ライフサイエンスコーパス: penumbral

1 Penumbral and core were defined using quantitative voxel

2 n the lesion core, but declined in potential penumbral and ipsilateral normal tissue at later times.

3 of AD, mouse HspB1 (Hsp25) localized to the penumbral areas of plaques.

4 nts contribute to secondary deterioration in penumbral areas.

5 nd reduced neuronal damaged was found in the penumbral at day 14 apoptosis.

6 ovide a completely novel strategy to improve penumbral blood flow and neuronal survival in stroke or

7 ck it is assumed that the affected tissue is penumbral but rescued by early spontaneous reperfusion.

8 neuroprotective candidates against ischemic penumbral cell death.

9 tanding of molecular mechanisms that mediate penumbral cell death.

10 We note that failure to control for penumbral cone stimulation could be mistaken for a melan

11 ones in the shadow of retinal blood vessels (penumbral cones).

12 In penumbral cortex alkaline pH preceded acid pH and infarc

13 e addressed by continuous pH measurements in penumbral cortex and post-ischaemic alkalization of brai

14 entrations of prostaglandin E(2) in ischemic penumbral cortex as compared to the vehicle-treated grou

15 as recorded by DEVD-AMC cleavage, peaked in penumbral cortex at 6-12 h following ischemia, correlati

16 e, initially, the deficit was less severe in penumbral cortex.

17 There was a net tendency towards increased penumbral firing during the seizure, although only a min

18 and numbers of pixels with LCBF in the lower penumbral flow range (0.24-0.36 ml g-1 min-1) were reduc

19 /- 11.4) on the core, intermediate and outer penumbral gyri, respectively.

20 ological models, infarction of 'non-core-non-penumbral' (i.e. clinically silent) brain tissue may nev

21 hese trials will confirm the hypothesis that penumbral imaging can enhance patient selection and exte

22 Going forward, we believe that the use of penumbral imaging with validated MRI techniques, as well

23 The penumbral magnetic field has an intricate and unexpected

24 in of the interlocking-comb structure of the penumbral magnetic field, and the behaviour of other mag

25 As penumbral neurons are threatened by markedly constrained

26 or Nox-mediated free radical production from penumbral neurons during the ischemic period.

27 erimentally induces significant increases in penumbral O2 pressure and by such may maintain the penum

28 neurophysiological dysfunction in either the penumbral or the core territories.

29 ard care in patients with either a favorable penumbral pattern (mean score, 3.9 vs. 3.4; P=0.23) or a

30 rding to whether the patient had a favorable penumbral pattern (substantial salvageable tissue and sm

31 A favorable penumbral pattern on neuroimaging did not identify patie

32 lment was 5.5 hours, and 58% had a favorable penumbral pattern.

33 time-to-peak might not directly reveal true penumbral perfusion levels.

34 metabolically compromised tissue, expediting penumbral recruitment into the ischemic core.

35 To determine the metabolic response in the penumbral region of the cortex ipsilateral to the occlus

36 ounding the infarct, possibly representing a penumbral region similar to that seen in ischemic brain

37 umulate adjacent to prior lesions and have a penumbral region susceptible to further injury.

38 airment developed over time in the perifocal/penumbral region, so that the deficit was greater 4 h af

39 resenting non-ischemic (Region A), perifocal/penumbral (Region B) and core ischemic (Region C) region

40 Curves in the presumed penumbral regions (n = 8) showed varied morphology, but

41 nsion of core-infarcted tissue into adjacent penumbral regions of reversible injury and have been sho

42 nclear but may involve enhanced apoptosis in penumbral regions.

43 After stroke, penumbral salvage determines clinical recovery.

44 and above the established positive impact of penumbral salvage.

45 ant differences were noted for percentage of penumbral salvaged (68% [SD 28] for the tenecteplase gro

46 The first decade of penumbral science investigated the ischemic regulation o

47 l simulation of a sunspot pair, we show that penumbral structures with such outflows form when the av

48 Surface cortical perfusion in core and penumbral territories was imaged semiquantitatively at i

49 inct spatial territories: the ictal core and penumbral territories.

50 ding seizure core surrounded by a far larger penumbral territory.

51 y, we hypothesised that age has an impact on penumbral tissue and its acute determinants.

52 t that PIDs contribute to the recruitment of penumbral tissue into the infarct core even after the re

53 order to test this hypothesis, non-core-non-penumbral tissue was identified in two independent prosp

54 ng relative risk of hemorrhage and volume of penumbral tissue, and add valuable prognostic informatio

55 emperature elevation is highest in potential penumbral tissue.

56 To determine whether detrimental penumbral-type depolarizations occur in human brain trau

57 le age correlated negatively with normalised penumbral volume (Kendall's tau b=-0.234, p=0.048) and l