ライフサイエンスコーパス: white matter injury

1 amate receptor blockade for hypoxic-ischemic white matter injury.

2 ages are possibly involved in the process of white matter injury.

3 utic strategy exists against the IVH-induced white matter injury.

4 egion could play a role in radiation-induced white matter injury.

5 therapeutic outcomes in models of perinatal white matter injury.

6 provement in myelination, suggesting reduced white matter injury.

7 There is also evidence of more global white matter injury.

8 to the treatment of premature children with white matter injury.

9 (DEHSI), the predominant patterns of preterm white matter injury.

10 ived MMP9 induced early BBB disruption after white matter injury.

11 e importance of axon pathology in developing white matter injury.

12 at trend levels, confirming heterogeneity in white matter injury.

13 RI that allow more detailed investigation of white matter injury.

14 rovides a more flexible way of investigating white matter injury.

15 alacia (PVL), a distinctive form of cerebral white matter injury.

16 y has been implicated in the pathogenesis of white matter injury.

17 agonist caffeine can prevent hypoxia-induced white matter injury.

18 to the particular pathogenesis of perinatal white matter injury, (2) provide evidence that at least

19 human erythropoietin had abnormal scores for white matter injury (22% [17/77] vs 36% [32/88]; adjuste

20 [Ca(2+)]i) homeostasis might be one cause of white matter injury after HIV infection.

21 ack of Wnt repressor tone promoted permanent white matter injury after mild hypoxic insult.

22 d in patients with PCS, suggestive of axonal white matter injury and amyloid deposition.

23 results indicate that the evolution of grey/white matter injury and blood-brain barrier disruption a

24 rotective against selective hypoxic-ischemic white matter injury and decreases the subsequent neuromo

25 s important implications for treatment after white matter injury and disease.

26 The resulting white matter injury and gray matter injury scores were c

27 role of AMPA-kainate receptor in IVH-induced white matter injury and identifies a novel strategy of n

28 t cerebral ischemia, probably by alleviating white matter injury and modulating microglial/macrophage

29 udy reveals that OPCs can rapidly respond to white matter injury and produce MMP9 that disrupts the B

30 The goals of this study were to evaluate white matter injury and recovery thereof, simultaneously

31 uctive brain lesions that resulted in cystic white matter injury and secondary cortical and subcortic

32 HIP rats have brain microhemorrhages, white matter injury, and neurologic deficits.

33 tibody, significantly attenuated LPS-induced white matter injury, as indicated by decreases in ventri

34 hese findings demonstrate that the degree of white matter injury associated with cerebral microvascul

35 This suggests that diffuse white matter injury begins in utero for a significant pr

36 ants are susceptible to inflammation-induced white matter injury but the exposures that lead to this

37 l cells can cause oligodendrocyte damage and white matter injury by release of inflammatory cytokines

38 a-induced DWMI.SIGNIFICANCE STATEMENTDiffuse white matter injury (DWMI) caused by hypoxia is a leadin

39 Diffuse white matter injury (DWMI) caused by hypoxia is associat

40 ments exist for preterm infants with diffuse white matter injury (DWMI) caused by hypoxia.

41 Diffuse white matter injury (DWMI) is a common finding in these

42 eonatal hypoxia (HX) that reproduces diffuse white matter injury (DWMI) of premature infants.

43 Diffuse white matter injury (DWMI), a leading cause of neurodeve

44 Early treatment of spinal cord white matter injury has been found beneficial.

45 Myelin damage and white matter injury have been frequently reported in HIV

46 Following white matter injury, however, there was no detectable im

47 to be a key mechanism in the pathogenesis of white matter injury; however, there has been no in vivo

48 White matter injuries in the 7-day-old BCAO rat brain we

49 MRI abnormalities consistent with cerebellar white matter injury in 3 of 4 subjects.

50 al NMDA glutamate receptors (NMDARs) mediate white matter injury in a variety of CNS diseases, includ

51 ed death, a mechanism that may contribute to white matter injury in CNS disease.

52 eterioration may contribute to both gray and white matter injury in CNS trauma.

53 n combined with hypothermia attenuates brain white matter injury in comatose survivors of out-of-hosp

54 Glutamate excitotoxicity plays a role in white matter injury in many neurological diseases.

55 rhage (IVH) results in neural cell death and white matter injury in premature infants.

56 iomarker for determining the pathogenesis of white matter injury in preterm infants during a period w

57 ar hemorrhage (IVH) remains a major cause of white matter injury in preterm infants with no viable th

58 uration arrest may predispose to more severe white matter injury in preterm survivors that sustain re

59 VBM is sensitive to detection of widespread white matter injury in SCD patients in borderzones betwe

60 hological sequela of chronic periventricular white matter injury in survivors of premature birth.

61 r activation contributes to hypoxic-ischemic white matter injury in the adult brain.

62 diated OL excitotoxicity in hypoxic/ischemic white matter injury in the developing brain.

63 of ROS and caspase activation, and leads to white matter injury in the neonatal rat brain.

64 the development of an effective treatment to white matter injuries including spinal cord trauma given

65 variety of neurological disorders involving white matter injury, including multiple sclerosis, acute

66 ry, we found that the mechanism of perinatal white matter injury involved maturation-dependent vulner

67 Axonal white matter injury is believed to be a major determinan

68 Subcortical white matter injury is often accompanied by orofacial mo

69 nic hypoxia-ischemia-induced periventricular white matter injury is related to persistent depletion o

70 Hypoxic/ischemic white matter injury is thought to mediate periventricula

71 iventricular leukomalacia (pre- or perinatal white matter injury leading to cerebral palsy), spinal c

72 s applied to capture spatially heterogeneous white matter injuries (lesions) in addition to standard

73 Neonatal white matter injury (NWMI) is a lesion found in preterm

74 These observations may be relevant to white matter injury observed in premature infants.

75 White matter injury on cranial ultrasound was associated

76 Chorioamnionitis, necrotizing enterocolitis, white matter injury on cranial ultrasound, and increasin

77 = 0.515) and quantitatively defined diffuse white matter injury (p = 0.183).

78 enteral nutrition, pulmonary hemorrhage, and white matter injury (p<0.01 for each; relative differenc

79 ative arterial Pco2 as a risk factor for new white matter injury (P=0.04).

80 Unique white matter injury patterns were seen for two major pos

81 tter astrocytes in a rodent model of diffuse white matter injury produced by exposing neonatal mice t

82 Periventricular white matter injury (PVWMI) in premature babies is a maj

83 Periventricular white matter injury (PWMI) is the leading cause of cereb

84 Although periventricular white matter injury (PWMI) is the leading cause of chron

85 Periventricular white matter injury (PWMI) is the leading cause of neuro

86 Periventricular white matter injury (PWMI) is the major cause of cerebra

87 fants frequently arises from periventricular white matter injury (PWMI), a condition associated with

88 in the preterm population is periventricular white matter injury (PWMI), a pathology associated with

89 lacia is a form of hypoxic-ischemic cerebral white matter injury seen most commonly in premature infa

90 anial ultrasound abnormalities suggestive of white matter injury significantly increased risk for som

91 mental window of selective vulnerability for white matter injury, such as periventricular leukomalaci

92 ntal disabilities, most often resulting from white matter injury sustained during the neonatal period

93 hemia (H/I) in the premature infant leads to white matter injury termed periventricular leukomalacia

94 l and neonatal brain injury, and can lead to white matter injury that is a precursor for a number of

95 yte lineage progression is implicated in the white-matter injury that occurs in cerebral palsy.

96 Periventricular white matter injury, that is, periventricular leukomalac

97 The contribution of tract-specific white matter injury to dysfunction in different cognitiv

98 The cellular basis for the propensity of white matter injury to occur in the developing brain and

99 e a mouse model of ischemia-induced neonatal white matter injury to study the biodistribution of gene

100 e resistance of SPNs to insults that trigger white matter injury, transient hypoxemia disrupted SPN a

101 at OPCs in lesions of hypoxic human neonatal white matter injury upregulated markers of high Wnt acti

102 White matter injury was also ameliorated in s-NSC-treate

103 nsient oxygen and glucose deprivation (OGD), white matter injury was assessed by electrophysiology an

104 On diffusion tensor imaging, white matter injury was prominent in the corpus callosum

105 White matter injury was the most common type of injury i

106 White-matter injury was observed in 13 newborns with con

107 Using an H/I rat model of white matter injury, we show in vivo that post-H/I treat

108 method of diagnosing clinically significant white matter injury when conventional imaging is normal.

109 e applied to capture spatially heterogeneous white matter injuries, which minimize implicit assumptio

110 for 1 hr) resulted in selective, subcortical white matter injury with a marked ipsilateral decrease i

111 nd/or ventricular enlargement (suggestive of white matter injury) with or without germinal matrix-int

112 chniques resulted in a high incidence of new white matter injury, with central infarctions occurring

113 se with normal findings (n = 23), those with white matter injury (WMI) (n = 9), those with grade I ge

114 r form of magnetic resonance imaging-defined white matter injury (WMI) comprises diffuse lesions wher

115 White matter injury (WMI) was the commonest type of inju

116 OL differentiation during development, after white matter injury (WMI), and is expressed in human whi

117 h preterm birth include focal and/or diffuse white matter injury (WMI).

118 optimal imaging modality to define cerebral white-matter injury (WMI) in preterm survivors, the hist