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1 stay and at long-term follow-up (up to 2 yrs postinjury).
2 uge of sympathetic hyperreflexia, for months postinjury.
3 ortex as early as few hours and up to 5 days postinjury.
4 ionally injured patients within 7 to 9 years postinjury.
5 disability, vegetative, or dead) at 6 months postinjury.
6 nning 30 minutes and persisting up to 1 week postinjury.
7 bradykinin receptors was gradual after day 3 postinjury.
8 mechanism may drive sex outcome differences postinjury.
9 m injured and control mice collected at 3 mo postinjury.
10 ve mechanism responsible for sex differences postinjury.
11 lood samples were obtained from days 1 to 14 postinjury.
12 (TLR) pathway thought to drive inflammation postinjury.
13 ce compared with wild-type mice at 2-4 weeks postinjury.
14 imit reparative processes in the early-phase postinjury.
15 t hospital admission and 3, 6, and 12 months postinjury.
16 ry outcome was mortality within 7 to 9 years postinjury.
17 e status and less hyperchloremia at 24 hours postinjury.
18 jury, with another probe test performed 3 mo postinjury.
19 ic episodes increasing as a function of time postinjury.
20 ere euthanized at 2 hours, 1 day, and 3 days postinjury.
21 ed Glasgow Outcome Scale (GOS-E) at 3 months postinjury.
22 eo-electrocorticography (ECoG) 2 to 16 weeks postinjury.
23 ecovery and neurodegeneration up to 3 months postinjury.
24 current is larger for intact neurons at 2 d postinjury.
25 onocytes rolled on a thrombus 3 to 5 minutes postinjury.
26 5 degrees C) initiated approximately 2.0 hrs postinjury.
27 n of CD68, CCL-2, TNF-alpha, and IL-6 at 1 d postinjury.
28 how these changes at 1 d, but recover by 2 d postinjury.
29 decreased in axotomized neurons at 1 and 2 d postinjury.
30 antly increased in axotomized neurons at 1 d postinjury.
31 rebral blood flow were measured 30 min-6 hrs postinjury.
32 ward regained size back to normal by 2 weeks postinjury.
33 roup) or at 1, 2, and 3 days (EPO-24h group) postinjury.
34 thymidine analog incorporation was observed postinjury.
35 and repeated subsequently for up to 32 days postinjury.
36 /15-lipoxygenase inhibitor) at 10-15 minutes postinjury.
37 Similar results were seen at 1-year postinjury.
38 stered intraperitoneally at days 1, 2, and 3 postinjury.
39 e delayed wound healing at early time points postinjury.
40 rn-injured mice was 50 x 10(3) CFU at 7 days postinjury.
41 in modulating phrenic function normally and postinjury.
42 th unilateral ACL insufficiency, 32-364 days postinjury.
43 Outcome was assessed 6-9 months postinjury.
44 e aerosolized every 4 hrs, starting at 2 hrs postinjury.
45 IB4 vascular profiles decreasing by 21 days postinjury.
46 cts who developed adverse events at 6 months postinjury.
47 atio, and decreased shunt fraction at 48 hrs postinjury.
48 itive dysfunction persisted for up to 16 wks postinjury.
49 tients survived, 9 (47%) developed infection postinjury.
50 s performed at baseline and at 24 and 48 hrs postinjury.
51 cular samples obtained over the first 48 hrs postinjury.
52 tion, gender, and time (p = .0035) by 24 hrs postinjury.
53 red cell viability to control values at 24 h postinjury.
54 time (p = .0045) throughout the first 48 hrs postinjury.
55 lammation were similar during the first week postinjury.
56 rome c release peaked at approximately 4-8 h postinjury.
57 rom injured samples between 1 day and 7 days postinjury.
58 expressed in the same direction at 24 hours postinjury.
59 ) and restored cognitive performance 14 days postinjury.
60 e happens almost entirely in the first weeks postinjury.
61 was strongly expressed in odontoblasts 4 wk postinjury.
62 one interview at 6-, 12-, 24-, and 36-months postinjury.
63 muscle action potential starting at 14 days postinjury.
64 n admission, compared to only 33 at 24 hours postinjury.
65 immune cell activation between 1 and 8 weeks postinjury.
66 activity during intestinal epithelium repair postinjury.
67 hysical activity participation within 7 days postinjury.
68 f axons and neurons during the first 2 weeks postinjury.
69 uestionnaires in the ED and at days 7 and 28 postinjury.
70 ric moderate-to-severe TBI sample 1-5 months postinjury.
71 cognitive function recovery through 3 months postinjury.
72 wounds were aggravated or minimally handled postinjury.
73 evels differentially in the initial 24 hours postinjury.
74 005) or 1 month (neuropsychiatric; P < .005) postinjury.
75 fer-treated animals at 18 hours and 24 hours postinjury.
76 crophage polarization markers at 3 h and 7 d postinjury.
80 lined from 4.6 preinjury to 3.7 at 12 months postinjury, a decline of nearly 1 full ADL (P < .05).
81 ated genes (false discovery rate <2) at d 14 postinjury, a subset of which were enriched for T-cell-r
82 rimotor function, evident as early as 1 week postinjury, a time point when increased neuronal surviva
84 aparotomy was followed by growing reports of postinjury abdominal compartment syndrome and prophylact
87 vels were drawn twice daily for up to 9 days postinjury; AI was defined as two consecutive cortisols
88 tudes of both CAP components were suppressed postinjury, although this deficit was 16% greater for th
89 subsequently demonstrated that pharmacologic postinjury AMPK activation was sufficient to delay muscl
92 icipation in physical activity within 7 days postinjury and incidence of persistent postconcussive sy
93 synthase inhibitor, during the first 12 hrs postinjury and infusion of BBS-2, a specific inducible n
96 g independent predictor of MOF and mortality postinjury and represents a common variant with prognost
97 ing pathways that govern cartilage responses postinjury and suggest that delivery of NF-kappaB siRNA
98 demonstrate the importance of TLR signaling postinjury and supports that a genetic mechanism may dri
100 ary vascular hyperpermeability peaked 12 hrs postinjury and was related to vascular endothelial growt
101 pregulated during the repair phase (2-3 days postinjury) and returned to the control level when repai
102 GB1 at 2 hr, 6 hr, 24 hr, 3 days, and 7 days postinjury, and serum was collected for enzyme-linked im
103 e collection was performed on days 17 and 29 postinjury, and urinary C-terminal telopeptide of type I
104 n that in controls during the first 24 hours postinjury, and was not affected by inhibitors of biosyn
106 is both necessary and sufficient to inhibit postinjury arterial VSMC proliferation, whereas membrane
108 (+) astrocytes that persisted for >/=6 weeks postinjury, as well as increased intraspinal GLT1 protei
109 SD and depression were assessed at 12 months postinjury, as were the following functional outcomes: a
111 pproximating 1:1:1 during the first 24 hours postinjury, based on US military retrospective experienc
112 hippocampal-onset seizures began 16-25 days postinjury, before hippocampal atrophy developed, as dem
113 n heavy chain 2) were increased on d 2 and 4 postinjury but later returned to baseline levels on d 8
114 ain constant in the SVZ and RMS until 5 days postinjury but then rapidly expanded by 150,000 cells by
115 medial VSMCs from injured vessels at 2 weeks postinjury but was restored when the up-regulation of ei
116 ever, MAC was down-regulated on days 5 and 7 postinjury but was still higher than in non-injured mice
117 0%) were known to have survived to 36-months postinjury but were lost to follow-up at all time points
120 tepped care that consisted of (1) continuous postinjury case management, (2) motivational interviews
121 n of IL-10 amplified the Th1 response at 1 d postinjury, causing increases in IL-6 and CCL2, while pr
122 FR2(+) cells and suppressed replenishment of postinjury CD34(+)/VEGFR2(+) cells in peripheral blood (
125 ding to recent evidence-also participates in postinjury CNS recovery, chronic neurodegenerative condi
126 ality that allows 'point-of-care' testing of postinjury coagulopathy and monitoring of transfusion st
127 Existing limitations in the management of postinjury coagulopathy include the lack of a uniform de
129 with life threatening hemorrhage at risk for postinjury coagulopathy should receive component therapy
130 secutive patients over 14 months at risk for postinjury coagulopathy were stratified by transfusion r
131 PF occurs early in severe shock, leading to postinjury coagulopathy, and ultimately hemorrhage-relat
132 This review examines the current approach to postinjury coagulopathy, including identification of pat
134 tion of spinal neurons and axons at 12 weeks postinjury, compared with control (LV-GFP)-treated anima
135 moderate-to-severe TBI (msTBI) at 1-5 months postinjury, compared with well matched healthy control c
137 h a lower GCS score at 24 hrs, in those with postinjury complications, in those with 6-wk mortality,
138 ophysiological recordings, conducted at 24 h postinjury, compound action potentials (CAPs) were evoke
140 ns in monocyte and T-cell responses on day 2 postinjury correlates with the development of adverse cl
141 xamine synaptic profiles in Vc/C2 at 3 weeks postinjury, corresponding to the time of peak behavioral
143 n lactulose permeability from day 1 to day 2 postinjury could not be demonstrated in the B and EF gro
149 a significantly dysregulated repair process postinjury, despite having a higher proliferative capaci
150 0.9% of tracer-flooded neurons revealed only postinjury dextran uptake, consistent with delayed membr
152 xotomy, we reveal a critical period of 4-5 h postinjury during which the course of Wallerian axonal d
154 spontaneous seizures.SIGNIFICANCE STATEMENT Postinjury epilepsy is an unpreventable and devastating
156 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
163 tional, do not include data on preinjury and postinjury health care visits and related costs, and use
166 present a network-level mechanism underlying postinjury hippocampal dysfunction and epileptic network
168 ormant basket cell" hypothesis suggests that postinjury hippocampal network hyperexcitability results
169 tate/pyruvate ratio remained elevated beyond postinjury hour 100 in the seizure group but not the non
174 sought to determine if differences in early postinjury immune-related gene expression are associated
177 , indicated that FK506 reduced the extent of postinjury impairments to axonal transport and subsequen
178 served reduced cortical cell loss at 5 weeks postinjury in mannose-binding lectin (-/-) mice compared
179 significantly elevated over the first 7 days postinjury in the hypotensive versus normotensive patien
180 studied the population of cells that divide postinjury in the injury epicenter by delivering BrdU or
181 l evaluation of the spinal lesion at 4 weeks postinjury indicated less collagen IV immunostaining in
182 erlines a pathogenic contribution of sterile postinjury inflammation in APAP-induced acute liver inju
183 ical and basic science literature related to postinjury inflammation in childhood, focusing on the de
187 ventions for the prevention and treatment of postinjury inflammatory dysregulation depends on continu
188 ealing how OPCs themselves contribute to the postinjury inflammatory milieu by producing cytokines th
191 he prevalence of ongoing problems at 3-years postinjury is high, confirming that serious injury is fr
192 ated neural control of systemic inflammation postinjury is likely exaggerated in patients with trauma
196 lose permeability in the B+EF group on day 2 postinjury markedly decreased from day 1 but was still s
197 g the early molecular and cellular responses postinjury may provide targets for therapeutic intervent
198 l experiments for a further understanding of postinjury mechanisms of motor control and recovery.
201 monocyte (Mphi) dysfunctions could result if postinjury Mphi differentiation preferentially favored i
202 This M1 to M2 sequence is observed during postinjury muscle regeneration, which provides an excell
205 tropium bromide 1 hr before injury (n=6) and postinjury nebulization protocols of 18 mug (n=6), 36 mu
209 her regional brain edema formation at 24 hrs postinjury nor the extent of cortical tissue loss assess
211 al contusion lesion sites between 1 and 90 d postinjury of athymic nude (AN) and Sprague Dawley (SD)
212 increased in all injured rat groups on day 1 postinjury; on day 2 it remained elevated post-B, decrea
213 4 administration schedules (preinjury only, postinjury only, for 24 hr postsurgery, or for 72 hr pos
214 ocking cPLA2 pharmacologically at 30 minutes postinjury or genetically deleting cPLA2 in mice amelior
216 lyses, blood lead levels increased with time postinjury (p < 0.0005) up to 3 months, with number of r
217 er PTSR than the assessment group at 4 weeks postinjury, p < .01, and at 12 weeks postinjury, p < .05
218 4 weeks postinjury, p < .01, and at 12 weeks postinjury, p < .05, and significantly lower depressive
219 nd longitudinal (1 day and 1 week vs 1 month postinjury; P < .001) evidence of CBF recovery in the ri
221 onsidered when designing acute and long-term postinjury patient intervention strategies aimed to enha
222 nt guidelines advocate rest in the immediate postinjury period until symptoms resolve, no clear evide
226 e immune status of patients in the immediate postinjury phase and how this might influence patient ou
228 on brain injury in untreated, preinjury, and postinjury phenylephrine (1 microg/kg/min intravenously)
229 ogrammed NIH3T3 cells significantly improved postinjury physiological functions and showed anatomic e
233 lation of NMDA receptors by NMDA 24 and 48 h postinjury produced a significant attenuation of neurolo
234 ovide one molecular mechanism underlying the postinjury protective effects of oligodendrocytes by str
235 tionship of preinjury psychiatric status and postinjury PTSD with conflicting results, but no prospec
236 Animals were euthanized at five timepoints postinjury, ranging from 6 hours to 9 weeks after BrdU d
237 ction (i.e., the point at which the earliest postinjury recovery of phrenic activity has been reporte
238 vivo evidence that FGF signaling facilitates postinjury recovery of the mouse hematopoietic system by
239 suppressed after injury and increased during postinjury recovery, whereas chlorzoxazone metabolism wa
241 peritoneal cholecalciferol treatment 6 hours postinjury reduced alveolar inflammation, cellular damag
242 n of RANKL, given either prophylactically or postinjury, reduces liver injury in a manner associated
244 nificantly elevated at the early acute phase postinjury relative to baseline and both control groups
245 Glial fibrillary acidic protein was elevated postinjury relative to baseline in concussed athletes wi
253 mg/kg) by subcutaneous injection 30 minutes postinjury restores levels of barrier sealing glucocorti
254 tested the function of Wnt signaling in the postinjury retina, focusing on its ability to influence
256 Interestingly, after halting GCV at 14 d postinjury, scar elements and vessels entered the lesion
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 reach the wound decreased after the first h postinjury, suggesting that the knockdown specifically a
267 sion increased in IL-10 mutant muscle at 1 d postinjury, suggesting that the mutation amplified the t
270 time) and neuropsychiatric symptoms at 1 day postinjury that resolved at either 1 week (cognitive; P
271 ciated neuropathological changes at 3 months postinjury; these included a smaller cortical lesion, re
273 itor of sTNFalpha, at a clinically feasible, postinjury time point (i.e., 3 d after complete SCI) suf
275 In this study, we showed how the hyperacute postinjury time window contained a focused, specific sig
276 -155 deletion improves locomotor function at postinjury times corresponding with the arrival and maxi
280 ice, treatment accelerated recovery, reduced postinjury tubular atrophy and interstitial fibrosis, an
281 The two groups underwent preinjury, weekly postinjury (up to 4 wks) somatosensory-evoked potential
284 revalence of reporting problems at 36-months postinjury was 37% for mobility, 21% for self-care, 47%
285 the phagocytic macrophage marker CD68 at 3 d postinjury was followed by increased CD206 expression at
286 dmission with systemic disease preinjury and postinjury was higher in both injury groups than in CC a
288 t of cortical tissue loss assessed at 7 days postinjury was significantly aggravated by superimposed
289 GAG release during the period 24-72 hours postinjury was similar to that in uninjured controls, bu
290 cipants with adjustment disorder at 3 months postinjury were significantly more likely to meet criter
292 in the first 24 hr and then from days 1 to 7 postinjury) were assessed for 24 inflammatory mediators
293 ing isolectin B4+ nonpeptidergic neurons 1 d postinjury, whereas peptidergic neurons did not display
294 ticular, ATP receptors up-regulated on day 1 postinjury, whereas the increase in bradykinin receptors
295 loping major depressive episode by 3 months' postinjury, which could facilitate selective referral fo
296 cyte growth factor in hepatic stellate cells postinjury, which, in turn, results in an earlier onset
298 uma and could be administered at least 3 hrs postinjury with only a small reduction in efficacy.
299 netic resonance imaging (MRI) out to 30 days postinjury, with a subset of animals selected for histop