ライフサイエンスコーパス: nervous system injury

1 growth during development, and after central nervous system injury.

2 s the recovery of adult mammals from central nervous system injury.

3 failed to be activated in a model of central nervous system injury.

4 Angiogenesis is a key feature of central nervous system injury.

5 sidered detrimental to recovery from central nervous system injury.

6 ndent ionic homoeostasis in areas of central nervous system injury.

7 ribe a previously unrecognized mechanism for nervous system injury.

8 peutic strategies for recovery after central nervous system injury.

9 e device delivery, and prevention of central nervous system injury.

10 ) to limit axonal regeneration after central nervous system injury.

11 ggable targets for treating victims of acute nervous system injury.

12 tion may limit functional outcomes following nervous system injury.

13 functional recovery following many types of nervous system injury.

14 of neurodegeneration after the acute central nervous system injury.

15 ssue reorganization and repair after central nervous system injury.

16 tension and neuronal migration after central nervous system injury.

17 een posited to affect outcomes after central nervous system injury.

18 microglial activation in response to central nervous system injury.

19 an important role in the response to central nervous system injury.

20 ated in the pathophysiology of acute central nervous system injury.

21 promote further recovery after adult central nervous system injury.

22 ion during development and following central nervous system injury.

23 r axonal damage and other aspects of central nervous system injury.

24 s with neurodegenerative diseases or central nervous system injury.

25 into mechanisms of and recovery from central nervous system injury.

26 larger issue of network remodeling following nervous system injury.

27 eurologic outcomes in children after central nervous system injury.

28 ducing stressors as might occur with central nervous system injury.

29 ory features characteristic of other central nervous system injuries.

30 egulated along pain-signaling pathways after nervous system injuries.

31 pment of NgR1-based therapeutics for central nervous system injuries.

32 nt of neuropathic pain after SCI and related nervous system injuries.

33 immune response may be of benefit in central nervous system injury, although T cells may have either

34 elopment and have important implications for nervous system injuries and diseases because disruption

35 very after brachial plexus avulsion or other nervous system injuries and diseases.

36 an attractive strategy for the treatment of nervous system injuries and neurodegenerative and demyel

37 ead to development of therapeutics to combat nervous system injuries and neurodegenerative diseases.

38 overy may inspire new treatments for central nervous system injuries and neurodegenerative diseases.

39 In central nervous system injury and disease, apolipoprotein E (APO

40 inhibitors that limit recovery from central nervous system injury and disease.

41 immune equilibrium by stroke in both central nervous system injury and repair responses.

42 ping our understanding of basic mechanism of nervous system injury and repair.

43 vated during embryogenesis or in response to nervous-system injury and disease.

44 neuronal excitability, axon outgrowth after nervous system injury, and protein folding in neurodegen

45 ), myocardial necrosis, the level of central nervous system injury, and the secondary multiple system

46 measurement of S100B as a marker of central nervous system injury; and 4) follow-up head computed to

47 ls (RGCs), used as a common model of central nervous system injury, are particularly vulnerable to me

48 0% of all fatalities, second only to central nervous system injury as a cause of death.

49 w cells to replace those lost due to central nervous system injury, as well as a source of trophic mo

50 The specific mechanisms by which nervous system injury becomes a chronic pain state remai

51 ricle have multiple risk factors for central nervous system injury, both before and after the Fontan

52 te neurodegenerative dysfunction and central nervous system injuries, but reprogrammed neurons are di

53 may be helpful in preventing serious central nervous system injury, but studies in children are lacki

54 iple traumas but without evidence of central nervous system injury constituted the control group.

55 y causes, immaturity, infection, and central nervous system injury decreased, while necrotizing enter

56 ly-onset IVH followed by significant central nervous system injury had low PPVT-R scores that decline

57 onset IVH and subsequent significant central nervous system injury had the lowest PPVT-R scores initi

58 ion and edema across the spectrum of central nervous system injury has driven extensive investigation

59 al stem cell (NSC) response to acute central nervous system injury; however, it is unclear whether th

60 ultrasound on memory impairment and central nervous system injury in a rat model of vascular dementi

61 te (FBP) has been shown to attenuate central nervous system injury in adult animals.

62 ration and functional recovery after central nervous system injury in adult mammals.

63 in the study of axonal growth after central nervous system injury in an attempt to provide guidance

64 s, (2) the mechanism and etiology of central nervous system injury in children with CHD, (3) perioper

65 as potential biomarkers for ischemic central nervous system injury in humans.

66 jective tool to assess the degree of central nervous system injury in individuals with PCS and to dis

67 s limited information on the pathogenesis of nervous system injury in these infections.

68 acellular nucleotides in response to central nervous system injury including trauma and ischemia have

69 ecovery when initiated shortly after central nervous system injury, including blockade of myelin-deri

70 detection and management of ischemic central nervous system injury, including for mild damage associa

71 neuroprotective effects in models of central nervous system injury, including in a contusive spinal c

72 add further strength to the model of central nervous system injury-induced efflux of L-glutamate thro

73 Patients with central nervous system injuries, injury requiring medical care i

74 ficial in the treatment of traumatic central nervous system injuries involving the excitotoxic action

75 Nervous system injury is a frequent result of cancer the

76 Manganese is known to cause central nervous system injury leading to parkinsonism and to con

77 have hypothesized that irreversible central nervous system injury may up-regulate proinflammatory me

78 covery of mammalian axonal projections after nervous system injury observed to date, highlighting an

79 extracorporeal membrane oxygenation, central nervous system injury (odds ratio, 26.5; 95% CI, 7.3-96.

80 Central nervous system injury often results in a pervasive inhib

81 Nervous system injury or disease leads to activation of

82 ay offer therapeutic opportunities following nervous system injury or disease where myelin inhibits n

83 he circulation, cardiac dysfunction, central nervous system injury, or sepsis.

84 d do not exhibit motor disturbances, central nervous system injury, or ultrastructural evidence of mi

85 complicated by infection (P=0.04) or central nervous system injury (P<0.001); however, there were inc

86 SC receptors that detect peripheral nervous system injury remain incompletely understood.

87 growth and functional recovery after central nervous system injury remains elusive.

88 the mechanism underlying its role in central nervous system injury remains unclear.

89 Functional regeneration after nervous system injury requires transected axons to recon

90 cond-order dorsal horn sensory neurons after nervous system injury, showing that SCI can trigger chan

91 ical researchers in disciplines from central nervous system injury/stroke, mental/addictive disorders

92 oke pain in patients with chronic pain after nervous system injury than in patients without somatosen

93 ly recognize and clear cellular debris after nervous system injury to maintain brain homeostasis, but

94 ce of cumulative end organ damage or central nervous system injury was observed.

95 rotective cytokine in models of ischemic and nervous system injury, where it reduces neuronal apoptos

96 d to T3D and a restricted pattern of central nervous system injury with damage limited to the hippoca