ライフサイエンスコーパス: controlled cortical impact

1 oblotting within mouse parietal cortex after controlled cortical impact.

2 ely-moving rats at 14 days following lateral controlled cortical impact.

3 eatment following mechanical brain lesion by controlled cortical impact.

4 on is associated with reduced sequelae after controlled cortical impact.

5 Mechanical brain lesion by controlled cortical impact.

6 Mechanical brain lesion by controlled cortical impact.

7 treatment with candesartan for 5 days after controlled cortical impact.

8 ) and traumatic brain injury (TBI) caused by controlled cortical impact.

9 ced in adult EPOR-null and wild-type mice by controlled cortical impact.

10 ered to tail pinch, and TBI was delivered by controlled cortical impact.

11 ve, sham-operated, TBI) underwent a moderate controlled cortical impact.

12 perimental traumatic brain injury induced by controlled cortical impact and (2) to evaluate whether m

13 /6J mice (weight, 21-26 g) were injured with controlled cortical impact and divided into 2 groups (n=

14 Adult male Wistar rats were injured with controlled cortical impact and treated either with salin

15 erimental TBI in C57BL/6 mice was induced by controlled cortical impact, and (64)Cu uptake in the inj

16 Using controlled cortical impact as a model of traumatic brain

17 At the time of controlled cortical impact, body weight, brain and body

18 function and histopathologic sequelae after controlled cortical impact brain injury were evaluated i

19 In the controlled cortical impact (CCI) animal model of pediatr

20 havioral and histopathological outcome after controlled cortical impact (CCI) brain injury in mice de

21 chromosome (YAC), we examined the effects of controlled cortical impact (CCI) brain injury on neuromo

22 ution within the hippocampus also occur post controlled cortical impact (CCI) demonstrating a reducti

23 Severe TBI was produced using controlled cortical impact (CCI) in a rat model, and TNS

24 changes during the first several days after controlled cortical impact (CCI) in mice.

25 (n=35) Sprague-Dawley rats underwent either controlled cortical impact (CCI) injury (2.7 mm; 4 m/s)

26 d that hippocampal synaptic damage caused by controlled cortical impact (CCI) injury in mice results

27 -Dawley rats were subjected to TBI using the controlled cortical impact (CCI) injury model.

28 his hypothesis, we used Nlrx1(-/-) mice in a controlled cortical impact (CCI) injury murine model of

29 We therefore performed controlled cortical impact (CCI) injury on mice to inves

30 However, the effect of controlled cortical impact (CCI) injury on TH in the nig

31 on was investigated by microarray 24 h after controlled cortical impact (CCI) injury or sham injury i

32 ere anesthetized and surgically prepared for controlled cortical impact (CCI) injury or sham surgery.

33 Histopathological changes at 7 days after controlled cortical impact (CCI) injury were examined.

34 We subjected adult mice to controlled cortical impact (CCI) injury, and isolated RN

35 unctional and histological outcome following controlled cortical impact (CCI) injury.

36 ronal injury in a rodent model of unilateral controlled cortical impact (CCI) injury.

37 The controlled cortical impact (CCI) model is one of the mos

38 In this study, using a controlled cortical impact (CCI) model of head injury, w

39 ive and migratory response of the brain to a controlled cortical impact (CCI) model of traumatic brai

40 ges of both the closed head injury (CHI) and controlled cortical impact (CCI) models, we developed a

41 imvastatin will render maximum recovery in a controlled cortical impact (CCI) mouse model of TBI.

42 trocytes after contusion injury generated by controlled cortical impact (CCI) of different severities

43 ANC, GCSF to increase ANC, or saline before controlled cortical impact (CCI) of moderate overall sev

44 trophic factor (AdGDNF), one week prior to a controlled cortical impact (CCI) over the forelimb senso

45 Using a controlled cortical impact (CCI) procedure in rats, we s

46 e autoradiography was performed 45 min after controlled cortical impact (CCI) to left parietal cortex

47 in rat brains up to 2 months after digitally controlled cortical impact (CCI) to produce traumatic br

48 In a model of controlled cortical impact (CCI) with secondary hypoxemi

49 Following controlled cortical impact (CCI), bolus administrations

50 g/kg at 5 min, 6 h and 24 h; i.p.) following controlled cortical impact (CCI)-induced traumatic brain

51 4-month-old PDAPP and wild type (WT) mice by controlled cortical impact (CCI).

52 (n = 9) and were sacrificed at 6 weeks after controlled cortical impact (CCI).

53 in injury (TBI) induced in adult rats with a controlled cortical impact device.

54 Brain trauma by use of a controlled cortical impact device.

55 C57BL6 mice received controlled cortical impact followed by hemorrhagic hypot

56 After controlled cortical impact in mice, MMP-9 was increased

57 mins, 3 hrs, 6 hrs, 12 hrs, and 24 hrs after controlled cortical impact in mice.

58 We generated controlled cortical impacts in adult rats.

59 Controlled cortical impact-induced cognitive impairment

60 AT1R knockout mice were less vulnerable to controlled cortical impact-induced injury suggesting tha

61 Both candesartan and telmisartan ameliorated controlled cortical impact-induced injury with a therape

62 f propofol (36 or 72 mg/kg/hr) either during controlled cortical impact induction or in a delayed app

63 Traumatic brain injury was produced by controlled cortical impact injury (4 m/sec, 2.6 mm of ti

64 Brain from rats (n=24) subjected to controlled cortical impact injury and sham operated (n=3

65 Controlled cortical impact injury caused immediate hyper

66 sensory-motor cortex was implemented by the controlled cortical impact injury device.

67 We used a controlled cortical impact injury model to determine the

68 ains following traumatic brain injury (TBI), controlled cortical impact injury of mild to moderate se

69 We demonstrate that controlled cortical impact injury of rats causes a long-

70 her characterize this response, we performed controlled cortical impact injury on male mice and deter

71 a TBI mouse model that received 1.8 mm deep controlled cortical impact injury or craniectomy only (c

72 Specifically, animal cohorts sustaining a controlled cortical impact injury received an intravenou

73 m mild, moderate, and severe TBI produced by controlled cortical impact injury technique.

74 als were sedated with sevoflurane during the controlled cortical impact injury, and propofol was give

75 Following TBI induced by controlled cortical impact injury, scaffold with hMSCs (

76 Using a validated mouse model of controlled cortical impact injury, we determined effecti

77 iced at 2 h, 6 h, 24 h, 72 h and 168 h after controlled cortical impact injury.

78 IV propofol bolus application delayed after controlled cortical impact injury.

79 8 wk old C57BL/6J mice 30 min after moderate controlled cortical impact injury.

80 ale Wistar rats were subjected to unilateral controlled cortical impact injury.

81 ulated in neurons throughout the brain after controlled cortical impact injury.

82 liosides in normal brain and the effect of a controlled cortical impact model (CCI) of traumatic brai

83 en Cav-1 (SynCav1 Tg)] and subjected it to a controlled cortical impact model of brain trauma and mea

84 man adipose-derived stem cells (hADSCs) in a controlled cortical impact model of mild TBI using young

85 temic administration of TAT-CBD3 following a controlled cortical impact model of TBI decreased hippoc

86 al edema by increasing the AQP4 level in the controlled cortical impact model of TBI in mice.

87 served BBB integrity/permeability in a mouse controlled cortical impact model of TBI when studied usi

88 In the present study, we used a controlled cortical impact model of TBI with pertinent l

89 but normal cytoprotective activity, using a controlled cortical impact model of TBI.

90 eceived sham, mild or moderate injury in the controlled cortical impact model of TBI.

91 wild-type control mice were subjected to the controlled cortical impact model of TBI.

92 Using a controlled cortical impact model of traumatic brain inju

93 Here, using a controlled cortical impact model of traumatic brain inju

94 er analysis, and applied the method to a rat controlled cortical impact model to identify the specifi

95 ation of posttraumatic epilepsy in the mouse controlled cortical impact model was first performed usi

96 Using a murine controlled cortical impact model, we used adoptive trans

97 Wistar rats were subjected to TBI using the controlled cortical impact model.

98 day, 1 week, and 4 weeks after TBI using the controlled cortical impact model.

99 o facilitate behavioral recovery following a controlled cortical impact of rats.

100 rformed on rats with moderate TBI induced by controlled cortical impact on one cerebral hemisphere.

101 e head injury by lateral fluid percussion, a controlled cortical impact or impact acceleration.

102 ubcutaneously twice per day for 7 days after controlled cortical impact or sham injury (n = 16).

103 nce, and lesion volume were determined after controlled cortical impact or sham injury.

104 Male mice received a controlled cortical impact or sham surgery at postnatal

105 Wistar rats were subjected to controlled cortical impact or sham surgery.

106 TBI was induced by controlled cortical impact over the left parietal cortex

107 TBI was induced by controlled cortical impact over the left parietal cortex

108 improved Morris water maze performance after controlled cortical impact (p < .05, repeated-measures a

109 bjected to sham or traumatic brain injury by controlled cortical impact received human amniotic mesen

110 In brain tissue subjacent to 1.0 mm depth controlled cortical impact, surviving hippocampal neuron

111 When subjected to a controlled cortical impact, SynCav1 Tg mice demonstrated

112 Here, we report that controlled cortical impact TBI in 3xTg-AD mice resulted

113 FGF-2(-/-) and FGF-2(+/+) mice subjected to controlled cortical impact, the number of dividing cells

114 , 12, 24, 48, and 96 hours; and 1 week after controlled cortical impact using anti-mouse mannose-bind

115 Controlled cortical impact was performed to the left par

116 Controlled cortical impact was used to induce traumatic

117 type 1A decreased by 42% within 24 hrs after controlled cortical impact, whereas angiotensin II recep