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1 jury time points in a preclinical TBI model (controlled cortical impact).
2 ered to tail pinch, and TBI was delivered by controlled cortical impact.
3 oblotting within mouse parietal cortex after controlled cortical impact.
4 ely-moving rats at 14 days following lateral controlled cortical impact.
5 Rats were subjected to TBI by pneumatic controlled cortical impact.
6 ve, sham-operated, TBI) underwent a moderate controlled cortical impact.
7 eatment following mechanical brain lesion by controlled cortical impact.
8 on is associated with reduced sequelae after controlled cortical impact.
9 Mechanical brain lesion by controlled cortical impact.
10 treatment with candesartan for 5 days after controlled cortical impact.
11 ) and traumatic brain injury (TBI) caused by controlled cortical impact.
12 ced in adult EPOR-null and wild-type mice by controlled cortical impact.
13 perimental traumatic brain injury induced by controlled cortical impact and (2) to evaluate whether m
14 /6J mice (weight, 21-26 g) were injured with controlled cortical impact and divided into 2 groups (n=
15 subjected to sham surgery or moderate-level controlled cortical impact and infected intranasally wit
16 experimental traumatic brain injury (TBI) by controlled cortical impact and investigated cortical spr
17 Adult male Wistar rats were injured with controlled cortical impact and treated either with salin
18 erimental TBI in C57BL/6 mice was induced by controlled cortical impact, and (64)Cu uptake in the inj
21 function and histopathologic sequelae after controlled cortical impact brain injury were evaluated i
24 havioral and histopathological outcome after controlled cortical impact (CCI) brain injury in mice de
25 chromosome (YAC), we examined the effects of controlled cortical impact (CCI) brain injury on neuromo
26 ution within the hippocampus also occur post controlled cortical impact (CCI) demonstrating a reducti
27 d 7 months after unilateral mild-to-moderate controlled cortical impact (CCI) in 5-7-month-old Tg/hta
31 ucted a temporal analysis of the response to controlled cortical impact (CCI) in rat microglia betwee
32 xpression of neuroinflammatory markers after controlled cortical impact (CCI) induced experimental TB
33 (n=35) Sprague-Dawley rats underwent either controlled cortical impact (CCI) injury (2.7 mm; 4 m/s)
34 P donor mice and subjected the recipients to controlled cortical impact (CCI) injury 14 days post-tra
35 d that hippocampal synaptic damage caused by controlled cortical impact (CCI) injury in mice results
37 his hypothesis, we used Nlrx1(-/-) mice in a controlled cortical impact (CCI) injury murine model of
40 on was investigated by microarray 24 h after controlled cortical impact (CCI) injury or sham injury i
41 ere anesthetized and surgically prepared for controlled cortical impact (CCI) injury or sham surgery.
51 ive and migratory response of the brain to a controlled cortical impact (CCI) model of traumatic brai
52 ed PAI-1 as a possible new target in a mouse controlled cortical impact (CCI) model of traumatic brai
55 ges of both the closed head injury (CHI) and controlled cortical impact (CCI) models, we developed a
57 imvastatin will render maximum recovery in a controlled cortical impact (CCI) mouse model of TBI.
58 trocytes after contusion injury generated by controlled cortical impact (CCI) of different severities
59 ANC, GCSF to increase ANC, or saline before controlled cortical impact (CCI) of moderate overall sev
61 trophic factor (AdGDNF), one week prior to a controlled cortical impact (CCI) over the forelimb senso
63 pecific EphA4 knockout and subjected them to controlled cortical impact (CCI) to investigate the role
64 e autoradiography was performed 45 min after controlled cortical impact (CCI) to left parietal cortex
65 in rat brains up to 2 months after digitally controlled cortical impact (CCI) to produce traumatic br
66 ons in an experimental rat model of moderate controlled cortical impact (CCI) while considering diffe
69 wing 2 different models of experimental TBI, controlled cortical impact (CCI), and closed head injury
72 g/kg at 5 min, 6 h and 24 h; i.p.) following controlled cortical impact (CCI)-induced traumatic brain
76 in serum miRNAs using two rat models of TBI (controlled cortical impact [CCI] and fluid percussion in
80 ical and behavioural outcomes, mice received controlled cortical impact followed by initiation of pio
82 oxic neuroinflammatory loop at 1-month after controlled cortical impact in mice by pharmacological re
87 AT1R knockout mice were less vulnerable to controlled cortical impact-induced injury suggesting tha
88 Both candesartan and telmisartan ameliorated controlled cortical impact-induced injury with a therape
89 f propofol (36 or 72 mg/kg/hr) either during controlled cortical impact induction or in a delayed app
95 ains following traumatic brain injury (TBI), controlled cortical impact injury of mild to moderate se
97 her characterize this response, we performed controlled cortical impact injury on male mice and deter
98 a TBI mouse model that received 1.8 mm deep controlled cortical impact injury or craniectomy only (c
100 Specifically, animal cohorts sustaining a controlled cortical impact injury received an intravenou
101 minutes after the induction of a unilateral controlled cortical impact injury resulted in their inco
102 ted with adeno-associated virus-Prok2 before controlled cortical impact injury show reduced neuronal
104 als were sedated with sevoflurane during the controlled cortical impact injury, and propofol was give
114 liosides in normal brain and the effect of a controlled cortical impact model (CCI) of traumatic brai
115 between the injured brain and lung, using a controlled cortical impact model followed by secondary S
116 N-beta in secondary injury after TBI using a controlled cortical impact model in adult male IFN-beta-
117 en Cav-1 (SynCav1 Tg)] and subjected it to a controlled cortical impact model of brain trauma and mea
118 74-days post-injury (DPI)) in mice using the controlled cortical impact model of experimental TBI.
119 man adipose-derived stem cells (hADSCs) in a controlled cortical impact model of mild TBI using young
120 temic administration of TAT-CBD3 following a controlled cortical impact model of TBI decreased hippoc
123 s a novel therapeutic target for TBI using a controlled cortical impact model of TBI on adult male mi
124 served BBB integrity/permeability in a mouse controlled cortical impact model of TBI when studied usi
132 er analysis, and applied the method to a rat controlled cortical impact model to identify the specifi
133 ation of posttraumatic epilepsy in the mouse controlled cortical impact model was first performed usi
134 is of rat microglia 24 h after TBI using the controlled cortical impact model, validated with a bioin
140 rformed on rats with moderate TBI induced by controlled cortical impact on one cerebral hemisphere.
141 Male C57Bl/6 mice were subjected to severe controlled cortical impact or a sham control surgery, at
143 astrointestinal dysfunction, mice received a controlled cortical impact or sham brain injury and inte
144 ubcutaneously twice per day for 7 days after controlled cortical impact or sham injury (n = 16).
150 improved Morris water maze performance after controlled cortical impact (p < .05, repeated-measures a
151 bjected to sham or traumatic brain injury by controlled cortical impact received human amniotic mesen
153 olamine oxidation and improved outcome after controlled cortical impact, suggesting that 15-lipoxygen
154 In brain tissue subjacent to 1.0 mm depth controlled cortical impact, surviving hippocampal neuron
157 FGF-2(-/-) and FGF-2(+/+) mice subjected to controlled cortical impact, the number of dividing cells
158 to adult male C57BL/6J mice at 1 month after controlled cortical impact to remove chronically activat
159 , 12, 24, 48, and 96 hours; and 1 week after controlled cortical impact using anti-mouse mannose-bind
163 type 1A decreased by 42% within 24 hrs after controlled cortical impact, whereas angiotensin II recep