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1 e fludarabine phosphate and cyclophosphamide conditioning therapy.
2 r fludarabine phosphate and cyclophosphamide conditioning therapy.
3 -based nonmyeloablative and irradiation-free conditioning therapy.
4 chronic myeloid leukemia after myeloablative conditioning therapy.
5 with systemic acute GVHD and full-intensity conditioning therapy.
6 mited to patients who received myeloablative conditioning therapy.
7 were started on day -3 to avoid overlap with conditioning therapy.
9 lasma antioxidant status was measured before conditioning therapy and serially at days 1, 3, 7, 10, a
10 LC2s) in the lower GI tract are sensitive to conditioning therapy and show very limited ability to re
11 under nonmyeloablative and irradiation-free conditioning therapy, and the blocking the CD40/CD154 pa
14 who successfully underwent nonmyeloablative conditioning therapy followed by infusion of partially m
15 used intravenous busulfan and fludarabine as conditioning therapy for allogeneic hematopoietic stem c
16 transplantation after standard myeloablative conditioning therapy for haematological malignant disord
17 having laboratory values before the start of conditioning therapy for unconjugated serum bilirubin co
18 ve days immediately before the initiation of conditioning therapy (fractionated total-body irradiatio
21 monoclonal antibodies (mAb) and intensified conditioning therapy, including fractionated total body
26 high level of safety and fast recovery from conditioning therapy-related side effects after the Bu-F
27 c mechanisms are altered by donor T cells or conditioning therapy, resulting in exacerbation of GVHD.
28 g daily) were administered with the start of conditioning therapy, until at least 120 days after SCT.
29 from haploidentical family members following conditioning therapy using total body irradiation (TBI)
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