ライフサイエンスコーパス: aortic disease

1 ntial therapeutic agents to prevent thoracic aortic disease.

2 ntly associated with development of thoracic aortic disease.

3 netic variants in LOX predispose to thoracic aortic disease.

4 ular pathway that leads to familial thoracic aortic disease.

5 c features have a family history of thoracic aortic disease.

6 in MAT2A predispose individuals to thoracic aortic disease.

7 he most devastating complication of thoracic aortic disease.

8 r) have revolutionized treatment of thoracic aortic disease.

9 vascular smooth muscle cells will ameliorate aortic disease.

10 and subclinical coronary artery disease and aortic disease.

11 is available for evaluation of patients with aortic disease.

12 d decisions regarding early intervention for aortic disease.

13 is patient population, which had substantial aortic disease.

14 AD), but only half of mutation carriers have aortic disease.

15 ich loss of smooth muscle alpha-actin causes aortic disease.

16 creased carotid and proximal atherosclerotic aortic disease.

17 patients referred for evaluation of thoracic aortic disease.

18 urbo SE sequences for evaluation of thoracic aortic disease.

19 and possible target for treatment for human aortic diseases.

20 alterations that predispose persons to these aortic diseases.

21 sheaths (15%), and progression of underlying aortic disease (15%).

22 r extremity (41%), upper extremity (3%), and aortic disease (33%).

23 Patients with severe atheromatous aortic disease (AAD) who undergo coronary artery bypass

24 nderwent combined repair of renal artery and aortic disease (abdominal aortic aneurysm [AAA]: 47 pati

25 econstruction remains greater than repair of aortic disease alone.

26 Affected family members also had descending aortic disease and aneurysms of other arteries.

27 aortic growth, Smad4 deficiency exacerbated aortic disease and caused premature death in MFS mice.

28 ng of distant relatives affected by thoracic aortic disease and subsequent Sanger sequencing of addit

29 it is unclear which of these pathways drives aortic disease and, when inhibited, which result in dise

30 sis and has been established in a variety of aortic diseases and ischemic cardiomyopathy.

31 sis and Management of Patients With Thoracic Aortic Disease" and the "2014 AHA/ACC Guideline for the

32 ng has shown great promise for evaluation of aortic disease, and may soon augment conventional assess

33 tive aorta is the primary driver of thoracic aortic disease, and that TGF-beta overactivity in diseas

34 ose persons without known syndromes to these aortic diseases, and a major locus for this condition, t

35 protein function but do not cause inherited aortic disease are common in the general population and

36 Temporal trends in mortality from thoracic aortic disease are unclear.

37 study highlights the relevance of miR-29b in aortic disease but also raises questions about its speci

38 te imaging modality in diagnosis of thoracic aortic disease but is insensitive to intramural hematoma

39 Endograft therapy for thoracic aortic disease can be performed safely in elderly patien

40 eaths resulting from nonrheumatic mitral and aortic diseases clustered among both close and distant r

41 The altered genes predisposing to thoracic aortic disease either disrupt smooth muscle cell (SMC) c

42 uction was performed or for other cardiac or aortic disease elsewhere.

43 contained in Section 9.2.2.1 of the thoracic aortic disease guideline and Section 5.1.3 of the valvul

44 l risk markers proposed in the 2010 thoracic aortic disease guidelines and their application as part

45 an had been recommended by the 2010 Thoracic Aortic Disease guidelines, the 2013 Society of Thoracic

46 obands from unrelated families with thoracic aortic disease identified another MAT2A rare variant, c.

47 f additional probands with familial thoracic aortic disease identified the same rare variant, PRKG1 c

48 ble, is the treatment of choice for thoracic aortic disease in elderly patients.

49 missense mutation in LOX is associated with aortic disease in humans, likely through insufficient cr

50 h STAAD, suggesting a common pathogenesis of aortic disease in Marfan syndrome and STAAD.

51 ) TGFbeta signaling is a prominent driver of aortic disease in MFS mice, and inhibition of the ERK1/2

52 This mutation segregated with aortic disease in these families with a combined two-poi

53 insights into the molecular pathogenesis of aortic disease in TSC patients and identify a potential

54 emerging knowledge of the characteristics of aortic disease in Turner syndrome in comparison with Mar

55 The natural history of aortic diseases in patients with TGFBR1 or TGFBR2 mutati

56 Risk factors for thoracic aortic disease include increased hemodynamic forces on t

57 Thoracic aortic diseases, including aneurysms and dissections of

58 ence and extent of congenital abnormalities, aortic disease, intracardiac masses, and pericardial dis

59 The complexity of aortic disease is more fully revealed with new functiona

60 Endograft therapy for thoracic aortic disease is rapidly evolving.

61 ns, a multidisciplinary approach to thoracic aortic disease management, and a standardized protocol f

62 ited aortopathy and tested 248 probands with aortic disease or Marfan syndrome.

63 utation were more prone to developing severe aortic disease or valvular disease.

64 y rest on a broad knowledge base of thoracic aortic disease processes and experience in both open and

65 omposed of LTBP-3 and TGFbeta contributes to aortic disease progression.

66 ion mutation in PRKG1 as a cause of thoracic aortic disease provides further evidence that proper SMC

67 rities in the care of patients with thoracic aortic disease seem warranted and may reduce the inciden

68 enetics has heightened awareness of familial aortic disease such as the Marfan syndrome, bicuspid aor

69 Thoracic aortic diseases that involve progressive enlargement, ac

70 In addition to hypertension and inflammatory aortic disease, these hereditary aortopathies are import

71 ntly reported data may indicate IgG4-related aortic disease to be more common than widely realized.

72 Aortic disease was caused by a perturbed contractile app

73 Severe atherosclerotic proximal aortic disease was found in 39.6% of Group 1 and 10.8% o

74 ldwide that specialize in heritable thoracic aortic diseases, was used to gather data on 441 patients

75 sis and management of patients with thoracic aortic disease, which identified high-risk clinical feat

76 est reported cohort of Chinese patients with aortic disease who have undergone genetic testing.

77 Abdominal aortic aneurysm (AAA) is a common aortic disease with a progressive nature.