ライフサイエンスコーパス: aortic disease

1 ontribute to strategies to prevent and treat aortic disease.

2 M) a-actin, predispose to heritable thoracic aortic disease.

3 on the association between FBN2 variants and aortic disease.

4 nes for diagnosis and management of thoracic aortic disease.

5 team expertise in the care of patients with aortic disease.

6 in valvular heart disease, arrhythmias, and aortic disease.

7 he subgroup of patients with more aggressive aortic disease.

8 es regarding the management of patients with aortic disease.

9 s with distinct clinical features, including aortic disease.

10 ly increasing deltaK forming the hallmark of aortic disease.

11 ntial therapeutic agents to prevent thoracic aortic disease.

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

13 ntly associated with development of thoracic aortic disease.

14 netic variants in LOX predispose to thoracic aortic disease.

15 ular pathway that leads to familial thoracic aortic disease.

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

17 in MAT2A predispose individuals to thoracic aortic disease.

18 he most devastating complication of thoracic aortic disease.

19 r) have revolutionized treatment of thoracic aortic disease.

20 vascular smooth muscle cells will ameliorate aortic disease.

21 and subclinical coronary artery disease and aortic disease.

22 is available for evaluation of patients with aortic disease.

23 d decisions regarding early intervention for aortic disease.

24 is patient population, which had substantial aortic disease.

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

26 creased carotid and proximal atherosclerotic aortic disease.

27 patients referred for evaluation of thoracic aortic disease.

28 urbo SE sequences for evaluation of thoracic aortic disease.

29 regard to our understanding and treatment of aortic disease.

30 with suspected connective tissue or thoracic aortic diseases.

31 tic variants predispose individuals to these aortic diseases.

32 smooth muscle cell contraction and heritable aortic diseases.

33 nsidered as a therapeutic target for diverse aortic diseases.

34 and possible target for treatment for human aortic diseases.

35 alterations that predispose persons to these aortic diseases.

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

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

38 xpression of 14-3-3 proteins in inflammatory aortic disease, a rare human autoimmune disorder with in

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

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

41 and long-term surveillance of patients with aortic disease across its multiple clinical presentation

42 econstruction remains greater than repair of aortic disease alone.

43 derstanding of the genetic basis of thoracic aortic disease and abdominal aortic aneurysm disease.

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

45 al region predispose individuals to thoracic aortic disease and are less associated with the typical

46 racterizes familial associations of thoracic aortic disease and BAV, as well as cardiovascular and ao

47 Thoracic aortic disease and bicuspid aortic valve (BAV) likely ha

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

49 current biological understanding of thoracic aortic disease and describe how these new findings can c

50 pecific alpha-actin, predisposes to thoracic aortic disease and early onset coronary artery disease i

51 le identification of individuals at risk for aortic disease and facilitate prioritization of therapeu

52 abnormalities, resulting in life-threatening aortic disease and high risk of early death from aneurys

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

54 en identified for the management of thoracic aortic disease and the only options capable of preventin

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

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

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

58 rtrophic cardiomyopathy, channelopathies, or aortic diseases), and 124 098 external controls (individ

59 lves, 2 women (10%) with a family history of aortic disease, and 1 woman (5%) with familial thoracic

60 s, valvular disease, thromboembolic disease, aortic disease, and cerebrovascular diseases.

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

62 -onset <50 years, family history of thoracic aortic disease, and no history of hypertension.

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

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

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

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

67 specially in the management of patients with aortic disease both before and during pregnancy.

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

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

70 total of 60% of these patients had thoracic aortic disease, but only 20% were diagnosed with congeni

71 del of MFS to test for drugs that can revert aortic disease by enhancing Tfam levels and mitochondria

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

73 Our results indicate that BAV and thoracic aortic disease carry a significant familial association

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

75 ms, but the relative infrequency of thoracic aortic disease compared with other cardiovascular condit

76 , organ or limb malperfusion attributable to aortic disease, complications of reinterventions, or aor

77 Acta2(R149C/+) mice do not develop thoracic aortic disease despite decreased contraction of aortic s

78 channelopathies, cardiomyopathies, thoracic aortic disease, dyslipidemias, and congenital/structural

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

80 AND2, TBX20) and Mendelian forms of thoracic aortic disease (ELN, FBN1).

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

82 A categorical model composed of genetic aortic disease (GAD) (hazard ratio [HR], 3.4 [95% CI: 1.

83 nts associated with these heritable thoracic aortic disease genes, highlighting the importance of tai

84 ic aortic aneurysm and dissections (thoracic aortic disease), genetic data can be used to identify so

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

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

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

88 Aortic disease has many forms including aortic aneurysm

89 ressing comprehensive care for patients with aortic disease have been developed.

90 tcomes after surgical management of thoracic aortic disease have improved; however, the impact of sex

91 predispose individuals to heritable thoracic aortic disease (HTAD), but limited data are available to

92 es that cause BAV (9%) or heritable thoracic aortic disease (HTAD, 19%).

93 (LDS) compared with other heritable thoracic aortic diseases (HTADs).

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

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

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

97 g (19% versus 45%), and greater incidence of aortic disease in family members.

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

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

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

101 n on SMC function and potentially preventing aortic disease in the Acta2(R149C/+) mice.

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

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

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

105 d was a significant predictor of age-related aortic diseases in humans.

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

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

108 Thoracic aortic diseases, including aneurysms and dissections of

109 holistic approach to understanding thoracic aortic disease, integrating its embryological developmen

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

111 Thoracoabdominal aortic disease is a rare but life-threatening condition

112 Ascending thoracic aortic disease is an important cause of sudden death in

113 Aortic disease is defined by anatomic scalars quantifyin

114 Heritable thoracic aortic disease is due to altered genes that confer a hig

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

116 Endograft therapy for thoracic aortic disease is rapidly evolving.

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

118 .6; 95% CI, 1.4-22.3), and family history of aortic disease (mother: OR, 5.7; 95% CI, 1.4-22.3, sibli

119 , management and outcomes of the most common aortic diseases, namely, aortic aneurysms and acute aort

120 tion during pregnancy in women with thoracic aortic disease necessitates a multidisciplinary approach

121 ) (n = 861), nonsyndromic heritable thoracic aortic disease (nsHTAD) (n = 378), Turner syndrome (TS)

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

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

124 sly published AHA/ACC guidelines on thoracic aortic disease, peripheral artery disease, and bicuspid

125 sly published AHA/ACC guidelines on thoracic aortic disease, peripheral artery disease, and bicuspid

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

127 scalars quantifying aortic size, even though aortic disease progression initiates complex shape chang

128 rolled VSMC phenotypic modulation underlying aortic disease progression.

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

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

131 uideline for the Diagnosis and Management of Aortic Disease" provides recommendations to guide clinic

132 n-based studies highlight that the burden of aortic diseases remains high.

133 eatment of cerebrovascular diseases, central aortic disease, renovascular disease, and peripheral art

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

135 e Receptor 2 (CCR2) is a tissue biomarker of aortic disease severity, particularly in patients with a

136 Classification accuracy for predicting aortic disease state (normal, diseased with successful s

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

138 istinguish MFS from other heritable thoracic aortic disease syndromes that can present with skeletal

139 Thoracic aortic diseases that involve progressive enlargement, ac

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

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

142 The Registry of Aortic Diseases to Model Adverse Events and Progression

143 ive multicenter cohort (ROADMAP [Registry of Aortic Diseases to Model Adverse Events and Progression]

144 Aortic disease was caused by a perturbed contractile app

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

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

147 ard deviation]) suspected of having thoracic aortic disease were used to evaluate the proposed recons

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

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

150 Abdominal aortic aneurysm (AAA) is a severe aortic disease with a high mortality rate in the event o

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

152 in Sm22Cre+Wnk1(lox/lox) mice aggravated the aortic disease, with the formation of lethal abdominal a

153 scular Diseases (VASCERN, Heritable Thoracic Aortic Disease Working Group) and the Association for Eu