ライフサイエンスコーパス: primary graft dysfunction

1 The patient experienced no primary graft dysfunction.

2 e damage to subpleural pulmonary vessels and primary graft dysfunction.

3 uction immunosuppression and the presence of primary graft dysfunction.

4 olonged ventilation, renal insufficiency and primary graft dysfunction.

5 risk is directly related to the severity of primary graft dysfunction.

6 mong subjects who died by 30 days, 43.6% had primary graft dysfunction.

7 nical ventilation or the incidence of severe primary graft dysfunction.

8 ggested that HOPE was beneficial in reducing primary graft dysfunction.

9 was 298 min with no observed cases of severe primary graft dysfunction.

10 t contributor to donor heart dysfunction and primary graft dysfunction.

11 e prevented vascular leakage and ameliorated primary graft dysfunction.

12 ences in early post-HTx morbidity, including primary graft dysfunction (2.9% vs 1.7% vs 5.3%, P = .5)

13 ts at our program and graded the severity of primary graft dysfunction according to the International

14 ical circulatory support have been achieved, primary graft dysfunction after cardiac transplantation

15 Although many prognostic factors of primary graft dysfunction after liver transplantation (L

16 emia-reperfusion injury is the main cause of primary graft dysfunction after lung transplantation and

17 fidence interval [CI], 3.2-19.4%) for severe primary graft dysfunction after lung transplantation and

18 reperfusion injury is a major determinant of primary graft dysfunction after lung transplantation, an

19 y be a novel therapeutic strategy to prevent primary graft dysfunction after lung transplantation.

20 ility, and lung edema, is the major cause of primary graft dysfunction after lung transplantation.

21 needed in 3 patients (15%) because of severe primary graft dysfunction; all were eventually weaned.

22 However, there was no association between primary graft dysfunction and acute rejection or lymphoc

23 Primary graft dysfunction and allograft rejection repres

24 etion may help to predict the development of primary graft dysfunction and avoid the need for retrans

25 The incidence of primary graft dysfunction and cardiac allograft vasculop

26 ence of major complications including severe primary graft dysfunction and early mortality rates were

27 d a significantly higher incidence of severe primary graft dysfunction and higher short- and long-ter

28 ue sources identify patients at high risk of primary graft dysfunction and other pre- and post-transp

29 l-free DNA levels and the primary outcome of primary graft dysfunction and other transplant outcomes,

30 Postoperatively, the incidence of severe primary graft dysfunction and the incidence of acute ren

31 regression), 1-y patient and graft survival, primary graft dysfunction, and nonanastomotic biliary st

32 care unit and hospital length of stay (LOS), primary graft dysfunction at postoperative day 3, and ne

33 ms of MR and post-LTx complications, such as primary graft dysfunction, complicates its diagnosis and

34 Primary graft dysfunction contributes to nearly half of

35 Secondary endpoints included primary graft dysfunction, early posttransplant bleeding

36 coatomer subunit alpha [COPA] syndrome), and primary graft dysfunction following lung transplantation

37 ificant reduction in the incidence of severe primary graft dysfunction from 35% (8/23) to 8% (4/51) i

38 hypoalbuminemia, thrombocytopenia, and high primary graft dysfunction grade were multivariate predic

39 onal Society for Heart & Lung Tranplantation primary-graft dysfunction grade 3 (PGD3) within 72 h pos

40 Among the 334 recipients, 65 did not have primary graft dysfunction (grade 0), 130 had grade 1, 69

41 Postoperatively, the rates of primary graft dysfunction (grades 1 to 3) within 72 hour

42 nts surviving at least 1 year, those who had primary graft dysfunction had significantly worse surviv

43 Survivors of primary graft dysfunction have increased risk of death e

44 Long-term outcomes of subjects with primary graft dysfunction have not been studied.

45 Grade 3 primary graft dysfunction, higher degree of donor/recipi

46 the lung for ischemia reperfusion injury and primary graft dysfunction in the recipient.

47 d; 95% CI, 0.81-6.40; P = 0.011), and higher primary graft dysfunction incidence at day 3 (odds ratio

48 nonanastomotic biliary strictures frequency, primary graft dysfunction incidence, 1-y patient, and gr

49 ed use of cardiopulmonary bypass, and severe primary graft dysfunction increased the risk for death i

50 ve outcomes such as hospital length of stay, primary graft dysfunction, inotrope score, mechanical ci

51 Primary graft dysfunction is a common complication after

52 Primary graft dysfunction is a severe acute lung injury

53 Primary graft dysfunction is an important cause of morbi

54 Primary graft dysfunction is associated with an increase

55 which are now discarded because the risk of primary graft dysfunction is considered too great.

56 observational study cohorts at risk for ALI: primary graft dysfunction (N = 619) and acute respirator

57 ion injury, which may lead to lower rates of primary graft dysfunction necessitating extracorporeal m

58 The main outcome was primary graft dysfunction necessitating postoperative in

59 ansplant cell-free DNA increased the risk of primary graft dysfunction (odds ratio, 1.60; 95% confide

60 We evaluated the impact of primary graft dysfunction on acute rejection, lymphocyti

61 We examined the impact of primary graft dysfunction on bronchiolitis obliterans sy

62 r 3 y, or differences in incidence of severe primary graft dysfunction or acute cellular rejection.

63 o significant differences in rates of severe primary graft dysfunction or acute rejection within 1 y.

64 out the early posttransplant course, such as primary graft dysfunction or hyperacute rejection.

65 er lung allocation score was associated with primary graft dysfunction (P < 0.0001), postoperative ex

66 a/reperfusion injury-mediated (IRI-mediated) primary graft dysfunction (PGD) adversely affects both s

67 Severe primary graft dysfunction (PGD) after lung transplantati

68 e clinical use of circulating biomarkers for primary graft dysfunction (PGD) after lung transplantati

69 evels are associated with the development of primary graft dysfunction (PGD) after lung transplantati

70 1) levels in plasma would be associated with primary graft dysfunction (PGD) after lung transplantati

71 od cell (PRBC) transfusion and occurrence of primary graft dysfunction (PGD) and associated outcomes.

72 We investigated associations between primary graft dysfunction (PGD) and development of acute

73 Primary graft dysfunction (PGD) continues to be a potent

74 strongly predispose to the fatal syndrome of primary graft dysfunction (PGD) following lung transplan

75 (pTLC) is associated with a reduced risk of primary graft dysfunction (PGD) following lung transplan

76 Primary graft dysfunction (PGD) is a common complication

77 Primary graft dysfunction (PGD) is a leading cause of mo

78 Primary graft dysfunction (PGD) is a major complication

79 Primary graft dysfunction (PGD) is a major determinant o

80 Rationale: Primary graft dysfunction (PGD) is a severe form of acut

81 Primary graft dysfunction (PGD) is a significant cause o

82 Primary graft dysfunction (PGD) is a significant contrib

83 Primary graft dysfunction (PGD) is associated with incre

84 Severe primary graft dysfunction (PGD) is the leading cause of

85 Rationale: Primary graft dysfunction (PGD) is the leading cause of

86 Rationale: Primary graft dysfunction (PGD) is the leading cause of

87 Primary graft dysfunction (PGD) is the leading cause of

88 Primary graft dysfunction (PGD) is the leading cause of

89 Primary graft dysfunction (PGD) is the main cause of ear

90 Primary graft dysfunction (PGD) is the most important ca

91 Rationale: Primary graft dysfunction (PGD) is the principal cause o

92 er cardiac-related death, moderate or severe primary graft dysfunction (PGD) of the left ventricle, P

93 Noninvasive detection of primary graft dysfunction (PGD) remains a major challeng

94 Twenty-three patients with Grade 3 primary graft dysfunction (PGD) were frequency matched w

95 an transplant recipients, largely because of primary graft dysfunction (PGD), a major form of acute l

96 We sought to determine if primary graft dysfunction (PGD), a syndrome of acute lun

97 s) are associated with a higher incidence of primary graft dysfunction (PGD), although it remains unc

98 l allografts may be at an increased risk for primary graft dysfunction (PGD), the leading cause of ea

99 demographics may influence the incidence of primary graft dysfunction (PGD).

100 y of donor organs and by mortality following primary graft dysfunction (PGD).

101 of acceptability for transplant and risk of primary graft dysfunction (PGD).

102 implicates complement in the pathogenesis of primary graft dysfunction (PGD).

103 with poor early post-HT outcomes, including primary graft dysfunction (PGD).

104 with respect to graft loss, CLAD onset, and primary graft dysfunction (PGD).

105 n duration beyond 4 hours is associated with primary graft dysfunction (PGD).

106 antation with good early outcome [absence of primary graft dysfunction- (PGD) grade 3]; (II) PGD3: bi

107 0.001) were associated with higher rates of primary graft dysfunction (PGD3).

108 with a significantly reduced risk of severe primary graft dysfunction, postbypass severe right ventr

109 intensive care unit stay (P = 0.74), highest primary graft dysfunction score (P = 0.67) and hospital

110 e care unit stay, hospital stay, and highest primary graft dysfunction score within 72 hours) and lon

111 Wisconsin solution in grafts with subsequent primary graft dysfunction, suggesting a slower recovery

112 oups in 1-year survival, incidence of severe primary graft dysfunction, treated rejection during the

113 on study to predict recipients' post-surgery primary graft dysfunction using donors' gene expressions

114 All-cause mortality at 30 days was 42.1% for primary graft dysfunction versus 6.1% in patients withou

115 The overall incidence of primary graft dysfunction was 10.2% (95% confidence inte

116 hiolitis obliterans syndrome associated with primary graft dysfunction was independent of acute rejec

117 The incidence of severe primary graft dysfunction was not significantly differen

118 Severe edema resembling primary graft dysfunction was observed at 24 hours after

119 nterval significantly associated with severe primary graft dysfunction was the asystolic warm ischemi

120 In multivariable regression analysis, primary graft dysfunction was the predominant perioperat

121 In the univariable analysis, all grades of primary graft dysfunction were associated with a signifi

122 We sought to test the relationship of primary graft dysfunction with both short- and long-term