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1 tive sarcoma virus leads to the formation of erythroid bursts.
2 lted in a significant increase in numbers of erythroid bursts and the proportion of hemoglobinized ce
3 of markers that define cells giving rise to erythroid burst- and erythroid colony-forming unit (BFU-
4 event, but the possibility that the induced erythroid burst formation is mediated via interaction wi
6 nulocyte-macrophage colony forming unit, and erythroid burst forming unit growth in rats subjected to
7 anulocyte-macrophage colony forming unit and erythroid burst forming unit) hematopoietic progenitor c
8 throid, monocyte, megakaryocyte [CFU-GEMM]), erythroid (burst-forming unit-erythroid [BFU-E]), and gr
9 (colony-forming granulocytic-macrophage) and erythroid (burst-forming unit-erythroid) progenitor colo
10 lony-forming unit-granulocyte-monocytic) and erythroid (burst-forming unit-erythroid) progenitors.
11 ormal donor and chemotherapy patient-derived erythroid (burst-forming units-erythroid [BFU-E]), myelo
14 into adulthood showed a moderate decrease in erythroid burst-forming unit (BFU-E) and erythroid colon
16 well as in early erythropoiesis encompassing erythroid burst-forming unit (BFU-E) differentiation to
18 fetal hemoglobin-containing erythroblasts in erythroid burst-forming unit (BFUe) cultures from health
20 absolute number and frequency of both early (erythroid burst-forming unit [BFU-E]) and late erythroid
23 ed with their wild-type littermates, splenic erythroid burst-forming unit and high-proliferative pote
24 persons with discordant results and also in erythroid burst-forming unit colonies but not in those w
25 anulocyte-macrophage colony-forming unit and erythroid burst-forming unit colonies compared with plas
26 anulocyte-macrophage colony-forming unit and erythroid burst-forming unit colony formation compared w
27 +) hematopoietic cells and completely blocks erythroid burst-forming unit formation in normal human b
29 lose cultures, as indicated by more numerous erythroid burst-forming unit-derived colonies in low Epo
30 more CD34(+) cells (2.7-fold/kg/apheresis), erythroid burst-forming units (1.8-fold/kg/apheresis), a
31 the SP600125 inhibitor reduced the number of erythroid burst-forming units (BFU-e's) but not the more
34 macrophage colony-forming units (CFU-GM) and erythroid burst-forming units (BFU-E) were performed on
35 egaly accompanied with decreased bone marrow erythroid burst-forming units (BFU-Es) and colony-formin
36 toxicity of EFA to hematopoietic progenitors erythroid burst-forming units (BFU-Es) and granulocyte-m
38 d reduction in erythroid progenitors (mature erythroid burst-forming units [BFUEs]) was observed betw
39 9 than the normal hematopoietic progenitors, erythroid burst-forming units and granulocyte/monocyte c
40 fects because granulocyte-macrophage CFU and erythroid burst-forming units from STAT1(-/-) mice were
42 ells that can generate BMP4-dependent stress erythroid burst-forming units when cultured under stress
43 erm HSCs, common myeloid progenitors (CMPs), erythroid burst-forming units, colony-forming units in s
44 rogenitor cells (19-39% growth inhibition of erythroid burst-forming units, multilineage colony-formi
46 plete mobilization of BMP4-responsive stress erythroid burst-forming units; therefore, new stress pro
48 of 29 individuals with normal frequencies of erythroid bursts in culture responded to immunomodulatin
49 ated from patients with del(5q) MDS, whereas erythroid burst recovery increased proportionally to the
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