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1 to induce neuroinflammation and subsequently white matter injury.
2 y has been implicated in the pathogenesis of white matter injury.
3 agonist caffeine can prevent hypoxia-induced white matter injury.
4 amate receptor blockade for hypoxic-ischemic white matter injury.
5 ages are possibly involved in the process of white matter injury.
6 egion could play a role in radiation-induced white matter injury.
7 gnitive impairment, particularly subcortical white matter injury.
8 s in reactivity, locally also in relation to white matter injury.
9  mitigate disturbed myelination in premature white matter injury.
10 ntial targets for promoting repair following white matter injury.
11  mitigate disturbed myelination in premature white matter injury.
12 utic strategy exists against the IVH-induced white matter injury.
13  therapeutic outcomes in models of perinatal white matter injury.
14 provement in myelination, suggesting reduced white matter injury.
15        There is also evidence of more global white matter injury.
16  to the treatment of premature children with white matter injury.
17 (DEHSI), the predominant patterns of preterm white matter injury.
18 ived MMP9 induced early BBB disruption after white matter injury.
19 inical utility of this model to detect focal white matter injury.
20 e importance of axon pathology in developing white matter injury.
21 at trend levels, confirming heterogeneity in white matter injury.
22 RI that allow more detailed investigation of white matter injury.
23 rovides a more flexible way of investigating white matter injury.
24 alacia (PVL), a distinctive form of cerebral white matter injury.
25  to the particular pathogenesis of perinatal white matter injury, (2) provide evidence that at least
26 human erythropoietin had abnormal scores for white matter injury (22% [17/77] vs 36% [32/88]; adjuste
27 [Ca(2+)]i) homeostasis might be one cause of white matter injury after HIV infection.
28 ack of Wnt repressor tone promoted permanent white matter injury after mild hypoxic insult.
29                       This review focuses on white matter injury after TBI and the multifactorial pro
30 d not fully rescue microglial activation and white matter injury after TBI.
31 d in patients with PCS, suggestive of axonal white matter injury and amyloid deposition.
32  the pro-inflammatory microglial activation, white matter injury and behavioural deficits.
33  results indicate that the evolution of grey/white matter injury and blood-brain barrier disruption a
34 rotective against selective hypoxic-ischemic white matter injury and decreases the subsequent neuromo
35 s important implications for treatment after white matter injury and disease.
36                                The resulting white matter injury and gray matter injury scores were c
37 role of AMPA-kainate receptor in IVH-induced white matter injury and identifies a novel strategy of n
38       These events ultimately attenuated the white matter injury and improved anxiety and depressive-
39 t cerebral ischemia, probably by alleviating white matter injury and modulating microglial/macrophage
40 udy reveals that OPCs can rapidly respond to white matter injury and produce MMP9 that disrupts the B
41     The goals of this study were to evaluate white matter injury and recovery thereof, simultaneously
42 uctive brain lesions that resulted in cystic white matter injury and secondary cortical and subcortic
43 godendrocytes, leading to neuroinflammation, white matter injury, and cognitive dysfunction.
44        HIP rats have brain microhemorrhages, white matter injury, and neurologic deficits.
45         We discuss clinical data implicating white matter injury as a key feature of these disorders,
46 tibody, significantly attenuated LPS-induced white matter injury, as indicated by decreases in ventri
47 hese findings demonstrate that the degree of white matter injury associated with cerebral microvascul
48 between biomechanical forces and patterns of white matter injuries, associated with persistent diffus
49 in the axon, with important implications for white matter injury, axonal growth, and axonal degenerat
50                   This suggests that diffuse white matter injury begins in utero for a significant pr
51 ants are susceptible to inflammation-induced white matter injury but the exposures that lead to this
52 l cells can cause oligodendrocyte damage and white matter injury by release of inflammatory cytokines
53 ls and infiltration of Th1 cells resulted in white matter injury, characterized by impaired myelin ba
54 godendrocyte (OL) maturation arrest in human white matter injury contributes significantly to the fai
55 a-induced DWMI.SIGNIFICANCE STATEMENTDiffuse white matter injury (DWMI) caused by hypoxia is a leadin
56                                      Diffuse white matter injury (DWMI) caused by hypoxia is associat
57 ments exist for preterm infants with diffuse white matter injury (DWMI) caused by hypoxia.
58                                      Diffuse white matter injury (DWMI) is a common finding in these
59 eonatal hypoxia (HX) that reproduces diffuse white matter injury (DWMI) of premature infants.
60                                      Diffuse white matter injury (DWMI), a leading cause of neurodeve
61 njury) 3 T MRI measures of lesion volume and white matter injury (fractional anisotropy).
62 d vasculature in MS that distinguishes human white matter injury from normal rodent demyelinating inj
63               Early treatment of spinal cord white matter injury has been found beneficial.
64                            Myelin damage and white matter injury have been frequently reported in HIV
65                                    Following white matter injury, however, there was no detectable im
66 to be a key mechanism in the pathogenesis of white matter injury; however, there has been no in vivo
67  and 7 more times at 2 d intervals mitigated white matter injury, improved axonal conduction, and enh
68                                              White matter injuries in the 7-day-old BCAO rat brain we
69 MRI abnormalities consistent with cerebellar white matter injury in 3 of 4 subjects.
70 al NMDA glutamate receptors (NMDARs) mediate white matter injury in a variety of CNS diseases, includ
71 ed death, a mechanism that may contribute to white matter injury in CNS disease.
72 eterioration may contribute to both gray and white matter injury in CNS trauma.
73 n combined with hypothermia attenuates brain white matter injury in comatose survivors of out-of-hosp
74     Glutamate excitotoxicity plays a role in white matter injury in many neurological diseases.
75  new insights into the mechanisms underlying white matter injury in premature infants with IVH and hi
76 rhage (IVH) results in neural cell death and white matter injury in premature infants.
77 iomarker for determining the pathogenesis of white matter injury in preterm infants during a period w
78 ar hemorrhage (IVH) remains a major cause of white matter injury in preterm infants with no viable th
79 uration arrest may predispose to more severe white matter injury in preterm survivors that sustain re
80  VBM is sensitive to detection of widespread white matter injury in SCD patients in borderzones betwe
81 hological sequela of chronic periventricular white matter injury in survivors of premature birth.
82 r activation contributes to hypoxic-ischemic white matter injury in the adult brain.
83 ells from venous vessels are correlated with white matter injury in the brain and poorer cognitive fu
84 diated OL excitotoxicity in hypoxic/ischemic white matter injury in the developing brain.
85  of ROS and caspase activation, and leads to white matter injury in the neonatal rat brain.
86 the development of an effective treatment to white matter injuries including spinal cord trauma given
87  variety of neurological disorders involving white matter injury, including multiple sclerosis, acute
88 ry, we found that the mechanism of perinatal white matter injury involved maturation-dependent vulner
89                                       Axonal white matter injury is believed to be a major determinan
90                                  Subcortical white matter injury is often accompanied by orofacial mo
91 nic hypoxia-ischemia-induced periventricular white matter injury is related to persistent depletion o
92                             Hypoxic/ischemic white matter injury is thought to mediate periventricula
93 bed in preterm infants affected with diffuse white matter injury, is incompletely understood.
94 bed in preterm infants affected with diffuse white matter injury, is incompletely understood.
95 iventricular leukomalacia (pre- or perinatal white matter injury leading to cerebral palsy), spinal c
96 s applied to capture spatially heterogeneous white matter injuries (lesions) in addition to standard
97                                     Neonatal white matter injury (NWMI) is a lesion found in preterm
98             Background It is well known that white matter injuries observed at birth are associated w
99        These observations may be relevant to white matter injury observed in premature infants.
100                                              White matter injury on cranial ultrasound was associated
101 Chorioamnionitis, necrotizing enterocolitis, white matter injury on cranial ultrasound, and increasin
102  = 0.515) and quantitatively defined diffuse white matter injury (p = 0.183).
103 enteral nutrition, pulmonary hemorrhage, and white matter injury (p<0.01 for each; relative differenc
104 ative arterial Pco2 as a risk factor for new white matter injury (P=0.04).
105                                       Unique white matter injury patterns were seen for two major pos
106 on is a promising option in treating diffuse white matter injury, previously called periventricular l
107 on is a promising option in treating diffuse white matter injury, previously called periventricular l
108 tter astrocytes in a rodent model of diffuse white matter injury produced by exposing neonatal mice t
109                              Periventricular white matter injury (PVWMI) in premature babies is a maj
110                              Periventricular white matter injury (PWMI) is the leading cause of cereb
111                     Although periventricular white matter injury (PWMI) is the leading cause of chron
112                              Periventricular white matter injury (PWMI) is the leading cause of neuro
113                              Periventricular white matter injury (PWMI) is the major cause of cerebra
114 fants frequently arises from periventricular white matter injury (PWMI), a condition associated with
115 in the preterm population is periventricular white matter injury (PWMI), a pathology associated with
116                                         This white matter injury results from a constellation of bloo
117                           Application toward white matter injury revealed CK2alpha-mediated Daam2 pho
118 lacia is a form of hypoxic-ischemic cerebral white matter injury seen most commonly in premature infa
119 anial ultrasound abnormalities suggestive of white matter injury significantly increased risk for som
120 mental window of selective vulnerability for white matter injury, such as periventricular leukomalaci
121 ntal disabilities, most often resulting from white matter injury sustained during the neonatal period
122 hemia (H/I) in the premature infant leads to white matter injury termed periventricular leukomalacia
123 l and neonatal brain injury, and can lead to white matter injury that is a precursor for a number of
124 yte lineage progression is implicated in the white-matter injury that occurs in cerebral palsy.
125                              Periventricular white matter injury, that is, periventricular leukomalac
126           The contribution of tract-specific white matter injury to dysfunction in different cognitiv
127     The cellular basis for the propensity of white matter injury to occur in the developing brain and
128 e a mouse model of ischemia-induced neonatal white matter injury to study the biodistribution of gene
129 e resistance of SPNs to insults that trigger white matter injury, transient hypoxemia disrupted SPN a
130 at OPCs in lesions of hypoxic human neonatal white matter injury upregulated markers of high Wnt acti
131 fficient (-0.16) that was similar to that of white matter injury volume (standardized beta = -0.22).
132                                              White matter injury was also ameliorated in s-NSC-treate
133 nsient oxygen and glucose deprivation (OGD), white matter injury was assessed by electrophysiology an
134 in the entire Fontan cohort; the presence of white matter injury was associated with worse paired ass
135  On preoperative imaging, moderate or severe white matter injury was present in 10 of 45 patients, wh
136                 On diffusion tensor imaging, white matter injury was prominent in the corpus callosum
137                                              White matter injury was significantly decreased in KI co
138                                              White matter injury was the most common type of injury i
139                                              White-matter injury was observed in 13 newborns with con
140                    Using an H/I rat model of white matter injury, we show in vivo that post-H/I treat
141  method of diagnosing clinically significant white matter injury when conventional imaging is normal.
142 e applied to capture spatially heterogeneous white matter injuries, which minimize implicit assumptio
143             Differentiation is a response to white matter injury, which is caused by tumour infiltrat
144 for 1 hr) resulted in selective, subcortical white matter injury with a marked ipsilateral decrease i
145 nd/or ventricular enlargement (suggestive of white matter injury) with or without germinal matrix-int
146 chniques resulted in a high incidence of new white matter injury, with central infarctions occurring
147 se with normal findings (n = 23), those with white matter injury (WMI) (n = 9), those with grade I ge
148 r form of magnetic resonance imaging-defined white matter injury (WMI) comprises diffuse lesions wher
149  proposed as a cellular mechanism of diffuse white matter injury (WMI) in premature infants.
150                Brain injuries in the form of white matter injury (WMI) or focal stroke and clinical f
151 oligodendrocyte dysfunction and repair after white matter injury (WMI) remains undefined.
152                                              White matter injury (WMI) was the commonest type of inju
153 OL differentiation during development, after white matter injury (WMI), and is expressed in human whi
154                    In the spinal cord, after white matter injury (WMI), NFIA-deficient astrocytes exh
155 h preterm birth include focal and/or diffuse white matter injury (WMI).
156  optimal imaging modality to define cerebral white-matter injury (WMI) in preterm survivors, the hist
157                                              White matter injuries (WMIs) are the leading cause of ne

 
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