ライフサイエンスコーパス: cerebral white matter

1 cavitations in the periventricular and deep cerebral white matter.

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

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

4 y reveals abnormality (leukoaraiosis) in 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 nal brain shrinkage and deterioration of the cerebral white matter.

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

9 equired for astrocyte differentiation in the cerebral white matter.

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

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

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

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

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

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

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

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

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

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

20 1rho values were found to be elevated in the cerebral white matter and cerebellum in the bipolar grou

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

42 Cerebral white matter from a patient with TUBB4A Asn414L

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

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

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

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

47 Cerebral white matter hyperintensities were measured for

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

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

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

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

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

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

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

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

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

57 The development of cerebral white matter involves multiple biological proce

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

74 A cerebral white matter reference region may improve the p

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

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

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

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

79 The cerebral white matter shows patchy gliosis and rarefacti

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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