1 These findings indicate that the new
antirejection agent rapamycin inhibits hepatic fibrosis
2 Reduced dependence on
antirejection agents, improved long-term allograft survi
3 Antirejection (
anti-CD154) therapy was discontinued, and
4 with the currently available transplantation
antirejection drugs are an increased susceptibility to i
5 Commonly used
antirejection drugs are excellent at inhibiting the adap
6 ical treatments such as cancer chemotherapy,
antirejection drugs used in organ transplantation, and c
7 dvantages of the most widely used transplant
antirejection drugs--CsA and the glucocorticoids.
8 These data describe a moderate
antirejection effect of G-CSF administration.
9 cribe a marker or possible mechanism of this
antirejection effect.
10 ting that these receptors have both pro- and
antirejection effects.
11 mposite tissue allograft model to assess the
antirejection efficacy and systemic toxicity of combinat
12 red to have occurred based on treatment with
antirejection medication and/or histology.
13 such that the recipient will not require any
antirejection medication.
14 Combined therapy with antibiotics and
antirejection medications (ART) was administered to 12 o
15 y acute rejection (AR) events using specific
antirejection medications and to validate rejected data
16 sm for at least 6 months were withdrawn from
antirejection medications for 1-3 years (mean, 28 months
17 body more than 20% (56% vs. 14%), and use of
antirejection medications in the first year (33% vs. 9.2
18 e still needed and will allow the use of new
antirejection medications, resulting in improved outcome
19 fer significant adverse effects from chronic
antirejection medications.
20 = 82), (2) recipients switched to FK506 for
antirejection or rescue therapy (n = 61), and (3) recipi
21 , and 21, we treated one group with a potent
antirejection regimen.
22 nature of post-LT recurrence and concurrent
antirejection regimens should not discourage systemic tr
23 In the
antirejection rescue group, patient survival rates at 6
24 immunosuppression, even when a high dose of
antirejection rescue therapy has failed.
25 sma cell-targeted therapy (bortezomib) as an
antirejection strategy.
26 This response may be caused by the
antirejection therapeutics, and in an earlier report we
27 ith important consequences for the design of
antirejection therapeutics.
28 Antirejection therapies are not always effective, must b
29 plasma (BKP) (group 1) and also tried other
antirejection therapies in 13 patients with BK virus in
30 Most
antirejection therapies target immune activation but may
31 ositive UFCs that completely normalized with
antirejection therapy (n=8); group III--stable patients
32 acute rejection showed complete response to
antirejection therapy (P=0.25 vs. patients with borderli
33 atients with BRR did not respond to standard
antirejection therapy and had a substantial increase in
34 sely associated with the initial response to
antirejection therapy and long-term graft failure.
35 ff defined acute TCMR should be treated with
antirejection therapy and maximized maintenance immunosu
36 r tubulitis, are correlated with response to
antirejection therapy and/or 1-yr clinical outcome.
37 outcome and novel therapeutic approaches for
antirejection therapy based on targeting of chemokines a
38 for graft loss, and the initial response to
antirejection therapy can predict long-term graft outcom
39 Initial
antirejection therapy in 12 cases led to clearance of th
40 ternative to the conventional drugs used for
antirejection therapy in renal transplantation.
41 reviewed the clinical course and response to
antirejection therapy of 24 patients with borderline cha
42 Following
antirejection therapy of acute TCMR, surveillance protoc
43 y single antigen bead assays 12 months after
antirejection therapy onset.
44 harge and at time of AR before initiation of
antirejection therapy or at matching timepoints in patie
45 Effective
antirejection therapy results in a rapid down-regulation
46 No other
antirejection therapy was given.
47 Usual
antirejection therapy was instituted in all but two epis
48 Complete response to
antirejection therapy was seen in 15/24 (63%), partial r
49 esponse, partial response and no response to
antirejection therapy were observed in 16/24 (66.7%), 3/
50 elatacept that are refractory to traditional
antirejection therapy with corticosteroids and polyclona
51 safe and allows the avoidance of unnecessary
antirejection therapy with its attendant side effects an
52 nal antibody or gallium nitrate was used for
antirejection therapy, (2) this immune status is charact
53 sAMRV), and AMRV showed similar responses to
antirejection therapy, whereas the grafts with v2- or v3
54 MSCs may serve as a new, safe, and effective
antirejection therapy.
55 evel of HCV RNA and genotype and the type of
antirejection therapy.
56 te rejection, and decreased after successful
antirejection therapy.
57 cute rejection, with a subsequent rise after
antirejection therapy.
58 -2 only) and immediately after completion of
antirejection therapy.
59 episodes of acute rejection and response to
antirejection therapy.
60 ting grafts could be targeted for additional
antirejection therapy.
61 he urine increases in response to successful
antirejection therapy.
62 uld permit the assessment of the efficacy of
antirejection therapy.
63 transplanted intestine, and the response to
antirejection therapy.
64 steroid and OKT3 resistance within 48 hr of
antirejection therapy.
65 d, but were not eliminated, after successful
antirejection therapy.
66 Both patients had received recent
antirejection treatment and presented with fever, hepati
67 (1) CB and PB prevented unnecessary
antirejection treatment in 44% of our recipients with su
68 level of enzymes in serum, glycemia, type of
antirejection treatment instituted, and response to trea
69 Cautious
antirejection treatment to patients with active BKP or B
70 Response to
antirejection treatment was 25%, 40%, 88%, 78%, 50%, and
71 The development of acute rejection or
antirejection treatment with methylprednisolone did not
72 The cumulative probability of receiving
antirejection treatment within 1 year was lower in the M
73 One loss was immediate despite
antirejection treatment, 1 secondary to nonresolving rej
74 esponse, partial response, or no response to
antirejection treatment, depending on whether the posttr
75 Given the potential adverse effects of
antirejection treatment, especially in hepatitis C virus
76 files reflect variability in the response to
antirejection treatment.
77 n, showed histological improvement following
antirejection treatment.
78 ith grade V, hyperglycemia persisted despite
antirejection treatment.
79 essary and could predict graft outcome after
antirejection treatment.
80 stently reliable and can lead to unnecessary
antirejection treatment.
81 agnosis (Banff criteria) and the response to
antirejection treatment.
82 mprovement of kidney allograft function upon
antirejection treatment.
83 ts in adverse outcomes, and neither requires
antirejection treatment.
84 re placed in three groups according to their
antirejection treatment: group I (n = 10), plasma exchan
85 ion to study the rejection process, test new
antirejection treatments, tolerance induction protocols