ライフサイエンスコーパス: acute graft rejection

1 ents in this study, irrespective of interval acute graft rejection.

2 R3 is a viable therapeutic target to prevent acute graft rejection.

3 s immune response in the clinical setting of acute graft rejection.

4 h a subnormal renal function and early-stage acute graft rejection.

5 tment is necessary for the efferent phase of acute graft rejection.

6 on has been limited by the high incidence of acute graft rejection.

7 t recipients correlates with the presence of acute graft rejection.

8 s in both the priming and effector phases of acute graft rejection.

9 ity in the transplanted hearts indicative of acute graft rejection.

10 hin host lymphoid tissue, is associated with acute graft rejection.

11 r antibodies nor CD8+ T cells participate in acute graft rejection.

12 human cardiac allograft specimens undergoing acute graft rejection.

13 d the incidence, timing, and risk factors of acute graft rejection.

14 for two decades to reverse steroid-resistant acute graft rejection.

15 CD4+ T cells are the primary mediators of acute graft rejection, although complement may contribut

16 reased recipient age, African American race, acute graft rejection and CMV infection were significant

17 sociated with the pharmacologic avoidance of acute graft rejection and the development of chronic tis

18 s strategy and could be used both to prevent acute graft rejection as well as for maintenance immunos

19 cells are both necessary and sufficient for acute graft rejection, as indicated by adoptive transfer

20 h cyclosporine, markedly attenuated not only acute graft rejection but also alloantibody elaboration

21 sk for posttransplant mortality, graft loss, acute graft rejection, chronic rejection, cancer, infect

22 actors during the first year posttransplant (acute graft rejection, chronically elevated anxiety, les

23 While on SJW, one patient developed acute graft rejection due to low CSA concentrations.

24 During acute graft rejection >90% of the anti-B10.A T cell repe

25 ells correlates closely with the presence of acute graft rejection in renal allograft recipients.

26 ogeneic blood transfusion causes accelerated acute graft rejection in the presence of the complete co

27 At six months, the rate of biopsy-confirmed acute graft rejection in the seronegative group was 52 p

28 These observations demonstrate that acute graft rejection in this model is associated with t

29 F) has been shown to reduce the incidence of acute graft rejection in three controlled trials of cada

30 normally observed and resulted in delayed or acute graft rejection (median survival times, 40 and 12

31 urvival advantage in Tg mice and resulted in acute graft rejection (n = 3).

32 t recipients to account for the avoidance of acute graft rejection or the development of chronic tiss

33 disease (OR = 2.67; 95% CI = 1.12-6.32), and acute graft rejection (OR = 3.01; 95% CI = 1.78-5.09).

34 : 18.76; 95% CI: 1.04-339.37; p = 0.047) and acute graft rejection (OR: 40.73, 95% CI: 3.63-456.98; p

35 ential to revise the clinical perspective on acute graft rejection, pending the results of larger stu

36 esponse is likely to be the driving force in acute graft rejection, posttransplantation induced autoi

37 ion of P5-activated syngeneic T cells led to acute graft rejection, suggesting that the homing of in

38 though it is believed that Th1 cells promote acute graft rejection, the role of these cells in chroni

39 e may expedite the noninvasive prediction of acute graft rejection, thus importantly assisting in est

40 To further investigate the role of LTs in acute graft rejection, we transplanted kidneys from CByD

41 Inductive OX40 stimulation induced acute graft rejection, which correlated with both IgG1 a