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1 ansplantation of ICAM-1 +/+, not ICAM-1 -/-, cardiac grafts).
2 phages that accumulated within the rejecting cardiac graft.
3 I-A(d)) or third-party (C3H, H2K(k), I-A(k)) cardiac grafts.
4 cells (MVEC) were developed from B6 and RIP3 cardiac grafts.
5  costimulation blockade to offspring-matched cardiac grafts.
6  exhibit delayed rejection of MHC-mismatched cardiac grafts.
7 reased in ischemia-reperfusion injury of the cardiac grafts.
8 aB-Luc) were used as donors or recipients of cardiac grafts.
9  to be relatively deficient in recipients of cardiac grafts.
10  rejected B10.D2, but not irrelevant B10.BR, cardiac grafts.
11 s had no effect on neutrophil trafficking in cardiac grafts.
12  major histocompatibility complex-mismatched cardiac grafts.
13 n molecule and cytokine expression in murine cardiac grafts.
14 ST 9 days) and even over Abeta (MST 20 days) cardiac grafts.
15 ased in mice receiving either Abeta or CIITA cardiac grafts.
16 may attenuate ischemia-reperfusion injury in cardiac grafts.
17 e endocrine tissue compared with that in the cardiac grafts.
18 ions) served as donors and recipients of the cardiac grafts.
19 transcripts were both expressed in rejecting cardiac grafts.
20  indefinite prolongation of (C57BL/10xCBA)F1 cardiac grafts.
21 s in cd39-deficient mice and in transplanted cardiac grafts.
22 in the endo-myocardium of AdCTLA4Ig-perfused cardiac grafts.
23 ion and vasculopathy compared with wild type cardiac grafts.
24 [PMNs]), T lymphocytes, and macrophages into cardiac grafts.
25  cyclosporine 15 mg/kg/day for 14 days after cardiac grafting.
26 nto rats that had been sensitized to hamster cardiac grafts 5 days earlier as a model for discordant
27 5/2 monotherapy uniformly produced permanent cardiac graft acceptance, whereas CTLA4Ig produced indef
28 ients (>100 days) challenged with second-set cardiac grafts accepted permanently donor-type (WF) graf
29 unction occurred in syngeneic and allogeneic cardiac grafts after transplantation.
30      In recipients bearing long-term beating cardiac grafts after treatment with anti-CD11a mAb, ther
31 into the lesions of chronic rejection in the cardiac grafts and homing of the cells to the bone marro
32 e permanently accept fully allogeneic (H-2d) cardiac grafts and secondary donor skin grafts, and that
33 eutrophil and macrophage chemoattractants in cardiac grafts and support the proposal that early infla
34 ce, failed to reject fully allogeneic (H-2d) cardiac grafts and that transgenic expression of antiapo
35 tion of arrhythmias, and formation of stable cardiac grafts are needed as the field advances toward t
36 ost important determinant of luminal loss in cardiac graft arteriosclerosis.
37 /endothelial cells could be detected in CoPP cardiac grafts, as compared with controls.
38 al and smooth muscle lineage potential after cardiac grafting, augmenting cardiac function although d
39 ation after circulatory death (DCD) enhances cardiac graft availability, but exposes hearts to potent
40                                              Cardiac graft beating was significantly better in the SO
41 mma (Mig) in acute rejection of A/J (H-2(a)) cardiac grafts by C57BL/6 (H-2(b)) recipients was tested
42 L/6 and B6.CCR5(-/-) recipients rejected A/J cardiac grafts by day 11, whereas rejection was delayed
43 n groups 2, 3, and 4 rejected their skin and cardiac grafts by postgrafting day 7.
44         Recipients of heterotopic allogeneic cardiac grafts (C3H donors into B6 recipients) were trea
45                                          All cardiac grafts continued to beat well throughout the inc
46                  In addition, IL-6-deficient cardiac grafts did not develop CAV after transplantation
47  which may contribute to early postoperative cardiac graft failure in the recipient.
48 ant CAD, posttransplant ischemic events, and cardiac graft failure.
49  for CAD, posttransplant ischemic events, or cardiac graft failure.
50 trategy to prevent the occurrence of primary cardiac graft failure.
51 e likely to be an important cause of primary cardiac graft failure.
52 ific hyporesponsiveness and maintained their cardiac grafts for markedly prolonged periods.
53 days of gestation (term = 145 days) received cardiac grafts from adult Wistar-Furth (275-350 g) rats.
54 swine following cotransplantation of VTL and cardiac grafts from fully MHC-mismatched donors.
55 ing preservation solution with AP39 protects cardiac grafts from prolonged ischemia, highlighting its
56                                              Cardiac grafts harvested on various days posttransplanta
57        Unfortunately, insufficient supply of cardiac grafts has become an obstacle.
58                                     WT donor cardiac grafts in CXCR3-/- recipients had a modest prolo
59                                     However, cardiac grafts in gammac(-/-)Rag(-/-) mice that received
60 olonged survival of MLR mismatched allogenic cardiac grafts in primates.
61                      Rejection of guinea pig cardiac grafts in rats depleted of complement takes plac
62 lucidate why CD154 blockade fails to protect cardiac grafts in sensitized recipients.
63                                 Furthermore, cardiac grafts in STAT4 -/- had fewer infiltrating CD45(
64  survival (P<0.0005), whereas CXCR3-/- donor cardiac grafts in WT recipients were rejected similar to
65          We have found that cold ischemia of cardiac grafts induces CAV after transplantation into Ra
66 emonstrate the approach to implantation of a cardiac graft into the intra-abdominal position in a bab
67                         The use of PCMV-free cardiac grafts is beneficial in reducing the direct effe
68                         In the clinic, donor cardiac graft ischemia time is limited to within a few h
69 -DMalpha and beta2-microglobulin (beta2m) in cardiac grafts lead to greater (8-10 times) graft surviv
70 c problem, resulting in the majority of late cardiac graft losses.
71 Transplant arteriosclerosis was evaluated in cardiac grafts placed into knockout recipients heterozyg
72             At day 55 after transplantation, cardiac grafts placed into STAT4 -/- (n=10) had reduced
73          We report several new biomarkers of cardiac graft quality, such as LV function and heart-typ
74 potential as novel biomarkers for evaluating cardiac graft quality, unlike lactate release after 10 m
75                  RESULT: CD4 T cell-mediated cardiac graft rejection is inhibited using RIP3 deficien
76 population that has been linked to renal and cardiac graft rejection, which was originally thought to
77 nd a shaper of T cell lineage development in cardiac graft rejection.
78 comprehensive analysis of gene expression in cardiac grafts secondary to I/R using microarray technol
79   The ability of epicardial cells to enhance cardiac graft size and function makes them a promising a
80 rates in vivo, resulting in 2.6-fold greater cardiac graft size and simultaneously augmenting graft a
81         It is not only useful for addressing cardiac graft-specific questions but also provides mecha
82  microg/mouse, i.p.; day -7) did not prolong cardiac graft survival (MST 12 days).
83 ytes from tolerant swine (group 6) prolonged cardiac graft survival as much as 123 days, whereas dono
84 yte infusion demonstrated slightly prolonged cardiac graft survival but all rejected their grafts, hi
85  the CD28/B7 costimulatory pathway prolonged cardiac graft survival for >100 days in 100% of wild-typ
86 /memory cells and abrogated acute rejection (cardiac graft survival for >30 days), paralleled by sele
87 rolonged the fully MHC mismatched allogeneic cardiac graft survival in a donor-specific fashion.
88  or by tissue allografts, increases skin and cardiac graft survival in mice receiving rapamycin, in a
89                              Prolongation of cardiac graft survival is associated with activation of
90 ant rejection in that its modulation affects cardiac graft survival.
91          Indeed, we identified 3234 genes in cardiac grafts that were down-regulated by MR1 in naive
92 ficient mice were used as donors of skin and cardiac grafts to eliminate the direct CD4(+) T cell res
93                       Euthymic recipients of cardiac grafts treated with an immunosuppressive regimen
94 y for the quantitative assessment of in vivo cardiac graft viability and tracking of passenger leukoc
95                   Modest prolongation of CBK cardiac grafts was induced in CBA mice fed with multiple
96      Nude or Lewis rats receiving guinea pig cardiac grafts were assigned to one of three groups: no
97                                     Skin and cardiac grafts were monitored by daily visual inspection
98                                 PVG.1A (C6-) cardiac grafts were rejected acutely (6-7 days) by untre
99                                   Allogeneic cardiac grafts were stored at 4 degrees C for 4 hr befor
100 ng allograft rejection and tolerance, BALB/c cardiac grafts were transplanted into wild-type or IL-6-
101                         ACI recipients of WF cardiac grafts were treated either with allochimeric [al
102  received two-haplotype fully MHC-mismatched cardiac grafts with a 12-day course of tacrolimus.
103 vealed high interleukin (IL)-6 expression in cardiac grafts with CAV.
104                                          The cardiac grafts with the attached aorta were harvested.
105 ipients depleted of CD8 T cells rejected A/J cardiac grafts within 10 days, allografts were not rejec
106 ls carrying host blood but relatively sparse cardiac grafts within engineered tissues, regardless of
107 its subsequent engraftment of donor islet or cardiac grafts without further treatment.

 
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