ライフサイエンスコーパス: cerebral white matter

1 atter were related to the lesion fraction in cerebral white matter.

2 thways leading to hypoxic-ischemic damage of cerebral white matter.

3 ws rarefaction and cystic destruction of the cerebral white matter.

4 llenges due to hypoxia-induced injury of the cerebral white matter.

5 rders leading to progressive degeneration of cerebral white matter.

6 sensory cortices of the hand and the entire cerebral white matter.

7 cavitations in the periventricular and deep cerebral white matter.

8 y accompanied by widespread abnormalities in cerebral white matter.

9 ultilayered ring-like lesions usually in the cerebral white matter.

10 observed tiny lesions arising de novo in the cerebral white matter.

11 y reveals abnormality (leukoaraiosis) in the cerebral white matter.

12 nal brain shrinkage and deterioration of the cerebral white matter.

13 ukomalacia (PVL), a disorder of the immature cerebral white matter.

14 equired for astrocyte differentiation in the cerebral white matter.

15 e understanding of the fibre pathways in the cerebral white matter.

16 -MRS) studies and it has not been studied in cerebral white matter.

17 leukomalacia (PVL), a lesion of the immature cerebral white matter.

18 ther such an association was also present in cerebral white matter.

19 ism of hypoxic-ischemic injury to developing cerebral white matter.

20 , 95% confidence interval [CI]: 1.80, 7.28), cerebral white matter (1.83, 95% CI: 0.56, 3.10), cerebr

21 determine whether nature and progression of cerebral white matter abnormalities in VWM differ accord

22 a useful tool for detecting and quantifying cerebral white matter abnormalities.

23 phy, can not only stabilize but even improve cerebral white matter abnormalities.

24 tly smaller volumes of cortical gray matter, cerebral white matter, amygdala, caudate, hippocampus, t

25 ed inclusion-bearing astrocytes prominent in cerebral white matter and (iii) the presence of intranuc

26 spin-density- and T2-weighted images and, in cerebral white matter and brain stem, a hypointense regi

27 1rho values were found to be elevated in the cerebral white matter and cerebellum in the bipolar grou

28 disorder and draw attention to roles of the cerebral white matter and cerebellum.

29 Loss of cerebral white matter and failure to develop white matte

30 repair mechanisms, including regeneration of cerebral white matter and improvement in neurocognitive

31 P positivity and were usually located in the cerebral white matter and internal capsule, and infreque

32 th higher ALFF and ReHo in PHIV in bilateral cerebral white matter and right cerebral white matter re

33 ective lipid peroxidation-mediated injury of cerebral white matter and targeted death of oligodendroc

34 e the border of demyelinated lesions in both cerebral white matter and the cortex in the brains of mu

35 linating lesion load in three volumes of the cerebral white matter and the loss of axons in NAWM of t

36 lative HDAC expression increases with age in cerebral white matter, and correlates with age-associate

37 Myelination disturbances in cerebral white matter are related to aberrant regenerati

38 es (OLs), the predominant cell type found in cerebral white matter, are essential for structural inte

39 of cortical and subcortical gray matter and cerebral white matter, brain lesion volume, spinal cord

40 nt between groups overall; and diencephalon, cerebral white matter, cerebellum and globus pallidus-pu

41 We sought to illustrate improvement of cerebral white matter changes in metachromatic leukodyst

42 The primary end point was cerebral white matter damage as evaluated by fractional

43 es that inflammation contributes to neonatal cerebral white matter damage have evolved over the last

44 ecially monocytes/macrophages, contribute to cerebral white matter damage in extremely low gestationa

45 siologic relationships among ischemia, acute cerebral white matter damage, and vulnerable target popu

46 hology of two affected family members showed cerebral white matter degeneration with axonal swellings

47 leukoencephalopathy (PML) is a usually fatal cerebral white matter disease found in patients with hum

48 The progressive loss of cerebral white matter during aging contributes to cognit

49 localize the glutamate transporters in human cerebral white matter during the age range of PVL.

50 ntly that late OL progenitors populate human cerebral white matter during the high risk period for PV

51 s (pre-OLs; O4(+)O1(-)) predominate in human cerebral white matter during the peak time frame for PVL

52 Until now, the ultrastructural analysis of cerebral white matter fiber tracts associated with front

53 Cerebral white matter from a patient with TUBB4A Asn414L

54 tudy, we analyzed the expression of EAAT2 in cerebral white matter from PVL and control cases.

55 erebrum was subdivided into cerebral cortex, cerebral white matter, hippocampus-amygdala, caudate nuc

56 of GWAS, in a joint analysis with a study of cerebral white matter hyperintensities (an aetiologicall

57 associated in the multi-trait analysis with cerebral white matter hyperintensities (n=42 310).

58 rphism (rs12445022) was also associated with cerebral white matter hyperintensities (OR [95% CI] = 1.

59 The burden of cerebral white matter hyperintensities (WMH) is associat

60 he most important parameters associated with cerebral white matter hyperintensities (WMH), in conside

61 Cerebral white matter hyperintensities are an important

62 Cerebral white matter hyperintensities on MRI are marker

63 Cerebral white matter hyperintensities were measured for

64 lationship between aortic distensibility and cerebral white matter hyperintensities, mechanistically

65 al disability, similar facies, myopathy, and cerebral white matter hyperintensities, with cardiac sys

66 Imaging studies reveal cerebral white matter hyperintensities, with delayed pos

67 leucocyte gene expression to progression of cerebral white matter hyperintensities.

68 whether these associations were modified by cerebral white matter hyperintensity (WMH) burden.

69 y revealed ZIKV in the brain and significant cerebral white matter hypoplasia, periventricular white

70 on of the processes that result in damage to cerebral white matter in the fetus and newborn.

71 were correlated with higher ALFF at the left cerebral white matter in the left medial orbital gyrus a

72 We found higher ALFF and ReHo in cerebral white matter in the medial orbital lobe for PHI

73 l orbital gyrus and higher ReHo at the right cerebral white matter in the PHIV patients.

74 cond, is there regional variation within the cerebral white matter in the rate of white matter hyperi

75 h in cultured OLs in vitro and in developing cerebral white matter in vivo, up-regulates GluR2, inhib

76 sities index structural abnormalities in the cerebral white matter, including axonal damage.

77 r leukomalacia is a form of hypoxic-ischemic cerebral white matter injury seen most commonly in prema

78 ar leukomalacia (PVL), a distinctive form of cerebral white matter injury.

79 I) is the optimal imaging modality to define cerebral white-matter injury (WMI) in preterm survivors,

80 e matter parcellation technique that divides cerebral white matter into an outer zone containing the

81 The development of cerebral white matter involves multiple biological proce

82 ypoxia-ischemia and/or infection in immature cerebral white matter is important in the pathogenesis o

83 including diffuse polymicrogyria, decreased cerebral white matter, large ventricles, and open opercu

84 Q and the total brain, cerebral gray matter, cerebral white matter, lateral ventricular, third ventri

85 ients with HL(95) had a higher microvascular cerebral white matter lesion load [1.4, interquartile ra

86 cantly associated with a smaller increase in cerebral white matter lesion volume and a greater decrea

87 We hypothesized that cerebral white matter lesions (WMLs)-an imaging surrogat

88 Cerebral white matter lesions prevent cortico-spinal des

89 brain injury in premature infants results in cerebral white matter lesions with prominent oligodendro

90 In addition, cerebral white matter lesions, peripheral neuropathy, an

91 evoked currents in developing OLs in situ in cerebral white matter of immature rats.

92 ecovery.SIGNIFICANCE STATEMENT Stroke in the cerebral white matter of the brain is common.

93 reased density of activated microglia in the cerebral white matter of the fetus (<37 PC weeks) relati

94 abundance of CD68-activated microglia in the cerebral white matter of the fetus suggests a potential

95 ify microglial morphology, revealed that the cerebral white matter of the human fetus and infant is d

96 ed microglial density occurs normally in the cerebral white matter of the human fetus during the peak

97 cellular glutamate in ischemic injury to the cerebral white matter of the preterm infant.

98 tients showed foci of T2 prolongation in the cerebral white matter, one had an enhancing lesion with

99 in associations by majority/minority status (cerebral white matter: p for interaction = 0.04).

100 Cerebral white matter pathology is a common CNS manifest

101 poxic-ischemic injury to the periventricular cerebral white matter [periventricular leukomalacia (PVL

102 ature infant, hypoxic-ischemic damage to the cerebral white matter [periventricular leukomalacia (PVL

103 , and higher relative HDAC expression in the cerebral white matter, pons, and cerebellum compared wit

104 A cerebral white matter reference region may improve the p

105 r of template-based cerebellar, pontine, and cerebral white matter reference regions to track 24-mo f

106 bserved in widespread areas of the patients' cerebral white matter relative to these controls.

107 in bilateral cerebral white matter and right cerebral white matter respectively after masking the out

108 y, and a severe inflammatory reaction in the cerebral white matter, resulting in demyelination.

109 ons, although not all in the same direction: cerebral white matter showed a trend towards being dispr

110 Bilateral cerebral white matter showed increased spontaneous regio

111 yte meningoencephalitis was present; and (v) cerebral white matter showed infiltration by macrophages

112 The cerebral white matter shows patchy gliosis and rarefacti

113 r 5 years with yearly follow-ups, the global cerebral white matter status as well as region-specific

114 ssociated these deficits with alterations in cerebral white matter structure and axonal pathology.

115 de a structural basis for the alterations in cerebral white matter structure widely reported in HD pa

116 ic injury to OPCs in disorders of developing cerebral white matter, such as PVL.

117 ed by neuronal/axonal disease, affecting the cerebral white matter, thalamus, basal ganglia, cerebral

118 (aNPCs) were injected bilaterally into major cerebral white matter tracts of myelin-deficient shivere

119 l anisotropy measurements were made on major cerebral white matter tracts, and DTI tractography was p

120 'tractography', reveals the trajectories of cerebral white matter tracts.

121 axons to structural development of selected cerebral white-matter tracts as determined by diffusion

122 Cerebral white matter undergoes a rapid and complex matu

123 lume (b = -7.8 [95% CI, -13.4 to -2.3] cm3), cerebral white matter volume (b = -5.9 [95% CI, -10.7 to

124 loss of (1) pre-oligodendrocytes at P4, (2) cerebral white matter volume and myelin at P14, (3) cere

125 A positive correlation between cerebral white matter volume and performance IQ was obse

126 le lesions did not differ significantly, but cerebral white matter volume decreased (MR2:MR1 ratio, 0

127 The smaller cerebral white matter volume mediated the association be

128 l microcephaly, hypomyelination, and reduced cerebral white-matter volume.

129 that transmit the risk for Sz also influence cerebral (white matter) volume.

130 tter volumes was present only in girls, with cerebral white matter volumes mediating the association

131 exposed to childhood poverty showed smaller cerebral white matter volumes than their control (B = -

132 er monoisobutyl phthalate (mIBP) and smaller cerebral white matter volumes was present only in girls,

133 and increased mean diffusivity in almost all cerebral white-matter voxels.

134 was measured to estimate brain atrophy; (b) cerebral white matter was visually scored as percentage

135 tural abnormalities in particular regions of cerebral white matter which are consistent between indiv

136 Although SPNs reside in close proximity to cerebral white matter, which is particularly vulnerable

137 ensor imaging (DTI) have revealed regions of cerebral white matter with decreased microstructural org

138 grey matter (GM), brainstem, cerebellum and cerebral white matter (WM) and diffusion measures (fract

139 neonatal MRI, the T2 hyperintensity (T2h) in cerebral white matter (WM) at term-equivalent age due to

140 Cerebral white matter (WM) damage has been reported in c

141 linated lesions, thalamic neuronal loss, and cerebral white matter (WM) lesions to thalamic volume.