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1 nits, multilineage colony-forming units, and granulocyte-macrophage colony-forming units).
2 early (cobblestone forming cells) and late (granulocyte-macrophage colony forming unit and erythroid
3 T/HS demonstrated a significant decrease in granulocyte-macrophage colony-forming unit and erythroid
4 rats caused a significant suppression of BM granulocyte-macrophage colony-forming unit and erythroid
5 y by expanding the pool of cells between the granulocyte-macrophage colony-forming unit and mature ne
6 ts by SP(1-4) on the proliferation of early (granulocyte-macrophage colony-forming units) and late (l
7 rrow cellularity, cobblestone forming cells, granulocyte-macrophage colony forming unit, and erythroi
8 inhibitor p21WAF1/Cip1 and Survivin enhance granulocyte macrophage colony-forming unit (CFU-GM) cell
9 peptides suppressed the colony formation of granulocyte macrophage colony-forming units (CFU-GMs) in
10 ched and mismatched CD56(+) cells to inhibit granulocyte macrophage-colony-forming unit (CFU-GM) form
11 oietic regulation: pro-proteinase 3 inhibits granulocyte macrophage-colony-forming unit (CFU-GM) grow
12 cts of imatinib mesylate on primary leukemic granulocyte macrophage-colony-forming unit (CFU-GM) prog
13 GFP) in primary mouse marrow cells increased granulocyte macrophage-colony-forming units (CFU-GM) by
14 ) in vivo in allogeneic recipients, and more granulocyte macrophage-colony-forming units (CFU-GMs) in
15 NC) (median slope per day, -0.032; P = .03), granulocyte-macrophage colony-forming unit (CFU-GM) (med
16 videnced by the presence of FLT3/ITD in both granulocyte-macrophage colony-forming unit (CFU-GM) and
17 protein induced a hypersensitive pattern of granulocyte-macrophage colony-forming unit (CFU-GM) colo
18 mice, reduced numbers of PMF CD34+ cells and granulocyte-macrophage colony-forming unit (CFU-GM) comp
20 ne marrow cells to examine GM-CSF-stimulated granulocyte-macrophage colony-forming unit (CFU-GM) grow
21 ions of CD34(+) and CD34(+)CD38(-) cells and granulocyte-macrophage colony-forming unit (CFU-GM).
24 s erythroid burst-forming units (BFU-Es) and granulocyte-macrophage colony-forming units (CFU-GMs) wa
25 P-1alpha enhanced colony formation of marrow granulocyte/macrophage colony-forming units (CFU-GM), re
26 one marrow stem cell proliferation, that is, granulocyte/macrophage colony-forming units (CFU-GMs) by
27 ultured for erythroid burst-forming unit and granulocyte-macrophage colony-forming unit colonies to a
28 (blast-forming unit-erythroid) and myeloid (granulocyte-macrophage colony-forming unit) colony forma
29 CD34+ cell concentrations correlate with granulocyte-macrophage colony-forming unit counts as wel
30 ma-secretase inhibitor directly promoted the granulocyte-macrophage colony-forming unit (GM-CFU).
31 To formally test the hypothesis that the granulocyte/macrophage colony-forming unit (GM-CFU) cell
32 (burst-forming unit-erythroid [BFU-E]), and granulocyte-macrophage (colony-forming unit-granulocyte-
34 % inhibition of in vitro colony formation of granulocyte-macrophage colony-forming units, multilineag
35 nfection-induced increases in proliferation, granulocyte macrophage colony-forming unit production, a
36 cial effect of Synthokine on the recovery of granulocyte-macrophage colony-forming units that was sig
38 BSCs was determined by measuring survival of granulocyte-macrophage colony-forming units with (90)Y i
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