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1 stay and at long-term follow-up (up to 2 yrs postinjury).
2 imit reparative processes in the early-phase postinjury.
3 t hospital admission and 3, 6, and 12 months postinjury.
4 ry outcome was mortality within 7 to 9 years postinjury.
5 e status and less hyperchloremia at 24 hours postinjury.
6 jury, with another probe test performed 3 mo postinjury.
7 ic episodes increasing as a function of time postinjury.
8 ere euthanized at 2 hours, 1 day, and 3 days postinjury.
9 ed Glasgow Outcome Scale (GOS-E) at 3 months postinjury.
10 was strongly expressed in odontoblasts 4 wk postinjury.
11 eo-electrocorticography (ECoG) 2 to 16 weeks postinjury.
12 current is larger for intact neurons at 2 d postinjury.
13 onocytes rolled on a thrombus 3 to 5 minutes postinjury.
14 5 degrees C) initiated approximately 2.0 hrs postinjury.
15 n of CD68, CCL-2, TNF-alpha, and IL-6 at 1 d postinjury.
16 how these changes at 1 d, but recover by 2 d postinjury.
17 one interview at 6-, 12-, 24-, and 36-months postinjury.
18 decreased in axotomized neurons at 1 and 2 d postinjury.
19 antly increased in axotomized neurons at 1 d postinjury.
20 rebral blood flow were measured 30 min-6 hrs postinjury.
21 ward regained size back to normal by 2 weeks postinjury.
22 roup) or at 1, 2, and 3 days (EPO-24h group) postinjury.
23 thymidine analog incorporation was observed postinjury.
24 and repeated subsequently for up to 32 days postinjury.
25 Similar results were seen at 1-year postinjury.
26 muscle action potential starting at 14 days postinjury.
27 stered intraperitoneally at days 1, 2, and 3 postinjury.
28 rn-injured mice was 50 x 10(3) CFU at 7 days postinjury.
29 in modulating phrenic function normally and postinjury.
30 th unilateral ACL insufficiency, 32-364 days postinjury.
31 Outcome was assessed 6-9 months postinjury.
32 e aerosolized every 4 hrs, starting at 2 hrs postinjury.
33 IB4 vascular profiles decreasing by 21 days postinjury.
34 atio, and decreased shunt fraction at 48 hrs postinjury.
35 itive dysfunction persisted for up to 16 wks postinjury.
36 tients survived, 9 (47%) developed infection postinjury.
37 s performed at baseline and at 24 and 48 hrs postinjury.
38 cular samples obtained over the first 48 hrs postinjury.
39 tion, gender, and time (p = .0035) by 24 hrs postinjury.
40 red cell viability to control values at 24 h postinjury.
41 time (p = .0045) throughout the first 48 hrs postinjury.
42 n admission, compared to only 33 at 24 hours postinjury.
43 lammation were similar during the first week postinjury.
44 rome c release peaked at approximately 4-8 h postinjury.
45 rom injured samples between 1 day and 7 days postinjury.
46 ) and restored cognitive performance 14 days postinjury.
47 mor necrosis factor alpha) peaked by 12-24 h postinjury.
48 Sheep were killed 48 hrs postinjury.
49 were collected on admission, 24, and 48 hrs postinjury.
50 expressed in the same direction at 24 hours postinjury.
51 immune cell activation between 1 and 8 weeks postinjury.
52 activity during intestinal epithelium repair postinjury.
53 hysical activity participation within 7 days postinjury.
54 f axons and neurons during the first 2 weeks postinjury.
55 uestionnaires in the ED and at days 7 and 28 postinjury.
56 ric moderate-to-severe TBI sample 1-5 months postinjury.
57 wounds were aggravated or minimally handled postinjury.
58 evels differentially in the initial 24 hours postinjury.
59 005) or 1 month (neuropsychiatric; P < .005) postinjury.
60 fer-treated animals at 18 hours and 24 hours postinjury.
61 crophage polarization markers at 3 h and 7 d postinjury.
62 ortex as early as few hours and up to 5 days postinjury.
63 ionally injured patients within 7 to 9 years postinjury.
64 disability, vegetative, or dead) at 6 months postinjury.
65 nning 30 minutes and persisting up to 1 week postinjury.
66 mechanism may drive sex outcome differences postinjury.
67 m injured and control mice collected at 3 mo postinjury.
68 e happens almost entirely in the first weeks postinjury.
69 ve mechanism responsible for sex differences postinjury.
70 lood samples were obtained from days 1 to 14 postinjury.
71 (TLR) pathway thought to drive inflammation postinjury.
72 ce compared with wild-type mice at 2-4 weeks postinjury.
77 lined from 4.6 preinjury to 3.7 at 12 months postinjury, a decline of nearly 1 full ADL (P < .05).
78 ated genes (false discovery rate <2) at d 14 postinjury, a subset of which were enriched for T-cell-r
79 rimotor function, evident as early as 1 week postinjury, a time point when increased neuronal surviva
81 aparotomy was followed by growing reports of postinjury abdominal compartment syndrome and prophylact
83 vels were drawn twice daily for up to 9 days postinjury; AI was defined as two consecutive cortisols
84 tudes of both CAP components were suppressed postinjury, although this deficit was 16% greater for th
85 subsequently demonstrated that pharmacologic postinjury AMPK activation was sufficient to delay muscl
86 T cells were determined on days 2, 5, and 10 postinjury and compared with similar measurements made i
87 ll numbers were highest between 3 and 7 days postinjury and declined by 50% over the next 3 weeks.
89 icipation in physical activity within 7 days postinjury and incidence of persistent postconcussive sy
90 synthase inhibitor, during the first 12 hrs postinjury and infusion of BBS-2, a specific inducible n
93 g independent predictor of MOF and mortality postinjury and represents a common variant with prognost
94 ing pathways that govern cartilage responses postinjury and suggest that delivery of NF-kappaB siRNA
95 demonstrate the importance of TLR signaling postinjury and supports that a genetic mechanism may dri
97 ary vascular hyperpermeability peaked 12 hrs postinjury and was related to vascular endothelial growt
98 pregulated during the repair phase (2-3 days postinjury) and returned to the control level when repai
99 ht microscopy at intervals from 1 to 56 days postinjury, and the area of damaged tissue (termed lesio
100 e collection was performed on days 17 and 29 postinjury, and urinary C-terminal telopeptide of type I
101 n that in controls during the first 24 hours postinjury, and was not affected by inhibitors of biosyn
104 is both necessary and sufficient to inhibit postinjury arterial VSMC proliferation, whereas membrane
106 (+) astrocytes that persisted for >/=6 weeks postinjury, as well as increased intraspinal GLT1 protei
107 SD and depression were assessed at 12 months postinjury, as were the following functional outcomes: a
109 pproximating 1:1:1 during the first 24 hours postinjury, based on US military retrospective experienc
110 hippocampal-onset seizures began 16-25 days postinjury, before hippocampal atrophy developed, as dem
111 n heavy chain 2) were increased on d 2 and 4 postinjury but later returned to baseline levels on d 8
112 ain constant in the SVZ and RMS until 5 days postinjury but then rapidly expanded by 150,000 cells by
113 medial VSMCs from injured vessels at 2 weeks postinjury but was restored when the up-regulation of ei
114 ever, MAC was down-regulated on days 5 and 7 postinjury but was still higher than in non-injured mice
115 0%) were known to have survived to 36-months postinjury but were lost to follow-up at all time points
119 tepped care that consisted of (1) continuous postinjury case management, (2) motivational interviews
120 n of IL-10 amplified the Th1 response at 1 d postinjury, causing increases in IL-6 and CCL2, while pr
121 FR2(+) cells and suppressed replenishment of postinjury CD34(+)/VEGFR2(+) cells in peripheral blood (
124 ality that allows 'point-of-care' testing of postinjury coagulopathy and monitoring of transfusion st
125 Existing limitations in the management of postinjury coagulopathy include the lack of a uniform de
127 with life threatening hemorrhage at risk for postinjury coagulopathy should receive component therapy
128 secutive patients over 14 months at risk for postinjury coagulopathy were stratified by transfusion r
129 PF occurs early in severe shock, leading to postinjury coagulopathy, and ultimately hemorrhage-relat
130 This review examines the current approach to postinjury coagulopathy, including identification of pat
132 tion of spinal neurons and axons at 12 weeks postinjury, compared with control (LV-GFP)-treated anima
133 moderate-to-severe TBI (msTBI) at 1-5 months postinjury, compared with well matched healthy control c
135 h a lower GCS score at 24 hrs, in those with postinjury complications, in those with 6-wk mortality,
136 ophysiological recordings, conducted at 24 h postinjury, compound action potentials (CAPs) were evoke
138 ns in monocyte and T-cell responses on day 2 postinjury correlates with the development of adverse cl
139 xamine synaptic profiles in Vc/C2 at 3 weeks postinjury, corresponding to the time of peak behavioral
141 n lactulose permeability from day 1 to day 2 postinjury could not be demonstrated in the B and EF gro
146 s was 40% to 70% lower in trauma patients on postinjury days 2, 5, and 10 than in healthy control sub
149 0.9% of tracer-flooded neurons revealed only postinjury dextran uptake, consistent with delayed membr
151 xotomy, we reveal a critical period of 4-5 h postinjury during which the course of Wallerian axonal d
153 spontaneous seizures.SIGNIFICANCE STATEMENT Postinjury epilepsy is an unpreventable and devastating
157 rd heightened fear learning during stressful postinjury events and provides a potential molecular mec
160 , plasma cfDNA levels, and IG count at day 1 postinjury gave good discriminatory power for the identi
164 present a network-level mechanism underlying postinjury hippocampal dysfunction and epileptic network
166 ormant basket cell" hypothesis suggests that postinjury hippocampal network hyperexcitability results
167 tate/pyruvate ratio remained elevated beyond postinjury hour 100 in the seizure group but not the non
172 sought to determine if differences in early postinjury immune-related gene expression are associated
175 , indicated that FK506 reduced the extent of postinjury impairments to axonal transport and subsequen
176 served reduced cortical cell loss at 5 weeks postinjury in mannose-binding lectin (-/-) mice compared
177 significantly elevated over the first 7 days postinjury in the hypotensive versus normotensive patien
178 studied the population of cells that divide postinjury in the injury epicenter by delivering BrdU or
180 erlines a pathogenic contribution of sterile postinjury inflammation in APAP-induced acute liver inju
181 ical and basic science literature related to postinjury inflammation in childhood, focusing on the de
185 ventions for the prevention and treatment of postinjury inflammatory dysregulation depends on continu
186 ealing how OPCs themselves contribute to the postinjury inflammatory milieu by producing cytokines th
188 l mice, and those microglia present at early postinjury intervals retained their resting morphology.
190 he prevalence of ongoing problems at 3-years postinjury is high, confirming that serious injury is fr
191 ated neural control of systemic inflammation postinjury is likely exaggerated in patients with trauma
195 lose permeability in the B+EF group on day 2 postinjury markedly decreased from day 1 but was still s
196 g the early molecular and cellular responses postinjury may provide targets for therapeutic intervent
197 l experiments for a further understanding of postinjury mechanisms of motor control and recovery.
200 monocyte (Mphi) dysfunctions could result if postinjury Mphi differentiation preferentially favored i
201 This M1 to M2 sequence is observed during postinjury muscle regeneration, which provides an excell
204 tropium bromide 1 hr before injury (n=6) and postinjury nebulization protocols of 18 mug (n=6), 36 mu
208 her regional brain edema formation at 24 hrs postinjury nor the extent of cortical tissue loss assess
209 al contusion lesion sites between 1 and 90 d postinjury of athymic nude (AN) and Sprague Dawley (SD)
210 increased in all injured rat groups on day 1 postinjury; on day 2 it remained elevated post-B, decrea
211 4 administration schedules (preinjury only, postinjury only, for 24 hr postsurgery, or for 72 hr pos
213 ocking cPLA2 pharmacologically at 30 minutes postinjury or genetically deleting cPLA2 in mice amelior
215 hildren with traumatic brain injury, 6-month postinjury outcome inversely correlated with Glasgow Com
217 lyses, blood lead levels increased with time postinjury (p < 0.0005) up to 3 months, with number of r
218 er PTSR than the assessment group at 4 weeks postinjury, p < .01, and at 12 weeks postinjury, p < .05
219 4 weeks postinjury, p < .01, and at 12 weeks postinjury, p < .05, and significantly lower depressive
220 nd longitudinal (1 day and 1 week vs 1 month postinjury; P < .001) evidence of CBF recovery in the ri
222 onsidered when designing acute and long-term postinjury patient intervention strategies aimed to enha
223 nt guidelines advocate rest in the immediate postinjury period until symptoms resolve, no clear evide
227 e immune status of patients in the immediate postinjury phase and how this might influence patient ou
229 on brain injury in untreated, preinjury, and postinjury phenylephrine (1 microg/kg/min intravenously)
230 ogrammed NIH3T3 cells significantly improved postinjury physiological functions and showed anatomic e
234 lation of NMDA receptors by NMDA 24 and 48 h postinjury produced a significant attenuation of neurolo
235 ovide one molecular mechanism underlying the postinjury protective effects of oligodendrocytes by str
236 tionship of preinjury psychiatric status and postinjury PTSD with conflicting results, but no prospec
237 Animals were euthanized at five timepoints postinjury, ranging from 6 hours to 9 weeks after BrdU d
238 ction (i.e., the point at which the earliest postinjury recovery of phrenic activity has been reporte
239 vivo evidence that FGF signaling facilitates postinjury recovery of the mouse hematopoietic system by
240 suppressed after injury and increased during postinjury recovery, whereas chlorzoxazone metabolism wa
243 peritoneal cholecalciferol treatment 6 hours postinjury reduced alveolar inflammation, cellular damag
244 n of RANKL, given either prophylactically or postinjury, reduces liver injury in a manner associated
254 mg/kg) by subcutaneous injection 30 minutes postinjury restores levels of barrier sealing glucocorti
255 tested the function of Wnt signaling in the postinjury retina, focusing on its ability to influence
257 Interestingly, after halting GCV at 14 d postinjury, scar elements and vessels entered the lesion
258 pacity of monocyte IL-12 production on day 2 postinjury showed a statistically significant correlatio
259 uggest the possibility of rapid, transmedian postinjury signals between homologous mirror-image neuro
261 ypothermia group showed significantly higher postinjury somatosensory-evoked potential amplitudes wit
264 cAMP into the L4 dorsal root ganglion, and a postinjury stimulus to the injured axon was administered
265 ater than that for the N1 CAPs, and improved postinjury strength-duration and refractoriness properti
266 rophages than scalpel wounds at days 2 and 7 postinjury, suggesting that free-electron laser irradiat
267 reach the wound decreased after the first h postinjury, suggesting that the knockdown specifically a
268 sion increased in IL-10 mutant muscle at 1 d postinjury, suggesting that the mutation amplified the t
271 nd CD-1 were significantly larger at 56 days postinjury than in the KA-resistant strains C57Bl/6 and
272 time) and neuropsychiatric symptoms at 1 day postinjury that resolved at either 1 week (cognitive; P
277 In this study, we showed how the hyperacute postinjury time window contained a focused, specific sig
278 -155 deletion improves locomotor function at postinjury times corresponding with the arrival and maxi
281 ice, treatment accelerated recovery, reduced postinjury tubular atrophy and interstitial fibrosis, an
282 The two groups underwent preinjury, weekly postinjury (up to 4 wks) somatosensory-evoked potential
285 revalence of reporting problems at 36-months postinjury was 37% for mobility, 21% for self-care, 47%
286 the phagocytic macrophage marker CD68 at 3 d postinjury was followed by increased CD206 expression at
287 dmission with systemic disease preinjury and postinjury was higher in both injury groups than in CC a
289 t of cortical tissue loss assessed at 7 days postinjury was significantly aggravated by superimposed
290 GAG release during the period 24-72 hours postinjury was similar to that in uninjured controls, bu
291 cipants with adjustment disorder at 3 months postinjury were significantly more likely to meet criter
293 in the first 24 hr and then from days 1 to 7 postinjury) were assessed for 24 inflammatory mediators
294 loping major depressive episode by 3 months' postinjury, which could facilitate selective referral fo
295 cyte growth factor in hepatic stellate cells postinjury, which, in turn, results in an earlier onset
297 uma and could be administered at least 3 hrs postinjury with only a small reduction in efficacy.
298 netic resonance imaging (MRI) out to 30 days postinjury, with a subset of animals selected for histop
299 t T-cell entry was not evident until 14 days postinjury, with T-cell numbers doubling between 2 and 6
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