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1 e important for the establishment of chronic white matter lesions.
2 tients with unilateral and bilateral frontal white matter lesions.
3 esions, with additional axonal dispersion in white matter lesions.
4 ence of deep subcortical and periventricular white matter lesions.
5  and Ig deposition in central nervous system white matter lesions.
6 t influences on early CBF deficits and later white matter lesions.
7 s with LMS and 26% of patients with LHON had white matter lesions.
8 osis Severity Score, cortical thickness, and white matter lesions.
9 tter injury (WMI), and is expressed in human white matter lesions.
10 thophysiological pathway in the formation of white matter lesions.
11 nstrated the presence of iron depositions in white matter lesions.
12 amma-herpesvirus was cultured from acute JME white matter lesions.
13 ivated macrophages/microglia at the edges of white matter lesions.
14 ascular risk factors, cerebral infarcts, and white matter lesions.
15 may not be directly related to demyelinating white matter lesions.
16 signs of tissue damage such as hemorrhage or white matter lesions.
17 btained in passing during biopsy sampling of white-matter lesions.
18  hemorrhages (8.5% versus 0%) and more small white matter lesions (23% versus 8% had > 5 such lesions
19 ith subjective cognitive complaints or brain white-matter lesions 5 to 10 years after the hypertensiv
20                          We assessed whether white-matter lesions affect the perioperative risk of st
21 p1) was also reduced in OPCs in human infant white matter lesions after hypoxia.
22 ronectin in TgNotch3(R169C) mice ameliorated white matter lesions, although CBF responses were unchan
23 sm, are altered in association with punctate white matter lesions and "diffuse excessive high signal
24 pendently evaluated the studies for punctate white matter lesions and DEHSI.
25                     R(2)' was measured in MS white matter lesions and in regions of interest in norma
26 ed qualitative histopathological analysis of white matter lesions and normal-appearing white matter r
27 s at postnatal day 7 (P7) produced selective white matter lesions and OL death.
28       (18)F-PBR111 binding was higher in the white matter lesions and perilesional volumes of MS pati
29 ic resonance imaging revealed nonprogressive white matter lesions and spinocerebellar atrophy similar
30 ging demonstrated cerebellar atrophy without white matter lesions and stereotactic biopsy showed sele
31 h these data, MCAM(+) cells were detected in white matter lesions, and in gray matter of multiple scl
32  of systemic atherosclerotic vessel changes, white matter lesions, and myocardial changes.
33 ncluding cerebral blood flow (CBF) deficits, white matter lesions, and Notch3(ECD) deposition, were e
34 le sclerosis; (ii) they occur independent of white matter lesions; and (iii) they are associated with
35      Pathology in MS is not confined only to white matter lesions; apparently normal appearing tissue
36 eason, illness outcome, and deep subcortical white matter lesions appear to be closely linked.
37 alities in normal-appearing white matter and white matter lesions are greatest near the ventricles.
38                                              White matter lesions are often located adjacent to the v
39                                 Inflammatory white-matter lesions are less evident but diffuse axonal
40                      The pattern of multiple white matter lesions arranged parallel to the lateral ve
41                               Iron status of white matter lesions, as determined by staining, was com
42 citotoxicity in the pathogenesis of punctate white matter lesions, but not necessarily in DEHSI, and
43 d be avoided in patients with more extensive white-matter lesions, but might be an acceptable alterna
44  the multiple sclerosis specimens containing white matter lesions by any of the methods employed, yet
45 ot CSF) levels of Abeta were associated with white matter lesions, cerebral microbleeds, hypertension
46 ll population within multiple sclerosis (MS) white matter lesions compared to control brains.
47 N had a significantly greater risk of having white matter lesions consistent with MS compared with ma
48                                  Compared to white matter lesions, cortical lesions contained 13 time
49  periependymal brainstem lesions, perivenous white matter lesions, Dawson's fingers, curved or S-shap
50 tered to patients with MRI-confirmed frontal white matter lesions due to sickle cell disease (SCD) va
51 in PET significantly improves predictions of white matter lesion enlargement in relapsing remitting p
52 hibits the same metabolic changes as chronic white matter lesions, even very early in the disease cou
53                    The unique combination of white matter lesions, hypohomocysteinaemia and increased
54 e matter masks were generated by subtracting white matter lesions identified on the proton density/T2
55                  Detection of this extensive white matter lesion in corticobasal degeneration and pro
56                       One subject had a pure white matter lesion in the location of the right IFOF an
57 in receptor TrkB is induced on astrocytes in white matter lesions in multiple sclerosis (MS) patients
58  sites of autoimmune inflammation, including white matter lesions in multiple sclerosis (MS), but its
59  a subpopulation of demyelinated subcortical white matter lesions in multiple sclerosis brains.
60 eviously associated with the distribution of white matter lesions in multiple sclerosis.
61 le demyelinating attack-when associated with white matter lesions in the brain-negatively impacts sub
62 e effect of gender on the risk of developing white matter lesions in the context of LHON.
63           We examined the impact of discrete white matter lesions in the frontal lobes on event-relat
64 melioration of cerebrovascular reactivity or white matter lesions in these mice was not associated wi
65 years, clinical and MRI (ie, gray matter and white matter lesions, including spinal cord lesions, and
66                             Additionally, in white matter lesions, iron precipitation in aggregates t
67  mechanism of myelination failure in chronic white matter lesions is related to a combination of dela
68 Patients with POAG had significantly greater white matter lesion load (p < 0.05), more PVS in the cen
69 sessment was negatively correlated with deep white matter lesion load (R(2) = -0.840, p < 0.01), tota
70 lesion load (R(2) = -0.840, p < 0.01), total white matter lesion load (R(2) = -0.928, p < 0.01) and t
71 h HL(95) had a higher microvascular cerebral white matter lesion load [1.4, interquartile range (IQR)
72              MR imaging was used to quantify white matter lesion load, frequency of dilated perivascu
73 ypothesis, wherein focal vascular damage and white matter lesion location is a crucial factor, influe
74                                              White matter lesion magnetization transfer ratio reducti
75 eptible population of preOLs renders chronic white matter lesions markedly more vulnerable to recurre
76                             Deep subcortical white matter lesions may be a marker of a toxic or infec
77 lity to detect a treatment effect in a focal white-matter lesion may be of use in studying therapies
78 essment to characterize cerebral parameters (white matter lesions, microbleeds), cardiovascular param
79 t of multiple sclerosis specimens containing white matter lesions (nine adult and three paediatric ca
80            Examination of NFIA expression in white matter lesions of human newborns with neonatal HIE
81 e oligodendrocyte progenitor cells (OLPs) in white matter lesions of human newborns with neonatal hyp
82 her, Nfasc140 is reexpressed in demyelinated white matter lesions of postmortem brain tissue from hum
83 Thirteen subjects exhibited deep subcortical white matter lesions, of whom nine (69.2%) were born in
84 ar-old woman with mild memory impairment and white matter lesions on magnetic resonance imaging, prov
85                              The presence of white-matter lesions on brain imaging should be taken in
86  higher function deficits that resulted from white matter lesions or lesions of the association corti
87 e infarcts, multiple microinfarcts, ischemic white matter lesions, or petechial hemorrhages.
88  carriers also showed an increased burden of white matter lesions (P-value=3.3 x 1(-02)) and a higher
89  carriers also showed an increased burden of white matter lesions (P-value=3.3 x 10(-02)) and a highe
90                        In addition, cerebral white matter lesions, peripheral neuropathy, and kidney
91  mice survived on high lysine, but developed white matter lesions, reactive astrocytes and neuronal l
92 erintensity (WMH) in older adults, a type of white matter lesion related to cerebral small vessel dis
93            Similar findings were observed in white matter lesions relative to normal-appearing white
94  with slightly abnormal MTR located close to white matter lesions (sa-WM Close); (3) NAWM regions wit
95 riventricular leukomalacia, an age-dependent white matter lesion seen in preterm infants and a common
96 ys within a 3D MRI volume helped to identify white matter lesion sites that could interfere with the
97          Due to its sensitivity in detecting white matter lesions, T(2)-weighted magnetic resonance i
98 ithin and adjacent to actively demyelinating white matter lesions that are associated with damaged ax
99 is study tests whether or not the structural white matter lesions that are characteristic of late-lif
100  proportion of infants, MRI detects punctate white matter lesions that are not seen on ultrasonograph
101 quantitative T2* changes, independently from white matter lesions, the greatest association being at
102 e I lesions were contiguous with subcortical white matter lesions; Type II lesions were small, confin
103 ere masked to treatment, for the severity of white-matter lesions using the age-related white-matter
104 r NT-proBNP level was associated with larger white matter lesion volume (mean difference in z score p
105 l infarcts, cerebral microbleeds, and higher white matter lesion volume), and neurodegenerative (lowe
106 metabolite levels also correlated with total white matter lesion volume, adjusting the Cr levels for
107 tive participants) and were used to quantify white matter lesion volume.
108 n volume (beta = 0.05, 95% CI: -0.34, 0.45), white matter lesions volume (beta = -0.10, 95% CI: -0.20
109 erebral microbleeds, total brain volume, and white matter lesions volume, as well as dementia, in lat
110 cingulate and caudate parcellations and with white matter lesion volumes.
111 also measured grey matter tissue volumes and white matter lesion volumes.
112                         A reproducible focal white matter lesion was used to reliably compare treatme
113 sufficiency of Timp3, although the number of white matter lesions was unaffected.
114                  MRI showed that subcortical white matter lesions were almost universal in both group
115                                     Punctate white matter lesions were associated with a 29% increase
116                                              White matter lesions were characterized by a centripetal
117           The birth seasons of patients with white matter lesions were compared with those of the gen
118                   Ischemic stroke and severe white matter lesions were more frequent among family A m
119 ic transgenic mice, multi-focal, plaque-like white matter lesions were present in cerebellum and brai
120 ultiple large contrast-enhancing subcortical white matter lesions, which regressed with glucose and h
121 estigated a link between season of birth and white matter lesions with magnetic resonance imaging (MR
122 ury in premature infants results in cerebral white matter lesions with prominent oligodendroglial inj
123 of cells and/or cell volumes in cortical and white matter lesions, with additional axonal dispersion
124                                     Punctate white matter lesions without associated cerebral lesions
125                                  We compared white matter lesion (WML) volume and prevalence of brain
126                         SVD was estimated as white matter lesions (WML) and lacunes.
127 mutation carriers with remarkable widespread white matter lesions (WML) associated with lobar atrophy
128 amined the influence of lacunar infarcts and white matter lesions (WML) on severity and course of dep
129                                              White matter lesions (WMLs) are frequently found in pati
130                                              White matter lesions (WMLs) detected on cerebral imaging
131                                              White matter lesions (WMLs) have been described as a del
132                                              White matter lesions (WMLs) were classified as "active"
133 ctional relationships with Abeta deposition; white matter lesions (WMLs), a marker of cerebrovascular
134                We hypothesized that cerebral white matter lesions (WMLs)-an imaging surrogate of smal

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