ライフサイエンスコーパス: transplant arteriosclerosis

1 ray of factors that favor the progression of transplant arteriosclerosis.

2 tolerance induction strategies that prevent transplant arteriosclerosis.

3 (T(reg) cells) expanded ex vivo can prevent transplant arteriosclerosis.

4 l wall from oxidative injury, and attenuates transplant arteriosclerosis.

5 ft itself, leading to increased formation of transplant arteriosclerosis.

6 hemokine receptor CCR7 in the development of transplant arteriosclerosis.

7 be used as cellular immunotherapy to control transplant arteriosclerosis.

8 ntigen can prevent CD25-CD4+ T-cell-mediated transplant arteriosclerosis.

9 ulatory T cells would reduce the severity of transplant arteriosclerosis.

10 Wegener granulomatosis, Behcet syndrome, and transplant arteriosclerosis.

11 cluding treatment of edema, endotoxemia, and transplant arteriosclerosis.

12 ts and xenografts correlates with absence of transplant arteriosclerosis.

13 fic regulation, which resulted in attenuated transplant arteriosclerosis.

14 for the development of chronic rejection and transplant arteriosclerosis.

15 nts with AGI-1096 decreases the incidence of transplant arteriosclerosis.

16 t, that is, the formation of microvessels in transplant arteriosclerosis.

17 raft, thereby attenuating the development of transplant arteriosclerosis.

18 essel wall from immune injury and attenuates transplant arteriosclerosis.

19 can play an important role in the process of transplant arteriosclerosis.

20 parity on the kinetics of the development of transplant arteriosclerosis.

21 nfluences the kinetics of the development of transplant arteriosclerosis.

22 play an important role in the development of transplant arteriosclerosis.

23 of FasL may have utility in the treatment of transplant arteriosclerosis.

24 ked evidence of chronic rejection, including transplant arteriosclerosis.

25 factor-I (IGF-I) is crucial in accelerating transplant arteriosclerosis.

26 beta treatment protects against experimental transplant arteriosclerosis.

27 plays a central role in the pathogenesis of transplant arteriosclerosis.

28 esent, immune sources of TGF-beta1 attenuate transplant arteriosclerosis.

29 hes to protect grafts against development of transplant arteriosclerosis.

30 NOS2, or iNOS) is upregulated in grafts with transplant arteriosclerosis.

31 ovide a genetic approach to the treatment of transplant arteriosclerosis.

32 mechanism whereby IGF-I exposure accelerates transplant arteriosclerosis.

33 survival of xenografts and the avoidance of transplant arteriosclerosis.

34 ted to the inhibitory effect of estradiol on transplant arteriosclerosis.

35 tion and luminal narrowing characteristic of transplant arteriosclerosis.

36 on within small arteries indicative of early transplant arteriosclerosis.

37 lls (SMCs) present in the intimal lesions of transplant arteriosclerosis?

38 blockade and CD8+ T-cell depletion abrogated transplant arteriosclerosis (9%+/-4% luminal occlusion 6

39 em cells are involved in the pathogenesis of transplant arteriosclerosis, an alloimmune initiated vas

40 jection by 16-24 weeks, including widespread transplant arteriosclerosis and focal and segmental glom

41 ibution of stem cells to the pathogenesis of transplant arteriosclerosis are controversial, eg, wheth

42 functional role of interferon (IFN)-gamma in transplant arteriosclerosis, BALB/c hearts were transpla

43 Acceleration of transplant arteriosclerosis by exposure to IGF-I is asso

44 onstrate that human T(reg) cells can inhibit transplant arteriosclerosis by impairing effector functi

45 odels of arterial injuries, vein grafts, and transplant arteriosclerosis, by which the major progress

46 of the infiltrate, but completely prevented transplant arteriosclerosis, diminished myocardial injur

47 recent research on the role of stem cells in transplant arteriosclerosis, discusses the mechanisms of

48 owed dense cellular infiltrates and moderate transplant arteriosclerosis (>75% of arteries showed 10-

49 rted via two separate strategies, to prevent transplant arteriosclerosis in a clinically relevant chi

50 rowth factor-I (IGF-I) on the development of transplant arteriosclerosis in a rat orthotopic aorta al

51 iac allografts, and prevented development of transplant arteriosclerosis in an MHC class II-mismatche

52 AR-C117977 also inhibited the development of transplant arteriosclerosis in aortic allografts partial

53 inical development of therapeutics targeting transplant arteriosclerosis in both allograft transplant

54 Estrogen prevents transplant arteriosclerosis in experimental cardiac and

55 We found that the in vivo development of transplant arteriosclerosis in human arteries was preven

56 ted the mechanisms of CD40-CD154-independent transplant arteriosclerosis in major histocompatibility

57 4 was not able to prevent the development of transplant arteriosclerosis in MHC class I-mismatched ao

58 val, but does not prevent the development of transplant arteriosclerosis in several models.

59 s age or recipient's age matters the most in transplant arteriosclerosis in the absence of such varia

60 o IGF-I prior to transplantation accelerates transplant arteriosclerosis in the rat aorta allograft m

61 Transplant arteriosclerosis initiated by CD4+ T cells wa

62 4(+) T cells resulted in a similar degree of transplant arteriosclerosis (intimal proliferation, 20+/

63 stradiol inhibition of SMC proliferation and transplant arteriosclerosis is down-regulation of IGF-IR

64 Although the pathogenesis of transplant arteriosclerosis is not yet fully understood,

65 Without immunosuppression, E2 inhibition of transplant arteriosclerosis is still associated with inh

66 Transplant arteriosclerosis is still the major complicat

67 Transplant arteriosclerosis is the hallmark of chronic a

68 The etiology of transplant arteriosclerosis is unknown, but current data

69 A4-4) to vascular cell injury and consequent transplant arteriosclerosis is unknown.

70 mmune events associated with acceleration of transplant arteriosclerosis may occur at an earlier time

71 This transplant arteriosclerosis model uses a 0.5% cholestero

72 CD80 and CD86, attenuated the development of transplant arteriosclerosis, mononuclear cell infiltrati

73 To determine the contribution to transplant arteriosclerosis of MHC and adhesion molecule

74 Cardiac transplant arteriosclerosis or cardiac allograft vasculo

75 eserving luminal geometry in mouse models of transplant arteriosclerosis or flow-induced vascular rem

76 During the development of transplant arteriosclerosis, PECAM-1 donor endothelial c

77 othelial cells attenuates the development of transplant arteriosclerosis, possibly by affecting macro

78 PD-L1.Ig use also prevented development of transplant arteriosclerosis post-CD154 mAb therapy.

79 nctional role of NOS2 in the pathogenesis of transplant arteriosclerosis remains unclear.

80 Protecting a vascularized graft from transplant arteriosclerosis requires inhibition of host

81 ortic allografts with 177/DST did not reduce transplant arteriosclerosis significantly (43.0+/-15.7%,

82 ed vascularized organ grafts will be lost to transplant arteriosclerosis sometime posttransplantation

83 lays a protective role in the development of transplant arteriosclerosis, suppressing neointimal smoo

84 sponses and vascular rejection that leads to transplant arteriosclerosis (TA) are poorly understood.

85 bone marrow-derived MSCs effectively control transplant arteriosclerosis (TA) by enhancing IL-10(+) a

86 apeutic T(reg) numbers on the development of transplant arteriosclerosis (TA) in human arterial graft

87 Transplant arteriosclerosis (TA) is the pathognomonic fe

88 flammation is central to the pathogenesis of transplant arteriosclerosis (TA).

89 may result from arterial injury, manifest as transplant arteriosclerosis (TA).

90 thway of allorecognition in the evolution of transplant arteriosclerosis, the main feature of chronic

91 t of cardiac allograft recipients attenuates transplant arteriosclerosis; this was associated with in

92 cludes spontaneous (native) atherosclerosis, transplant arteriosclerosis, vein graft atherosclerosis,

93 Transplant arteriosclerosis was evaluated in cardiac gra

94 f Fas to vascular cell injury and consequent transplant arteriosclerosis was investigated.

95 This CD40-CD154 pathway resistant transplant arteriosclerosis was mediated by IL-4, becaus

96 donor aortas into CCR7-deficient recipients, transplant arteriosclerosis was significantly elevated.

97 mediated pathways protect against or promote transplant arteriosclerosis, we used NOS2-deficient mice

98 ated that beta-gal+ cells of microvessels in transplant arteriosclerosis were derived from bone marro

99 tion, vessels of rejected hearts show florid transplant arteriosclerosis whereas those of accommodate