed patients' mood, post-traumatic stress disorder (PTSD) symptoms, and QOL 6 mon
255                                         Post-traumatic stress disorder (PTSD) was measured with the P
256 essive disorder (MDD), 50 patients with post-traumatic stress disorder (PTSD), and 122 healthy contro
257 s whether post-deployment screening for post-traumatic stress disorder (PTSD), depression, anxiety, o
258 g the effect of traumatic experience on post-traumatic stress disorder (PTSD), this study aims to exp
259 genetic response to traumatic stress on post-traumatic stress disorder (PTSD), this study examined lo
260 or type 2 (CRFR2) to be associated with post-traumatic stress disorder (PTSD)-like symptoms.
261 type is consistent with some aspects of post-traumatic stress disorder (PTSD).
262 ctional neurological disorder (FND) and post-traumatic stress disorder (PTSD).
263 ss-related psychopathologies, including post-traumatic stress disorder (PTSD).
264 reat is one of the defining features of post-traumatic stress disorder (PTSD).
265 highlight a unique sensory pathology of post-traumatic stress disorder (ruling out effects merely ref
266 ed symptoms of depression, anxiety, and post-traumatic stress disorder 1 year after flooding.
267 , for anxiety 1.66 (1.12-2.46), and for post-traumatic stress disorder 1.70 (1.17-2.48) than people w
268 s disorder (PTSD) was measured with the Post-traumatic Stress Disorder 8 items (PTSD-8) and severe me
269 rventions that might offset the risk of post-traumatic stress disorder after cardiovascular disease e
270            Interestingly, patients with post-traumatic stress disorder also showed heightened frontal
271                                         Post-traumatic stress disorder and anxiety are more prevalent
272 ndidate mechanisms for the link between post-traumatic stress disorder and cardiovascular disease, an
273 of symptoms of depression, anxiety, and post-traumatic stress disorder between participants displaced
274 umatic stress disorder (measured by the Post-Traumatic Stress Disorder Checklist [PCL]-6 scale).
275 carried mild traumatic brain injury and post-traumatic stress disorder diagnoses.
276                        We conclude that post-traumatic stress disorder is a risk factor for incident
277 tive control, fuelling and perpetuating post-traumatic stress disorder symptoms.
278 four studies, more women presented with post-traumatic stress disorder than did men in two studies, a
279 tions help construct a vicious cycle in post-traumatic stress disorder that is in action even at rest
280               Scores for depression and post-traumatic stress disorder were higher in people who were
281 ding (p=0.04 for depression, p=0.01 for post-traumatic stress disorder), although the difference in a
282  examined the apolipoprotein E4 allele, post-traumatic stress disorder, and genetic risk for schizoph
283 ictims reported a greater prevalence of post-traumatic stress disorder, anxiety, or depression than d
284 understanding mental disorders, such as post-traumatic stress disorder, little is known about the sou
285 energic system, a known risk factor for post-traumatic stress disorder, modulates the stress-induced
286     To elucidate a sensory pathology of post-traumatic stress disorder, we examined intrinsic visual
287  disorders, such as chronic anxiety and post-traumatic stress disorder.
288 threat-neutral sensory hyperactivity in post-traumatic stress disorder.
289 its levels are reduced in patients with post-traumatic stress disorder.
290 n additional aetiological mechanism for post-traumatic stress disorder.
291 ine the impact of the epigenetic response to traumatic stress on post-traumatic stress disorder (PTSD
292                 Life history events, such as traumatic stress, illness, or starvation, can influence
293 ed by existing evidence-based approaches for traumatic stress.
294 h Administration (VA) have a history of post-traumatic-stress-disorder (PTSD), and there exists a hig
295                           Patients with post-traumatic-stress-disorder reported higher pain scores, h
296     Our data suggests that a history of post-traumatic-stress-disorder was correlated with higher pai
297  Secondary outcomes included history of post-traumatic-stress-disorder, anesthesia type, first or sec
298                                The aggregate traumatic subarachnoid hemorrhage (tSAH) component of th
299 e that CN2097 significantly reduces the post-traumatic synthesis of proinflammatory mediators and inh
300 ean number of attempts, and the incidence of traumatic tap and backache did not differ significantly

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