ライフサイエンスコーパス: pulmonary vessel

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

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

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

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

5 inflammatory infiltrates surrounding larger pulmonary vessels.

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

7 usive and inflammatory diseases of the small pulmonary vessels.

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

9 d aggregation of platelets and leukocytes in pulmonary vessels.

10 d inhibited the structural remodeling of the pulmonary vessels.

11 ion and occlusion of the small- to mid-sized pulmonary vessels.

12 se involving proliferative remodeling of the pulmonary vessels.

13 ncreased medial wall thickness of peripheral pulmonary vessels (41.9 +/- 2.9% and 41.8 +/- 3.2%, vs 2

14 hial arteries, is seen in the walls of large pulmonary vessels after a period of chronic hypoxia.

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

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

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

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

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

20 ich result in selective damage to subpleural pulmonary vessels and primary graft dysfunction.

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

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

23 circulation system into the impedance of the pulmonary vessels and the harmonic response of the LH.

24 t of the harmonic frequency responses of the pulmonary vessels and the left heart attached in series.

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

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

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

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

29 onship between peel pulmonary vessels, small pulmonary vessels, and pulmonary hypertension (PH) is no

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

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

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

33 It is characterized by remodeled pulmonary vessels associated with perivascular and intra

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

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

36 ion defects caused by neutrophil adhesion to pulmonary vessels contribute to COVID-19 severity.

37 e alveolarization by radial alveolar counts, pulmonary vessel density, and right ventricle hypertroph

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

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

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

41 of persistently activated cell types in the pulmonary vessel exhibiting aberrant expression of genes

42 ar thrombosis and included calcifications in pulmonary vessels, focal cardiac fibrosis with calcifica

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

44 ound to be overexpressed in the SMC layer of pulmonary vessels from patients with PAH-congenital hear

45 Histologic analysis of pulmonary vessels in patients with Covid-19 showed wides

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

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

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

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

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

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

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

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

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

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

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

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

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

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

60 Measurements and Main Results: In pulmonary vessels of patients with PF-PH, increased coll

61 ite consideration of the potential impact on pulmonary vessels of strategies aimed at controlling cel

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

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

64 that proteins orchestrating inflammation or pulmonary vessel remodeling in group 1 pulmonary hyperte

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

66 seases characterized by abnormal dilation of pulmonary vessels, resulting in impaired oxygenation.

67 ground The in vivo relationship between peel pulmonary vessels, small pulmonary vessels, and pulmonar

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

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

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

71 In PH, small pulmonary vessel volume is associated with pulmonary fun

72 ratio of small blood vessel volume to total pulmonary vessel volume were increased compared with con

73 Purpose To quantitatively assess peel pulmonary vessel volumes (PPVVs) and small pulmonary ves

74 l pulmonary vessel volumes (PPVVs) and small pulmonary vessel volumes (SPVVs) as estimated from CT pu

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

76 .227+/-0.0252, P<0.05) and a decrease in the pulmonary vessel wall thickness index (36.87%, P<0.001),

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

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

79 Pulmonary vessels were automatically identified, segment

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

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

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

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

84 ing characteristic curve (AUC), CT volume of pulmonary vessels with cross-sectional area 5 mm(2) or s

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