ライフサイエンスコーパス: cardiac allograft vasculopathy

1 nhibitors protect against the development of cardiac allograft vasculopathy.

2 finitively link indirect allorecognition and cardiac allograft vasculopathy.

3 onary endothelial dysfunction contributes to cardiac allograft vasculopathy.

4 accelerated form of arteriosclerosis, termed cardiac allograft vasculopathy.

5 not STAT6, contribute to the development of cardiac allograft vasculopathy.

6 type of graft modification does not prevent cardiac allograft vasculopathy.

7 days and all long-surviving hearts developed cardiac allograft vasculopathy.

8 fter intracoronary stenting in patients with cardiac allograft vasculopathy.

9 giographic success in selected patients with cardiac allograft vasculopathy.

10 cularly immunosuppression, in these forms of cardiac allograft vasculopathy.

11 n coronary function in patients with diffuse cardiac allograft vasculopathy.

12 ms of angioscopically heterogeneous forms of cardiac allograft vasculopathy.

13 ting cellular trafficking, alloimmunity, and cardiac allograft vasculopathy.

14 eactive T cell activation and development of cardiac allograft vasculopathy.

15 pharmacotherapies to halt the progression of cardiac allograft vasculopathy.

16 No difference was found in deaths due to cardiac allograft vasculopathy.

17 modeling, may be an important determinant of cardiac allograft vasculopathy.

18 on and is associated with the development of cardiac allograft vasculopathy.

19 levels, which may in turn reduce the risk of cardiac allograft vasculopathy.

20 gnificant risk factor for the development of cardiac allograft vasculopathy.

21 well as to suppress the late development of cardiac allograft vasculopathy.

22 the association of mode of brain death with cardiac allograft vasculopathy.

23 arly and more severe allograft rejection and cardiac allograft vasculopathy.

24 ntrast with the known suppression by iNOS of cardiac allograft vasculopathy.

25 or and immunosuppressive agent, may suppress cardiac-allograft vasculopathy.

26 o be beneficial in preventing development of cardiac allograft vasculopathy, a long-term nemesis in c

27 se include a higher risk of acute rejection, cardiac allograft vasculopathy after heart transplantati

28 -segment-elevation myocardial infarction and cardiac allograft vasculopathy after heart transplantati

29 er transplantation, may increase the risk of cardiac allograft vasculopathy and allograft loss, but n

30 cant determinant for the late development of cardiac allograft vasculopathy and influences long-term

31 Understanding of the mechanisms surrounding cardiac allograft vasculopathy and insight into the poss

32 F may provide long-term benefits in reducing cardiac allograft vasculopathy and those evaluating the

33 ated by cohort for time until graft failure, cardiac allograft vasculopathy, and hospitalization for

34 ET-1 may also play a significant role in cardiac allograft vasculopathy, and in animal models, ER

35 antation and reflects diastolic dysfunction, cardiac allograft vasculopathy, and poor late outcome.

36 delayed alloantibody production, suppressed cardiac allograft vasculopathy, and tended to further pr

37 hogenesis, natural history, and diagnosis of cardiac allograft vasculopathy, and to outline new preve

38 ion and risk stratification of patients with cardiac allograft vasculopathy are problematic.

39 oronary IVUS data show that H+LTx attenuates cardiac allograft vasculopathy by decreasing the rate of

40 TAT4-mediated signaling pathways may promote cardiac allograft vasculopathy by directing Th1-specific

41 Moreover, imatinib mesylate enhanced rat cardiac allograft vasculopathy, cardiac fibrosis, and la

42 letion to modulate alloimmunity or attenuate cardiac allograft vasculopathy (CAV) (classic chronic re

43 acute antibody-mediated rejection (AMR) and cardiac allograft vasculopathy (CAV) after human heart t

44 Group 1 animals developed cardiac allograft vasculopathy (CAV) and rejection.

45 ual targets suggest their important roles in cardiac allograft vasculopathy (CAV) and rejection.

46 hort course of cyclosporine developed florid cardiac allograft vasculopathy (CAV) and were rejected w

47 e evaluated the association between Lp-PLA2, cardiac allograft vasculopathy (CAV) assessed by 3D intr

48 as associated with an increased incidence of cardiac allograft vasculopathy (CAV) at 1 year postcardi

49 ulted in prolonged graft survival and marked cardiac allograft vasculopathy (CAV) by histology (mean

50 Cardiac allograft vasculopathy (CAV) has a high prevalen

51 Cardiac allograft vasculopathy (CAV) has an incidence of

52 eous coronary intervention (PCI) to palliate cardiac allograft vasculopathy (CAV) has been associated

53 sessed clinical predictors of the process of cardiac allograft vasculopathy (CAV) in 39 consecutive p

54 tomography angiography (CCTA) for detecting cardiac allograft vasculopathy (CAV) in comparison with

55 elial dysfunction may be an early marker for cardiac allograft vasculopathy (CAV) in orthotopic heart

56 ls (APCs) do not reject acutely, but develop cardiac allograft vasculopathy (CAV) in untreated recipi

57 Cardiac allograft vasculopathy (CAV) is a common cause o

58 eful model that has evolved for the study of cardiac allograft vasculopathy (CAV) is a heterotopic (a

59 Cardiac allograft vasculopathy (CAV) is a major cause of

60 Cardiac allograft vasculopathy (CAV) is a major impedime

61 Cardiac allograft vasculopathy (CAV) is a major limitati

62 Chronic rejection in transplanted hearts or cardiac allograft vasculopathy (CAV) is the leading caus

63 Cardiac allograft vasculopathy (CAV) is the main cause o

64 Because cardiac allograft vasculopathy (CAV) is the major cause

65 Cardiac allograft vasculopathy (CAV) is the preeminent c

66 Cardiac allograft vasculopathy (CAV) is the principal ca

67 Although cardiac allograft vasculopathy (CAV) is typically charac

68 hy has been clearly established, its role in cardiac allograft vasculopathy (CAV) is unclear.

69 Cardiac allograft vasculopathy (CAV) limits the long-ter

70 el wall inflammation and its significance in cardiac allograft vasculopathy (CAV) progression.

71 of concomitant in-stent restenosis (ISR) and cardiac allograft vasculopathy (CAV) progression.

72 The mechanisms and treatment of cardiac allograft vasculopathy (CAV) remain elusive.

73 Cardiac allograft vasculopathy (CAV) remains a leading c

74 Cardiac allograft vasculopathy (CAV) remains the Achille

75 Cardiac allograft vasculopathy (CAV) remains the leading

76 Cardiac allograft vasculopathy (CAV) remains the leading

77 cular magnetic resonance (CMR) for detecting cardiac allograft vasculopathy (CAV) using contemporary

78 Cardiac allograft vasculopathy (CAV) was graduated in ac

79 A role for natural killer (NK) cells in cardiac allograft vasculopathy (CAV) was suggested by ou

80 Progressive arterial stenosis (cardiac allograft vasculopathy (CAV)) is a leading cause

81 graft arteriosclerosis (AGA), also known as cardiac allograft vasculopathy (CAV), after cardiac tran

82 Cardiac allograft vasculopathy (CAV), an unusually accel

83 on the initial TTE for recipient mortality, cardiac allograft vasculopathy (CAV), and primary graft

84 of CD8 lymphocytes, in chronic rejection or cardiac allograft vasculopathy (CAV), is incompletely un

85 Chronic rejection, or cardiac allograft vasculopathy (CAV), remains the leadin

86 f TSP-1 in allografts and the development of cardiac allograft vasculopathy (CAV).

87 ecruitment and precede intimal thickening in cardiac allograft vasculopathy (CAV).

88 rosis play a major role in the occurrence of cardiac allograft vasculopathy (CAV).

89 es of AR, graft survival, and development of cardiac allograft vasculopathy (CAV).

90 owth factors are postulated to contribute to cardiac allograft vasculopathy (CAV).

91 helium is associated with the development of cardiac allograft vasculopathy (CAV).

92 l homeostasis may prevent the development of cardiac allograft vasculopathy (CAV).

93 art is a central event in the development of cardiac allograft vasculopathy (CAV).

94 chronic rejection of transplanted hearts or cardiac allograft vasculopathy (CAV).

95 n the pathophysiologic mechanisms underlying cardiac allograft vasculopathy (CAV).

96 efficacy of immunotherapy or development of cardiac allograft vasculopathy (CAV).

97 chronic rejection of transplanted hearts, or cardiac allograft vasculopathy (CAV).

98 pressures to augment angiographic grading of cardiac allograft vasculopathy (CAV); however, no data e

99 gic risk factors with the different forms of cardiac allograft vasculopathy detected angioscopically.

100 icacy to prolong graft survival and to delay cardiac allograft vasculopathy development and antidonor

101 ngation of graft survival and suppression of cardiac allograft vasculopathy development.

102 munologic risk factors to the development of cardiac allograft vasculopathy distinguished angioscopic

103 ly events influence the later development of cardiac allograft vasculopathy following heart transplan

104 ed into STAT6 -/- (n=11), the development of cardiac allograft vasculopathy (frequency 62+/-8%, sever

105 4C T cells caused cardiac allograft vasculopathy in the absence of other T

106 y, we sought to examine the heterogeneity of cardiac allograft vasculopathy in vivo using coronary an

107 Cardiac allograft vasculopathy is a complicated interpla

108 These findings indicate that cardiac allograft vasculopathy is a heterogeneous diseas

109 Cardiac allograft vasculopathy is a key prognostic deter

110 Cardiac allograft vasculopathy is a major cause of death

111 Cardiac allograft vasculopathy is a major challenge to l

112 Cardiac allograft vasculopathy is a multifactorial proce

113 s to treat discrete lesions in patients with cardiac allograft vasculopathy is associated with higher

114 Cardiac allograft vasculopathy is the major cause of lat

115 Cardiac allograft vasculopathy is the major limiting fac

116 cacy in reducing restenosis in patients with cardiac allograft vasculopathy is unknown.

117 rferon-gamma--producing T cells and enhanced cardiac allograft vasculopathy lesion formation.

118 Cardiac allograft vasculopathy lesions contain alloreact

119 associated with intermediate-term mortality, cardiac allograft vasculopathy, or primary graft failure

120 imary immunosuppressant attenuates long-term cardiac allograft vasculopathy progression and may impro

121 ucing calcineurin inhibitor use, attenuating cardiac allograft vasculopathy progression and reducing

122 osuppressant in the long-term attenuation of cardiac allograft vasculopathy progression and the effec

123 SRL as primary immunosuppression attenuates cardiac allograft vasculopathy progression.

124 s a primary immunosuppressant in attenuating cardiac allograft vasculopathy progression.

125 rular filtration rate, previously documented cardiac allograft vasculopathy), relative perfusion defe

126 Cardiac transplant arteriosclerosis or cardiac allograft vasculopathy remains the leading cause

127 particular, by chronic rejection leading to cardiac allograft vasculopathy, remains a major cause of

128 IDEC-131-treated grafts had higher cardiac allograft vasculopathy severity scores during tr

129 Cardiac allograft vasculopathy severity varied with time

130 reased graft survival and the development of cardiac allograft vasculopathy, suggesting a contributio

131 ne in reducing the severity and incidence of cardiac-allograft vasculopathy, suggesting that everolim

132 Cardiac allograft vasculopathy, the nature of the inflam

133 study a mouse model of autoantibody-mediated cardiac allograft vasculopathy to clarify the alloimmune

134 tter understanding of the pathophysiology of cardiac allograft vasculopathy to direct interventions f

135 Similarly, cardiac allograft vasculopathy up to 5 years and primary

136 tect the heart graft from the development of cardiac allograft vasculopathy using coronary three-dime

137 a clinically relevant large animal model of cardiac allograft vasculopathy, we immunized MHC inbred

138 ption factor signaling pathways that mediate cardiac allograft vasculopathy, we used mice with target