ライフサイエンスコーパス: elastic lamina

1 d fragmentation of the internal and external elastic lamina.

2 ted with a higher frequency of breaks in the elastic lamina.

3 vascular contraction, and a proliferation of elastic lamina.

4 changes involve the intima and the internal elastic lamina.

5 re was extensive destruction of the internal elastic lamina.

6 area divided by the area within the internal elastic lamina), adjusted for injury score, by 47%.

7 as also found in the media near the external elastic lamina and in some periadventitial vessels.

8 ells forming a neointima inside the internal elastic lamina and luminal compromise, affected a greate

9 ffect permanent vasodilatation, the internal elastic lamina and medial elastin fibers must be degrade

10 of plaque area and area within the internal elastic lamina) and as the percent of vessel surface cov

11 ng intima, the fragmentation of the internal elastic lamina, and the presence of multinucleated giant

12 mbrane was also found to be thicker, and its elastic lamina appeared disorganized and discontinuous.

13 An increase in the external elastic lamina area in TGF-beta3-treated vessels (+0.73+

14 24.5 +/- 8.6 mm2, P = NS), and the external elastic lamina area was also quite constant in each vess

15 80 +/- 0.08 mm2, P=0.06) and larger external elastic lamina areas (3.32 +/- 0.21 versus 2.62 +/- 0.10

16 ing animals, lumen, neointimal, and external elastic lamina areas were 3.58 +/- 0.33, 3.16 +/- 0.35,

17 Longitudinal changes in external elastic lamina areas were highly correlated with changes

18 Lipid was layered against the internal elastic lamina as in human transplants.

19 using a specific reference segment external elastic lamina-based stent optimisation strategy was saf

20 Human macrophages mediate the dissolution of elastic lamina by mobilizing tissue-destructive cysteine

21 /-)/IDO(-/-) mice, which presented decreased elastic lamina degradation and aortic expansion.

22 decreased inflammatory cytokine expression, elastic lamina degradation and aortic expansion.

23 Elastic lamina degradation peptides extracted from arter

24 lammation, thin fibrous cap, severe internal elastic lamina degradation, and excessive expansive remo

25 ce had reduced aortic expansion and internal elastic lamina degradation; decreased numbers of macroph

26 oth muscle cell proliferation, fibrosis, and elastic lamina disruption observed in untreated animals

27 cle actin+ cell proliferation, fibrosis, and elastic lamina disruption).

28 The density of leukocytes within the elastic lamina-dominant media was about 58-70-fold lower

29 termine whether structural properties of the elastic lamina (EL) correspond to the region of the macu

30 thinning of the fibrous cap, severe internal elastic lamina fragmentation, and extracellular matrix r

31 yielded significantly increased tunica media elastic lamina fragmentation, decreased medial size, and

32 ted positively with the severity of internal elastic lamina fragmentation.

33 of MMPs and cathepsins, and severe internal elastic lamina fragmentation.

34 crophages in close proximity to the internal elastic lamina frequently coproduced matrix metalloprote

35 phosphatase resulted in calcification of the elastic lamina identified as hydroxyapatite by x-ray dif

36 Marked expansion of the internal elastic lamina (IEL) occurred in plaque hemorrhages with

37 Holes within the internal elastic lamina (IEL) of blood vessels are sites of fenes

38 hether interface changes, including internal elastic lamina (IEL) rupture, and medial and adventitial

39 The degeneration of internal elastic lamina (IEL), media thickness and CA size were e

40 d by endothelial cells (EC) and the internal elastic lamina (IEL).

41 nflations sufficient to disrupt the internal elastic lamina in a carotid artery of minipigs with hype

42 Age-related degradation of the elastic lamina in Bruch's membrane may have a permissive

43 d remodeling) and shortening of the internal elastic lamina in the ligated vessel.

44 The area within the internal elastic lamina increased with plaque area in the left an

45 wall dissection, fracturing of the internal elastic lamina, intimal hyperplasia, and eyelid vessel d

46 he supporting basement membrane and internal elastic lamina macromolecules with minimal deformation o

47 sion according to reference segment external elastic lamina measurements.

48 nd the plaque area (area within the external elastic lamina minus lumen area) were significantly (P <

49 likely resulted from the degradation of the elastic lamina of Bruch's membrane and up-regulation of

50 The elastic lamina of Bruch's membrane in the LOXL1-deficien

51 aracterized by calcification of the internal elastic lamina of muscular arteries and stenosis due to

52 essel circumference measured at the external elastic lamina of paclitaxel-treated vessels was signifi

53 isease in which infants calcify the internal elastic lamina of their medium and large arteries and ex

54 ces or in thin layers overlying the internal elastic lamina, often at the edges of atherosclerotic pl

55 ee of disruption of the internal or external elastic lamina or media was assigned.

56 dal arteries with disruption of the internal elastic lamina, patchy choroidal inflammation, and biref

57 mean change in the area within the external elastic lamina relative to a normal proximal reference s

58 considering the expected degree of internal elastic lamina tapering, remodeling was classified as po

59 BrM, an elastic lamina that is located between the retinal pigme

60 ne domains that project through the internal elastic lamina to adjacent smooth muscle membranes.

61 han the stent wire sites, where the internal elastic lamina was intact with underlying normal media (

62 collagen and fibrillin adjacent to internal elastic lamina was observed.

63 P:=0.0001), and the area within the internal elastic lamina was significantly less in healed ruptures

64 ction (as measured by the length of external elastic lamina) was the same in both groups, but the cir

65 EDTA) that were designed to target calcified elastic lamina when administrated by intravenous injecti

66 -1 immunostaining was increased in the inner elastic lamina, where fibulin-2 preferentially localizes

67 EDTA-loaded albumin NPs targeted the damaged elastic lamina while sparing healthy artery.

68 The morphologic characteristics of the elastic lamina within Bruch's membrane were examined in