ライフサイエンスコーパス: cerebral lesion

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 bsequently, only 4 of 33 subjects had silent cerebral lesions.

8 or urinary dysfunction; and total volume of cerebral lesions.

9 Twenty-six scans to assess newly diagnosed cerebral lesions, 24 scans for diagnosing tumor progress

10 Although cerebral lesions 3 mm or larger on imaging are associate

11 rioration of the motor functions by reducing cerebral lesion and edema.

12 nd complement studies in patients with known cerebral lesions and abnormal eye movements.

13 ion is dominated by rapid exclusion of acute cerebral lesions and further varies greatly depending on

14 rebrospinal fluid, sometimes coinciding with cerebral lesions and neuroendocrine symptoms, marked the

15 points included quantitative MRI analyses of cerebral lesions and neurological outcomes at 48 h and 3

16 n all patients with acquired non-progressive cerebral lesions and partial seizures.

17 ional information for the differentiation of cerebral lesions and the grading of gliomas.

18 e, severe bronchopulmonary dysplasia, severe cerebral lesions, and necrotizing enterocolitis).

19 ty, including for esophageal lesions, silent cerebral lesions, and PV stenosis.

20 tate white matter lesions without associated cerebral lesions are common in preterm infants currently

21 Background Detection of cerebral lesions at MRI may benefit from a chemically st

22 on the blood-brain barrier is hampered after cerebral lesions by proteasomal glucocorticoid receptor

23 Contralateral to the cerebral lesion (contralesional side), cells were smalle

24 virus, were associated with various types of cerebral lesions (e.g., microcephaly, atrophy, or perive

25 d time course of the enlargement of ischemic cerebral lesions following human stroke and to study the

26 ns neurologically stable, with resolution of cerebral lesions, >2 years after diagnosis.

27 Asymptomatic cerebral lesions have been observed on diffusion weighte

28 ndocarditis group, MRI revealed at least one cerebral lesion in 12 of 23 rats (52%), including brain

29 ion device reduced the frequency of ischemic cerebral lesions in potentially protected regions.

30 nance imaging showed bilateral and symmetric cerebral lesions, including microhemorrhages and hyperin

31 nfants are at increased risk of a variety of cerebral lesions, involving the white matter, cortex, ce

32 me-independent identification of an ischemic cerebral lesion is an important objective of magnetic re

33 een serum pNF-H status, disease severity and cerebral lesion load and activity.

34 Brain mechanisms compensating for cerebral lesions may mitigate the progression of chronic

35 ients (aged 16-73 years) suspected of having cerebral lesions on MR images who subsequently underwent

36 mia on neonatal cerebral injury, we assessed cerebral lesions on MRI scans of infants who participate

37 ls were largely attributable to pre-existing cerebral lesions or alcohol abuse.

38 The incidence of silent cerebral lesions (SCL) after atrial fibrillation (AF) ab

39 udy intended to evaluate the distribution of cerebral lesion sites and the potential presence of spec

40 Cerebral lesion sites were correlated voxel-wise with pr

41 ormance between the arms, and differences in cerebral lesion sizes and locations between patients.

42 We aimed to define the cerebral lesion spectrum in an infective endocarditis ra

43 ((18)F-FET) PET in the initial diagnosis of cerebral lesions suggestive of glioma.

44 These animals show no cerebral lesions that are reputed characteristics of hum

45 Despite the increased risk of cerebral lesions, the control of saccades and pursuit wa

46 In patients with newly diagnosed cerebral lesions, the highest accuracy (77%) to detect n

47 In three patients with nonneoplastic cerebral lesions, the ratio did not exceed 1.

48 Structural imaging reveals most cerebral lesions underlying focal epilepsy.

49 n addition, both thrombolytic agents reduced cerebral lesion volume (determined by magnetic resonance

50 owever, Microlyse, but not rh-tPA, decreased cerebral lesion volumes (13.9 +/- 11.4 mm3; P < .001; 23

51 lume maps were co-registered, segmented when cerebral lesion was present, and normalized cerebral blo

52 llocation to hypothermia or normothermia and cerebral lesions was assessed by logistic regression wit

53 The fate of OL lineage cells in chronic cerebral lesions was defined with OL lineage-specific ma

54 cerebral magnetic resonance imaging, silent cerebral lesions were detected in 4 of the first 6 subje

55 severe bronchopulmonary dysplasia, or severe cerebral lesions were observed.

56 Embolic cerebral lesions were often 6-10mm in diameter.

57 In 60% (36/60) of patients, pre-existing cerebral lesions were seen on the preprocedure MRI (8 le

58 e was 333+/-570 ml below the baseline value; cerebral lesions were unchanged.