戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (1語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
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.
77                               For 30-45 mins postinjury, 1 L of normal saline was administered.
78                                  At 6 months postinjury, 133 (19%) patients had a fatal outcome; of t
79                               For 30-60 mins postinjury, 500 mL of either normal saline (control, n =
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
83                                              Postinjury abdominal compartment syndrome (ACS) is an ex
84 aparotomy was followed by growing reports of postinjury abdominal compartment syndrome and prophylact
85                                              Postinjury administration of baicalein attenuated oxidat
86                                              Postinjury administration of sulforaphane reduced the lo
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
90          We demonstrate that LMO7 is induced postinjury and by TGF-beta in SMC in vitro.
91 tions (PTSR) were assessed at 4 and 12 weeks postinjury and depression at baseline and week 4.
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
94      Late phase of healing occurs a few days postinjury and involves interaction of injured myofibers
95              Fibrinolysis shutdown is common postinjury and predicts poor outcomes.
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
99 within physiologic ranges for a certain time postinjury and then suddenly deteriorate.
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
105 r discomfort increased from 24- to 36-months postinjury (ARR 1.06, 95% CI: 1.01, 1.12).
106  is both necessary and sufficient to inhibit postinjury arterial VSMC proliferation, whereas membrane
107 rotein immunoreactive clusters 7 and 14 days postinjury, as compared with nontreated rats.
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
110 ts were observed at the 6-, 9-, and 12-month postinjury assessments.
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
118                  The mechanisms that dictate postinjury cardiomyocyte proliferation early in life rem
119 s were developed and implemented to optimize postinjury care.
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 (
123                                              Postinjury changes in gut microbiota persist for at leas
124                                 Control over postinjury CNS plasticity is a major frontier of science
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
128                                  Progressive postinjury coagulopathy remains the fundamental rational
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
133 he injured rat groups (B, EF, B+EF) on day 1 postinjury compared with sham.
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
136                                   Six months postinjury, comparing good outcome (PCPC < or = 3, n = 2
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
139 care on mortality at discharge and 12 months postinjury, controlling for injury severity.
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
142                 Minocycline alone attenuated postinjury cortical lesion volume, hippocampal CA3 neuro
143 n lactulose permeability from day 1 to day 2 postinjury could not be demonstrated in the B and EF gro
144 ion on computed tomography and a complicated postinjury course.
145 CD4(-/-) mice with WT CD4(+) T cells reduced postinjury cytokine production to WT levels.
146 p were euthanized for histologic analysis at postinjury day 3 and day 28.
147                                       During postinjury days 1-8, 65 neurological wake-up tests were
148                                          The postinjury decrease in SGC tonic GABA currents is in dir
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
151 age that normally occurred between 1 and 4 d postinjury did not occur in IL-10 mutants.
152 xotomy, we reveal a critical period of 4-5 h postinjury during which the course of Wallerian axonal d
153                                              Postinjury epilepsy (PIE) is a devastating sequela of va
154  spontaneous seizures.SIGNIFICANCE STATEMENT Postinjury epilepsy is an unpreventable and devastating
155                                              Postinjury etomidate attenuated water maze deficits, but
156 rd heightened fear learning during stressful postinjury events and provides a potential molecular mec
157 rate injury, accelerate recovery, or prevent postinjury fibrosis after AKI.
158 onal cohort of brains was harvested at 3 day postinjury for immunofluorescence staining.
159  which resulted in a concomitant increase in postinjury functional recovery.
160 , plasma cfDNA levels, and IG count at day 1 postinjury gave good discriminatory power for the identi
161   Desensitization is most marked immediately postinjury, generally resolving by Day 7.
162 r studies suggest that Olig2 is critical for postinjury gliosis.
163 tional, do not include data on preinjury and postinjury health care visits and related costs, and use
164 ated that collagen V is a critical driver of postinjury heart function.
165                  Our research sheds light on postinjury heterogeneity.
166 present a network-level mechanism underlying postinjury hippocampal dysfunction and epileptic network
167                               The process of postinjury hippocampal epileptogenesis may involve gradu
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
170                                 After 7 days postinjury, however, the cellular responses differed bet
171                    The mechanisms underlying postinjury immune suppression are not known.
172                                  Reversal of postinjury immune suppression in SCI mice can be achieve
173 25+ T cells contribute to the development of postinjury immune suppression.
174  sought to determine if differences in early postinjury immune-related gene expression are associated
175 o and production of M-CSF and contributes to postinjury immunoaberrations.
176                     This could contribute to postinjury immunosuppression.
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
184                                              Postinjury inflammation markedly reduces newborn neuron
185 vival of young neurons is sharply reduced by postinjury inflammation.
186 d by HMGB1 neutralization and attenuation of postinjury inflammation.
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
189                                          The postinjury inflammatory response in the CNS leads to neu
190                                       At 2 d postinjury, intrinsic bursting activity is lost within t
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
193                                    Four days postinjury, laser-injured mouse retinas injected with IG
194       In pediatric burn patients at 6 months postinjury, leg muscle protein net deposition is unrespo
195                    Administered starting 4 h postinjury, LM11A-31 promotes functional recovery withou
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.
199  adverse inflammatory responses that lead to postinjury MOF.
200                                   Thirty-day postinjury motor function determined by CatWalk (Noldus
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
203 e neuroscore and beam walk tests for 4 weeks postinjury (n = 11).
204 uring hospitalization and at 3 and 12 months postinjury (N=826).
205 tropium bromide 1 hr before injury (n=6) and postinjury nebulization protocols of 18 mug (n=6), 36 mu
206 treated groups, including both preinjury and postinjury nebulization protocols.
207                                              Postinjury neurogenesis occurs as a burst of proliferati
208 as injected into the T9 dorsal horns 2 weeks postinjury/nontransection.
209 her regional brain edema formation at 24 hrs postinjury nor the extent of cortical tissue loss assess
210  class of VEGFD-derived peptide mimetics and postinjury nose-to-brain delivery.
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
215       There is considerable heterogeneity in postinjury outcome, which is only partially explained by
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
220 useful for follow-up evaluation of secondary postinjury pathologies.
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
223                               Over the acute postinjury period, patients with AI had lower trough mea
224           UCH-L1 performed best in the early postinjury period.
225                         We hypothesized that postinjury PF occurs early in severe shock, leading to p
226 e immune status of patients in the immediate postinjury phase and how this might influence patient ou
227 tissue loss increases throughout the chronic postinjury phase.
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
230 a), which modulates these two aspects of the postinjury physiological response.
231 ogen protein signals remodel the progressive postinjury (PI) niche.
232                                      One day postinjury, PP mixed cells were cultured in the presence
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
240 rophylactic measures, PE remains a threat to postinjury recovery.
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
243 n, which are a subset of cells necessary for postinjury regeneration of gut epithelium.
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
246 esponsible for sex-based outcome differences postinjury remain conflicting.
247 sed by the lesion or by processes related to postinjury reorganization.
248 opulation maintenance and crypt regeneration postinjury require mTOR.
249 in 81% and 85% of subjects at 3 and 6 months postinjury, respectively.
250 amined the effect of gender on the immediate postinjury response to major trauma.
251 se leads to activation of glia, which govern postinjury responses in the nervous system.
252 a therapeutic target for atherosclerosis and postinjury restenosis.
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
255            Ultrastructural analyses of axons postinjury revealed immediate breakage and buckling of m
256     Interestingly, after halting GCV at 14 d postinjury, scar elements and vessels entered the lesion
257 ed, however, this treatment failed to reduce postinjury seizure susceptibility.
258 ration which may be of particular use in the postinjury setting.
259 uggest the possibility of rapid, transmedian postinjury signals between homologous mirror-image neuro
260                                   At 1 month postinjury, smaller lesion area and midsagittal tissue b
261 ypothermia group showed significantly higher postinjury somatosensory-evoked potential amplitudes wit
262                                 In the acute postinjury stage, equine SF exhibits poor boundary lubri
263 ny interlimb constraints in promoting robust postinjury stepping behavior.
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
268                               Maintenance of postinjury T-lymphocyte immune paralysis or anergy could
269               Eleven rats were controls with postinjury temperature maintained at 37 +/- 0.5 degrees
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
272                                       Over a postinjury time course of 1 week, alphaCT1-treated IBZs
273 itor of sTNFalpha, at a clinically feasible, postinjury time point (i.e., 3 d after complete SCI) suf
274  regeneration is achievable at unprecedented postinjury time points.
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
277                        We transduced neurons postinjury to express a constitutively active Rheb to en
278       Patients were contacted 6 to 12 months postinjury to measure: presence of daily pain; screening
279                                              Postinjury treatments with tiotropium bromide were as ef
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
282 haAF1 is necessary and sufficient to inhibit postinjury VSMC proliferation.
283              Cumulative mortality at 3 years postinjury was 16% (95% confidence interval [CI], 15.8%-
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
287           Continued improvement to 36-months postinjury was only present for the usual activities ite
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
291                Immediate neurologic symptoms postinjury were used to identify mild TBI.
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
297 ontinuous infusion of ZK 234238 started 1 hr postinjury with a dose of 100 microg/kg/hr.
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
300 enous repair continues beyond the first week postinjury (wpi), however, is unknown.

 
Page Top