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1 severe bronchopulmonary dysplasia, or severe cerebral lesions.
2 ging revealed extensive liver, pulmonary and cerebral lesions.
3 ing to the formation of these characteristic cerebral lesions.
4  development of fatal neurological signs and cerebral lesions.
5 sorganization exists in occult epileptogenic cerebral lesions.
6 inically useful information in patients with cerebral lesions.
7  or urinary dysfunction; and total volume of cerebral lesions.
8   Twenty-six scans to assess newly diagnosed cerebral lesions, 24 scans for diagnosing tumor progress
9                                     Although cerebral lesions 3 mm or larger on imaging are associate
10 rioration of the motor functions by reducing cerebral lesion and edema.
11 nd complement studies in patients with known cerebral lesions and abnormal eye movements.
12 ion is dominated by rapid exclusion of acute cerebral lesions and further varies greatly depending on
13 rebrospinal fluid, sometimes coinciding with cerebral lesions and neuroendocrine symptoms, marked the
14 points included quantitative MRI analyses of cerebral lesions and neurological outcomes at 48 h and 3
15 n all patients with acquired non-progressive cerebral lesions and partial seizures.
16 ional information for the differentiation of cerebral lesions and the grading of gliomas.
17 e, severe bronchopulmonary dysplasia, severe cerebral lesions, and necrotizing enterocolitis).
18 tate white matter lesions without associated cerebral lesions are common in preterm infants currently
19 on the blood-brain barrier is hampered after cerebral lesions by proteasomal glucocorticoid receptor
20 d time course of the enlargement of ischemic cerebral lesions following human stroke and to study the
21 ns neurologically stable, with resolution of cerebral lesions, >2 years after diagnosis.
22                                 Asymptomatic cerebral lesions have been observed on diffusion weighte
23 ion device reduced the frequency of ischemic cerebral lesions in potentially protected regions.
24 nance imaging showed bilateral and symmetric cerebral lesions, including microhemorrhages and hyperin
25 nfants are at increased risk of a variety of cerebral lesions, involving the white matter, cortex, ce
26 me-independent identification of an ischemic cerebral lesion is an important objective of magnetic re
27 een serum pNF-H status, disease severity and cerebral lesion load and activity.
28            Brain mechanisms compensating for cerebral lesions may mitigate the progression of chronic
29 ients (aged 16-73 years) suspected of having cerebral lesions on MR images who subsequently underwent
30 mia on neonatal cerebral injury, we assessed cerebral lesions on MRI scans of infants who participate
31 ls were largely attributable to pre-existing cerebral lesions or alcohol abuse.
32                      The incidence of silent cerebral lesions (SCL) after atrial fibrillation (AF) ab
33 ormance between the arms, and differences in cerebral lesion sizes and locations between patients.
34  ((18)F-FET) PET in the initial diagnosis of cerebral lesions suggestive of glioma.
35                        These animals show no cerebral lesions that are reputed characteristics of hum
36                Despite the increased risk of cerebral lesions, the control of saccades and pursuit wa
37             In patients with newly diagnosed cerebral lesions, the highest accuracy (77%) to detect n
38         In three patients with nonneoplastic cerebral lesions, the ratio did not exceed 1.
39              Structural imaging reveals most cerebral lesions underlying focal epilepsy.
40 lume maps were co-registered, segmented when cerebral lesion was present, and normalized cerebral blo
41 llocation to hypothermia or normothermia and cerebral lesions was assessed by logistic regression wit
42      The fate of OL lineage cells in chronic cerebral lesions was defined with OL lineage-specific ma
43 severe bronchopulmonary dysplasia, or severe cerebral lesions were observed.
44     In 60% (36/60) of patients, pre-existing cerebral lesions were seen on the preprocedure MRI (8 le
45 e was 333+/-570 ml below the baseline value; cerebral lesions were unchanged.

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