ライフサイエンスコーパス: pulmonary vessel

1 their role in diseases of both systemic and pulmonary vessels.

2 a direct and specific effect of dasatinib on pulmonary vessels.

3 th muscle component of the bronchi and major pulmonary vessels.

4 inflammatory infiltrates surrounding larger pulmonary vessels.

5 r in appearance to normal structures such as pulmonary vessels.

6 usive and inflammatory diseases of the small pulmonary vessels.

7 in the smooth muscle component of the major pulmonary vessels.

8 d aggregation of platelets and leukocytes in pulmonary vessels.

9 d inhibited the structural remodeling of the pulmonary vessels.

10 in-positive endothelial cells in up to 5% of pulmonary vessels.

11 ET-1 causes contraction of isolated pulmonary vessels and bronchi and stimulates proliferati

12 A reduction in the number of pre-acinar pulmonary vessels and increased muscularization are the

13 Here we show that in pulmonary vessels and PASMCs of human and experimental P

14 In validation of this model, diseased pulmonary vessels and plasma from mammalian models and h

15 ly expressed in the endothelium of remodeled pulmonary vessels and plexiform lesions of patients with

16 aging to study neutrophil extravasation from pulmonary vessels and subsequent interstitial migration.

17 od cells that continuously circulate through pulmonary vessels and that have major effector activitie

18 rkers to identify the various cell layers of pulmonary vessels and to identify different endothelial

19 caused edema accumulation around airways and pulmonary vessels, and a large increase in the number of

20 ed edema accumulation around the airways and pulmonary vessels, and a significant increase in the num

21 ns are characterized by involvement of small pulmonary vessels, and pathologically they can be conven

22 lymphatics were abundant near major airways, pulmonary vessels, and visceral pleura.

23 venous gas emboli (via cardiac shunts or via pulmonary vessels) are introduced into the arterial circ

24 subjects had approximately a 20% increase in pulmonary vessel area in response to saline infusion, su

25 invariably accompanied by remodeling of the pulmonary vessels but the mechanism by which hypoxia inc

26 mic features in the thorax, such as ribs and pulmonary vessels, can greatly influence the detection o

27 sibility, defined as the percent increase in pulmonary vessel diameter per mm Hg increase in pressure

28 n MRA and catheterization measurements of 33 pulmonary vessel diameters was 0.5+/-1.5 mm, with a mean

29 Hypoxic wild-type pulmonary vessels displayed close temporal and spatial r

30 thelium and not in the endothelium of larger pulmonary vessels following treatment of mice with thora

31 hed in lung endothelial cells of obliterated pulmonary vessels in patients with idiopathic PAH.

32 we observed marked muscularization of distal pulmonary vessels in Prkg1(-/-) mice.

33 es that express VLA-4 bind preferentially to pulmonary vessels in sites of LIP: vessels that expresse

34 expression in the endothelium of dermal and pulmonary vessels, in the pulmonary parenchyma, and in r

35 , biochemical, and functional assessments of pulmonary vessels, including in vivo hemodynamic studies

36 m cells form human bronchioles, alveoli, and pulmonary vessels integrated structurally and functional

37 at extravasation of breast cancer cells from pulmonary vessels is a point of action of TGF-beta in th

38 hat smooth-muscle proliferation around small pulmonary vessels is an essential part of the pathogenes

39 The loss of blood volume in distal pulmonary vessels is associated with PA enlargement on c

40 mooth muscle cell proliferation around small pulmonary vessels is essential to the pathogenesis of pu

41 Prostacyclin (PGI2) analogues, which relax pulmonary vessels mainly through cAMP elevation, have a

42 Smooth muscle cell hyperplasia in pulmonary vessels (n = 11) in PPH and secondary PH was p

43 arkedly improved visualization of peripheral pulmonary vessels (n = 26) and improved spatial orientat

44 was also observed in smooth muscle cells of pulmonary vessels of mice exposed to hypoxia and rats ch

45 tensive pulmonary arteries but not to normal pulmonary vessels or other tissues.

46 as been extensively studied, their impact on pulmonary vessels remains less clear.

47 manifest diffuse medial thickening in small pulmonary vessels, resulting from smooth muscle cell hyp

48 g was seen in both mouse and human remodeled pulmonary vessels, supporting the use of Nutlins as a PH

49 e endothelial cell (EC) monolayer in nascent pulmonary vessels, thereby contributing to EC survival i

50 per mm Hg increase in pressure, permits the pulmonary vessels to increase in size to accommodate inc

51 increase, right ventricular hypertrophy, and pulmonary vessel wall thickening.

52 .227+/-0.0252, P<0.05) and a decrease in the pulmonary vessel wall thickness index (36.87%, P<0.001),

53 ng the transmigration of leukocytes into the pulmonary vessel wall.

54 ed that the proportion of muscularized small pulmonary vessels was almost fourfold greater in NOS3-de

55 Pulmonary vessels were automatically identified, segment

56 The airways and pulmonary vessels were measured at baseline and after i.

57 Initially, the cells attached to the pulmonary vessels were rounded.

58 Unstable alveoli stent open pulmonary vessels, which may explain the failure of hypo

59 e fibrin deposits were largely restricted to pulmonary vessels with a lumenal area greater than 100 m

60 th muscle component of the bronchi and major pulmonary vessels with decreased Fgf10 expression.