ライフサイエンスコーパス: white matter lesion

1 nd force control in a patient with a chronic white matter lesion.

2 nstrated the presence of iron depositions in white matter lesions.

3 amma-herpesvirus was cultured from acute JME white matter lesions.

4 ivated macrophages/microglia at the edges of white matter lesions.

5 ascular risk factors, cerebral infarcts, and white matter lesions.

6 may not be directly related to demyelinating white matter lesions.

7 signs of tissue damage such as hemorrhage or white matter lesions.

8 e important for the establishment of chronic white matter lesions.

9 tients with unilateral and bilateral frontal white matter lesions.

10 ence of deep subcortical and periventricular white matter lesions.

11 and Ig deposition in central nervous system white matter lesions.

12 od (56 days) increased oligodendrogenesis in white matter lesions.

13 Magnetic resonance imaging quantified white matter lesions.

14 ral pathways can improve motor control after white matter lesions.

15 al similarity index), brain morphometry, and white matter lesions.

16 , heart disease, APOE e4 carrier status, and white matter lesions.

17 This potentiation persists after white matter lesions.

18 age function at the border of chronic active white matter lesions.

19 o the activity of macrophages in the rims of white matter lesions.

20 ells are a source of elevated HMGB1 in human white matter lesions.

21 esions, with additional axonal dispersion in white matter lesions.

22 t influences on early CBF deficits and later white matter lesions.

23 s with LMS and 26% of patients with LHON had white matter lesions.

24 osis Severity Score, cortical thickness, and white matter lesions.

25 tter injury (WMI), and is expressed in human white matter lesions.

26 thophysiological pathway in the formation of white matter lesions.

27 btained in passing during biopsy sampling of white-matter lesions.

28 hemorrhages (8.5% versus 0%) and more small white matter lesions (23% versus 8% had > 5 such lesions

29 ith subjective cognitive complaints or brain white-matter lesions 5 to 10 years after the hypertensiv

30 ocortical, 0.7 +/- 1.9; P = .04), surpassing white matter lesion accrual (cortical, 2.0 +/- 2.8 vs wh

31 width within the first 5 years, allowing for white matter lesion accrual and Expanded Disability Stat

32 th, sulci, and gyri; (b) their relation with white matter lesion accrual; and (c) the contribution of

33 Chronic white matter lesion activity measured by longitudinal T1

34 weighted intensity-based measures of chronic white matter lesion activity predict clinical progressio

35 We assessed whether white-matter lesions affect the perioperative risk of st

36 p1) was also reduced in OPCs in human infant white matter lesions after hypoxia.

37 ronectin in TgNotch3(R169C) mice ameliorated white matter lesions, although CBF responses were unchan

38 sm, are altered in association with punctate white matter lesions and "diffuse excessive high signal

39 ging at 7 T was used to segment cortical and white matter lesions and 3 T imaging for cortical thickn

40 nfirmed in monocytes from multiple sclerosis white matter lesions and blood.

41 pendently evaluated the studies for punctate white matter lesions and DEHSI.

42 ULA to obtain brain volumes and thicknesses, white matter lesions and diffusion metrics.

43 reased cleaved caspase 3 and IL-1beta within white matter lesions and exacerbated OxPC-induced injury

44 l anisotropy) were measured from whole brain white matter lesions and from both lesions and normal ap

45 R(2)' was measured in MS white matter lesions and in regions of interest in norma

46 is, T1w/T2w ratio was significantly lower in white matter lesions and normal-appearing white matter a

47 ed qualitative histopathological analysis of white matter lesions and normal-appearing white matter r

48 s at postnatal day 7 (P7) produced selective white matter lesions and OL death.

49 (18)F-PBR111 binding was higher in the white matter lesions and perilesional volumes of MS pati

50 f molecular mechanisms underpinning ischemic white matter lesions and provides the potential for nove

51 ic resonance imaging revealed nonprogressive white matter lesions and spinocerebellar atrophy similar

52 ging demonstrated cerebellar atrophy without white matter lesions and stereotactic biopsy showed sele

53 led significant associations between frontal white-matter lesions and reduced ipsilesional parietal c

54 activity (NEDA; occurrence of relapses, new white matter lesions, and Expanded Disability Status Sca

55 tion in brain normal-appearing white matter, white matter lesions, and grey matter.

56 h these data, MCAM(+) cells were detected in white matter lesions, and in gray matter of multiple scl

57 of systemic atherosclerotic vessel changes, white matter lesions, and myocardial changes.

58 ncluding cerebral blood flow (CBF) deficits, white matter lesions, and Notch3(ECD) deposition, were e

59 le sclerosis; (ii) they occur independent of white matter lesions; and (iii) they are associated with

60 Pathology in MS is not confined only to white matter lesions; apparently normal appearing tissue

61 eason, illness outcome, and deep subcortical white matter lesions appear to be closely linked.

62 alities in normal-appearing white matter and white matter lesions are greatest near the ventricles.

63 e sclerosis (MS), a subset of chronic active white matter lesions are identifiable on magnetic resona

64 m NAWM into WMH is a continuous process, yet white matter lesions are often examined dichotomously, w

65 White matter lesions are often located adjacent to the v

66 While early stages of these white matter lesions are only weakly associated with cog

67 icroglia/macrophages associated with chronic white matter lesions are thought to be responsible for s

68 Inflammatory white-matter lesions are less evident but diffuse axonal

69 The pattern of multiple white matter lesions arranged parallel to the lateral ve

70 Iron status of white matter lesions, as determined by staining, was com

71 of baseline infratentorial lesions and deep white matter lesions at 1 year.

72 quencing to profile the edge of demyelinated white matter lesions at various stages of inflammation.

73 correlates, as well as T2-FLAIR hyperintense white matter lesion burden and microstructural abnormali

74 Future studies linking white matter lesion burden in the UF with treatment prog

75 within groups in MRI metrics of cortical and white matter lesion burden; regression analysis explored

76 citotoxicity in the pathogenesis of punctate white matter lesions, but not necessarily in DEHSI, and

77 d be avoided in patients with more extensive white-matter lesions, but might be an acceptable alterna

78 the multiple sclerosis specimens containing white matter lesions by any of the methods employed, yet

79 ot CSF) levels of Abeta were associated with white matter lesions, cerebral microbleeds, hypertension

80 tensities in U-fibers and cortex adjacent to white-matter lesions characteristic of the disease can b

81 pvWMHs represent white matter lesions characterized by regions of myelin

82 ll population within multiple sclerosis (MS) white matter lesions compared to control brains.

83 N had a significantly greater risk of having white matter lesions consistent with MS compared with ma

84 all patients demonstrated a distribution of white matter lesions consistently in all subcortical bra

85 Neurite density index in white matter lesions correlated with disability in patie

86 In contrast to white matter lesions, cortical lesion accrual was greate

87 Compared to white matter lesions, cortical lesions contained 13 time

88 periependymal brainstem lesions, perivenous white matter lesions, Dawson's fingers, curved or S-shap

89 tered to patients with MRI-confirmed frontal white matter lesions due to sickle cell disease (SCD) va

90 in PET significantly improves predictions of white matter lesion enlargement in relapsing remitting p

91 hibits the same metabolic changes as chronic white matter lesions, even very early in the disease cou

92 Polarized glial-cell activation, white-matter lesion formation and hippocampal neuronal l

93 ant of the Expanded Disability Status Scale, white matter lesion fractions in the spinal cord and bra

94 In white matter lesions from MS brain tissue, we noted the

95 e, studies in mouse demyelination models and white matter lesions from patients with multiple scleros

96 The unique combination of white matter lesions, hypohomocysteinaemia and increased

97 e matter masks were generated by subtracting white matter lesions identified on the proton density/T2

98 Detection of this extensive white matter lesion in corticobasal degeneration and pro

99 One subject had a pure white matter lesion in the location of the right IFOF an

100 in 368 (21%), microbleeds in 372 (22%), and white matter lesions in 1715 (99%).

101 longitudinal studies that track the onset of white matter lesions in MS with the emergence and resolu

102 in receptor TrkB is induced on astrocytes in white matter lesions in multiple sclerosis (MS) patients

103 sites of autoimmune inflammation, including white matter lesions in multiple sclerosis (MS), but its

104 a subpopulation of demyelinated subcortical white matter lesions in multiple sclerosis brains.

105 eviously associated with the distribution of white matter lesions in multiple sclerosis.

106 tine, we examined its effect on demyelinated white matter lesions in rabbits, which exhibit progenito

107 le demyelinating attack-when associated with white matter lesions in the brain-negatively impacts sub

108 identally identified demyelinating-appearing white matter lesions in the CNS within individuals lacki

109 e effect of gender on the risk of developing white matter lesions in the context of LHON.

110 We examined the impact of discrete white matter lesions in the frontal lobes on event-relat

111 melioration of cerebrovascular reactivity or white matter lesions in these mice was not associated wi

112 d the cortical hypointensity adjacent to the white-matter lesion in the T2-weighted gradient-echo seq

113 years, clinical and MRI (ie, gray matter and white matter lesions, including spinal cord lesions, and

114 T2-weighted MRI detected white matter lesions independently of T cells.

115 Additionally, in white matter lesions, iron precipitation in aggregates t

116 mechanism of myelination failure in chronic white matter lesions is related to a combination of dela

117 Patients with POAG had significantly greater white matter lesion load (p < 0.05), more PVS in the cen

118 th gadolinium; P < .001) and correlated with white matter lesion load (r = 0.39; 95% CI: 0.20, 0.55;

119 sessment was negatively correlated with deep white matter lesion load (R(2) = -0.840, p < 0.01), tota

120 lesion load (R(2) = -0.840, p < 0.01), total white matter lesion load (R(2) = -0.928, p < 0.01) and t

121 h HL(95) had a higher microvascular cerebral white matter lesion load [1.4, interquartile range (IQR)

122 d (c) the contribution of 7.0-T cortical and white matter lesion load and cortical thickness to neuro

123 MD and GM changes were associated with white matter lesion load and with physical and cognitive

124 he ROC analyses over grey matter atrophy and white matter lesion load in predicting EDSS worsening (a

125 Grey matter atrophy over 1 year and white matter lesion load were determined.

126 were constructed for grey matter atrophy and white matter lesion load, and the network measures and c

127 MR imaging was used to quantify white matter lesion load, frequency of dilated perivascu

128 ypothesis, wherein focal vascular damage and white matter lesion location is a crucial factor, influe

129 For white matter lesions, LowGAN increased lesion segmentati

130 White matter lesion magnetization transfer ratio reducti

131 eptible population of preOLs renders chronic white matter lesions markedly more vulnerable to recurre

132 Deep subcortical white matter lesions may be a marker of a toxic or infec

133 lity to detect a treatment effect in a focal white-matter lesion may be of use in studying therapies

134 connectivity in 26 uCP with periventricular white matter lesions (mean age (standard deviation): 12.

135 essment to characterize cerebral parameters (white matter lesions, microbleeds), cardiovascular param

136 ssel disease, such as covert brain infarcts, white matter lesions, microbleeds, and cortical microinf

137 Metabolic ratios were obtained in white matter lesions, NAWM, and CGM regions.

138 t of multiple sclerosis specimens containing white matter lesions (nine adult and three paediatric ca

139 ls, T1w/T2w ratio was significantly lower in white matter lesions of all multiple sclerosis phenotype

140 Examination of NFIA expression in white matter lesions of human newborns with neonatal HIE

141 e oligodendrocyte progenitor cells (OLPs) in white matter lesions of human newborns with neonatal hyp

142 dentified in SOX2(+) progenitor cells within white matter lesions of human progressive MS (PMS) autop

143 her, Nfasc140 is reexpressed in demyelinated white matter lesions of postmortem brain tissue from hum

144 Thirteen subjects exhibited deep subcortical white matter lesions, of whom nine (69.2%) were born in

145 PML in any patient with sarcoidosis and new white matter lesions on brain magnetic resonance imaging

146 ar-old woman with mild memory impairment and white matter lesions on magnetic resonance imaging, prov

147 In CIS patients, finding typical MS white matter lesions on the patient's MRI scan remains t

148 The presence of white-matter lesions on brain imaging should be taken in

149 Suspected causes of these deficits, such as white matter lesions or affective instability, become ap

150 higher function deficits that resulted from white matter lesions or lesions of the association corti

151 e infarcts, multiple microinfarcts, ischemic white matter lesions, or petechial hemorrhages.

152 -artery atherosclerosis stroke (P = .01) and white matter lesion (P < .001).

153 carriers also showed an increased burden of white matter lesions (P-value=3.3 x 1(-02)) and a higher

154 carriers also showed an increased burden of white matter lesions (P-value=3.3 x 10(-02)) and a highe

155 In addition, cerebral white matter lesions, peripheral neuropathy, and kidney

156 Cerebral white matter lesions prevent cortico-spinal descending i

157 mice survived on high lysine, but developed white matter lesions, reactive astrocytes and neuronal l

158 erintensity (WMH) in older adults, a type of white matter lesion related to cerebral small vessel dis

159 Similar findings were observed in white matter lesions relative to normal-appearing white

160 oimaging demonstrated cerebellar atrophy and white matter lesions, respectively, in 2 patients.

161 with slightly abnormal MTR located close to white matter lesions (sa-WM Close); (3) NAWM regions wit

162 riventricular leukomalacia, an age-dependent white matter lesion seen in preterm infants and a common

163 s (0.33 x 0.33 x 1.0 mm(3)) for cortical and white matter lesion segmentation and 3.0-T T1-weighted i

164 the number of objects is unknown, such as in white matter lesion segmentation of multiple sclerosis (

165 ys within a 3D MRI volume helped to identify white matter lesion sites that could interfere with the

166 Due to its sensitivity in detecting white matter lesions, T(2)-weighted magnetic resonance i

167 ithin and adjacent to actively demyelinating white matter lesions that are associated with damaged ax

168 is study tests whether or not the structural white matter lesions that are characteristic of late-lif

169 proportion of infants, MRI detects punctate white matter lesions that are not seen on ultrasonograph

170 quantitative T2* changes, independently from white matter lesions, the greatest association being at

171 Also, in 75% of white matter lesions, the reduction in neurite density i

172 ed that visceral obesity contributes to deep white matter lesions through increases in proinflammator

173 e I lesions were contiguous with subcortical white matter lesions; Type II lesions were small, confin

174 ere masked to treatment, for the severity of white-matter lesions using the age-related white-matter

175 r NT-proBNP level was associated with larger white matter lesion volume (mean difference in z score p

176 sociated with a smaller increase in cerebral white matter lesion volume and a greater decrease in tot

177 The primary outcome was change in total white matter lesion volume from baseline.

178 , based on a robust linear mixed model, mean white matter lesion volume increased from 4.57 to 5.49 c

179 erage white matter fractional anisotropy and white matter lesion volume showed statistically signific

180 whole brain parenchymal volume and total T2 white matter lesion volume was assessed.

181 l infarcts, cerebral microbleeds, and higher white matter lesion volume), and neurodegenerative (lowe

182 metabolite levels also correlated with total white matter lesion volume, adjusting the Cr levels for

183 For white matter lesion volume, we did not observe a signifi

184 tive participants) and were used to quantify white matter lesion volume.

185 ging features and risk factors: microbleeds; white matter lesion volume; stroke-related events (infar

186 n volume (beta = 0.05, 95% CI: -0.34, 0.45), white matter lesions volume (beta = -0.10, 95% CI: -0.20

187 erebral microbleeds, total brain volume, and white matter lesions volume, as well as dementia, in lat

188 p learning model to extract brain region and white matter lesion volumes from any single MRI contrast

189 cingulate and caudate parcellations and with white matter lesion volumes.

190 also measured grey matter tissue volumes and white matter lesion volumes.

191 A reproducible focal white matter lesion was used to reliably compare treatme

192 sufficiency of Timp3, although the number of white matter lesions was unaffected.

193 MRI showed that subcortical white matter lesions were almost universal in both group

194 e density index and myelin water fraction in white matter lesions were associated to serum neurofilam

195 Punctate white matter lesions were associated with a 29% increase

196 White matter lesions were characterized by a centripetal

197 White matter lesions were characterized by Loes MRI seve

198 White matter lesions were classified in T1-isointense, T

199 The birth seasons of patients with white matter lesions were compared with those of the gen

200 Similarly, brain white matter lesions were mapped voxel-wise as a functio

201 Ischemic stroke and severe white matter lesions were more frequent among family A m

202 ic transgenic mice, multi-focal, plaque-like white matter lesions were present in cerebellum and brai

203 ed up over 30 years, we explored (1) whether white matter lesions were prognostically more relevant e

204 ncortical infarcts (SNCIs), microbleeds, and white matter lesions were quantified by a central core l

205 ultiple large contrast-enhancing subcortical white matter lesions, which regressed with glucose and h

206 eta [Abeta], tau, and neurodegeneration) and white matter lesions with longitudinal neuropsychiatric

207 estigated a link between season of birth and white matter lesions with magnetic resonance imaging (MR

208 ury in premature infants results in cerebral white matter lesions with prominent oligodendroglial inj

209 at predicted by the model to detect punctate white matter lesions with very good accuracy (area under

210 of cells and/or cell volumes in cortical and white matter lesions, with additional axonal dispersion

211 Punctate white matter lesions without associated cerebral lesions

212 We compared white matter lesion (WML) volume and prevalence of brain

213 SVD was estimated as white matter lesions (WML) and lacunes.

214 mutation carriers with remarkable widespread white matter lesions (WML) associated with lobar atrophy

215 amined the influence of lacunar infarcts and white matter lesions (WML) on severity and course of dep

216 White matter lesions (WML) underlie multiple brain disor

217 trophy (MTA), global cortical atrophy (GCA), white matter lesions (WML), and posterior atrophy.

218 disease (FD) are at risk for progression of white matter lesions (WMLs) and brain infarctions and wh

219 White matter lesions (WMLs) are frequently found in pati

220 White matter lesions (WMLs) detected on cerebral imaging

221 White matter lesions (WMLs) have been described as a del

222 White matter lesions (WMLs) were classified as "active"

223 ctional relationships with Abeta deposition; white matter lesions (WMLs), a marker of cerebrovascular

224 sahexaenoic acid (DHA; 22:6) have more brain white matter lesions (WMLs), an association suggesting t

225 associated with brain amyloid accumulation, white matter lesions (WMLs), and brain atrophy.

226 fractional anisotropy (FA) and diffusivity), white matter lesions (WMLs), and cerebral blood flow (CB

227 gh cerebral arterial pulsatility index (PI), white matter lesions (WMLs), enlarged perivascular space

228 ndent risk factor for subclinical focal deep white matter lesions (WMLs), even in young and otherwise

229 BP1, p16, and lipofuscin as markers of CS in white matter lesions (WMLs), normal appearing white matt

230 We hypothesized that cerebral white matter lesions (WMLs)-an imaging surrogate of smal

231 CVS assessment; presence of T2-hyperintense white matter lesions (WMLs).