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 large vessel occlusion (LVO) stroke improves penumbral blood flow and clinical stability.

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

8 achromatic cues like contrast, texture, and penumbral blur remains poorly understood.

9 accuracy, and furthermore exhibits tuning to penumbral blur.

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

11 neuroprotective candidates against ischemic penumbral cell death.

12 tanding of molecular mechanisms that mediate penumbral cell death.

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

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

15 In penumbral cortex alkaline pH preceded acid pH and infarc

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

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

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

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

20 to spatial domains of seizures, showing that penumbral discharges are more broadly distributed and le

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

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

23 the best PW measure Tmax to detect the upper penumbral flow threshold in ischemic stroke is excellent

24 /- 11.4) on the core, intermediate and outer penumbral gyri, respectively.

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

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

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

28 The penumbral magnetic field has an intricate and unexpected

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

30 As penumbral neurons are threatened by markedly constrained

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

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

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

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

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

36 A favorable penumbral pattern on neuroimaging did not identify patie

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

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

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

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

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

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

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

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

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

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

47 nclear but may involve enhanced apoptosis in penumbral regions.

48 By contrast, neurons in "penumbral" regions (those receiving intense local synapt

49 After stroke, penumbral salvage determines clinical recovery.

50 Penumbral salvage in the active C-tDCS group was median

51 and above the established positive impact of penumbral salvage.

52 ings, with signals of beneficial effect upon penumbral salvage.

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

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

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

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

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

58 " territories invaded by the seizure versus "penumbral" territories is evident at the level of single

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

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

61 res (eg, time-to-maximum [Tmax]) to optimize penumbral tissue detection.

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

63 neurons are recruited to the seizure, while penumbral tissue shows stable action potentials, in keep

64 he-curve = 0.88) performed best in detecting penumbral tissue up to 48 hours after stroke onset.

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

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

67 r studies aimed at neuroprotection targeting penumbral tissue, especially in patients that do not res

68 emperature elevation is highest in potential penumbral tissue.

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

70 y 1 hour resulted in a decrease of 3.1 mL of penumbral volume (beta coefficient = -3.1; 95% CI, -4.6

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

72 core volume was 24 (IQR, 8-76) mL and median penumbral volume was 58 (IQR, 29-91) mL.

73 Mismatch volume (ie, the estimated penumbral volume) was calculated as critically hypoperfu

74 Penumbral volume, measured using automated software, was

75 The association of ischaemic core and penumbral volumes with 90-day mRS score was analysed wit

76 sociated with increasing core and decreasing penumbral volumes.