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1 CFU-GM were also reduced in these patients, but with con
5 ed that rhG-CSF-recruited CFU-Meg(blood) and CFU-GM(blood) were considerably more radiosensitive than
8 e expansion of total cells, CD34+ cells, and CFU-GM and enhances the pool of early CD34+ CD33(dim) ce
10 Trauma plasma inhibits bone marrow BFU-E and CFU-GM colony growth for up to 2 weeks after injury.
11 ors showed that this inhibition of BFU-E and CFU-GM colony growth was mediated by bone marrow stroma.
12 environment, we compared growth of BFU-E and CFU-GM from 7-14-wk-old FL, 11-20-wk-old fetal bone marr
15 2 antibody reduced femoral CFU-E, BFU-E, and CFU-GM content to less than half that found in phenylhyd
16 In addition, platelet, reticulocyte, and CFU-GM regeneration were significantly accelerated in mi
17 o control levels after 5 days treatment, and CFU-GM were significantly reduced (65%) after 7 days tre
18 n addition to osteoclast progenitors such as CFU-GM, earlier hematopoietic progenitors are also uniqu
19 reshly isolated CD34(+) cells; chemo-attract CFU-GM- and CFU-Meg-derived cells as well as other CD34(
20 significantly reduced while peripheral blood CFU-GM, BFU-E, and CFU-E was increased in the trauma pat
21 TBI caused a dose-dependent decrease of both CFU-GM(femur) (D0, 136 cGy) and CFU-Meg(femur) (D0, 148
25 -macrophage colony-forming progenitor cells (CFU-GM); in contrast, only Mll(PTD/WT) FLC had increased
27 ent pairs, donor CD56(+) cells inhibited CML CFU-GM comparably to effectors from 14 HLA-mismatched un
32 Average D0 values for TBI were 53 cGy for CFU-GM(blood) and 40 cGy for CFU-Meg(blood) D0 values fo
37 age [CFU-GM]) showed a threefold increase in CFU-GM from ARH-77 marrow versus controls (185 +/- 32 v
39 ated mice exhibited significant increases in CFU-GM compared with the saline-treated control groups.
40 th IFN-alpha showed a threefold reduction in CFU-GM amplification in responders (P = 0.03) but no sig
41 fect on BM CFU over time, FL alone increased CFU-GM and CFU-GEMM threefold and fivefold, respectively
42 lines, as determined by ELISA; and increased CFU-GM formation and osteoclastogenesis as determined ex
45 concentration used, the Vav AS ODN inhibited CFU-GM colony formation from 66% to 81% when compared wi
47 that NK-A (10(-7) to 10(-12) mol/L) inhibits CFU-GM proliferation but stimulates erythroid progenitor
48 neic T cells preferentially inhibit leukemic CFU-GM based on overexpression of proteinase 3, and that
50 ed on c-kit fluorescence, over 88% of CFU-M, CFU-GM, and CFU-SCF were found in the c-kithigh populati
51 colony-forming unit-granulocyte macrophage (CFU-GM) derived from transduced CD34+ cells was shown po
53 colony-forming unit-granulocyte macrophage (CFU-GM) formation in HLA-A2(+) healthy controls and CML
54 colony-forming unit-granulocyte macrophage (CFU-GM) infused was 27 x 10(4)/kg, and the number of CD3
57 igher numbers of CFU-granulocyte macrophage (CFU-GM), and greater than 10-fold higher numbers of burs
58 olony-forming unit-granulocyte, -macrophage (CFU-GM), burst-forming unit-erythroid (BFU-E), and colon
59 old increases in CFU-granulocyte-macrophage (CFU-GM) and CFU-granulocyte, erythrocyte, monocyte, mega
60 colony-forming unit-granulocyte-macrophage (CFU-GM) and colony-forming unit granulocyte, erythroid,
61 colony-forming unit-granulocyte-macrophage (CFU-GM) assay to quantitate the level of hematopoietic c
62 colony-forming unit-granulocyte-macrophage (CFU-GM) by the CD8+,CD57+ subset was shown by 1 FS patie
63 colony-forming unit-granulocyte-macrophage (CFU-GM) colonies, whereas Flt3low cells produced mostly
65 colony-forming unit-granulocyte-macrophage (CFU-GM) from the CD34+CD38dim fraction by 14.5- +/- 5.6-
66 colony-forming unit granulocyte-macrophage (CFU-GM) myeloid progenitors to differentiate into cells
67 colony-forming unit-granulocyte-macrophage (CFU-GM) or CFU-megakaryocyte colony formation was observ
69 colony-forming unit-granulocyte-macrophage (CFU-GM) recovery 23%, and estimated tumor-cell depletion
70 colony-forming unit granulocyte-macrophage (CFU-GM) were relatively resistant to these treatments.
71 colony-forming unit-granulocyte-macrophage (CFU-GM), and a 12-fold to 17-fold increase of cobbleston
72 colony-forming unit-granulocyte-macrophage (CFU-GM)-derived, burst forming unit-erythroid (BFU-E)-de
73 colony-forming unit-granulocyte/macrophage (CFU-GM) and burst-forming unit-erythroid derived from CM
74 colony-forming units-granulocyte/macrophage (CFU-GM) in the graft products for the three dose levels
75 colony-forming unit-granulocyte/macrophage (CFU-GM), burst-forming unit-erythroid (BFU-E), and CFU-e
76 colony-forming unit-granulocyte-macrophage [CFU-GM(blood)]) and megakaryocytopoietic (blood CFU-mega
79 (colony-forming unit-granulocyte-macrophage [CFU-GM]) showed a threefold increase in CFU-GM from ARH-
80 (colony-forming unit-granulocyte-macrophage [CFU-GM], colony-forming unit-megakaryocyte [CFU-Meg], an
81 colony forming unit-granulocyte-macrophage [CFU-GM]; 17% inhibition burst forming unit-erythroid [BF
82 colony-forming units-granulocyte/macrophage [CFU-GM]), and megakaryocyte (CFU-Meg) progenitor cell gr
84 ming units for granulocytes and macrophages (CFU-GM), and primitive progenitors, long term culture-in
87 ed colony-forming unit-granulocyte/monocyte (CFU-GM) cells to have a strong affinity for SBA because
91 development of erythbroid (BFU-E), myeloid (CFU-GM), and primitive progenitor (CFU-GEMM, HPP-CFC, or
92 e suppressed the growth of leukemic myeloid (CFU-GM) progenitors from such patients, whereas concomit
95 HLA-A2.1 gene was found in the DNA of 56% of CFU-GM colonies derived from lentivirus-transduced SP ce
98 brogated the IGF-II-dependent enhancement of CFU-GM and long term culture-initiating cell numbers.
99 ws, rHuMig also abrogated SCF enhancement of CFU-GM numbers in cultures of CD34+ cells stimulated wit
103 3 controls studied showed >40% inhibition of CFU-GM, and all but 2 showed at least some suppression.
104 U-E]) and 3.44 micromol/L (24% inhibition of CFU-GM; 57% inhibition BFU-E) of depsipeptide for 4 hour
106 nd p21 gene deletion accelerated the loss of CFU-GM upon growth factor deprivation, and wild-type Sur
110 transduction was apparent in the numbers of CFU-GM colonies formed in the presence or absence of Epo
111 ic and sustained increases in the numbers of CFU-GM per kilogram collected per harvest that represent
113 t and G-CSF in stimulating the production of CFU-GM colonies in a human bone marrow-derived CD34+ col
118 feline marrow yields a marked separation of CFU-GM and BFU-E progenitors, select CCE SBA(-) fraction
120 increased in the same time frame as those of CFU-GM and CFU-GEMM in BM, spleen, and PB, although the
122 By contrast, there was little effect on CFU-GM and BFU-E formulation or on long term culture ini
123 A similar suppressive effect was observed on CFU-GM number when ovariectomized rat marrow was treated
124 d the suppressive effect of trauma plasma on CFU-GM and BFU-E colony growth during the early but not
126 overexpression inhibited apoptosis of p21+/+ CFU-GM and c-kit+, Lin- cells but not p21-/- cells, sugg
129 ionships between p21 and Survivin in primary CFU-GM and c-kit+, lineage-negative (Lin-) cells and dem
135 ced BM progenitor expansion, whereas splenic CFU-GM/CFU-granulocyte-erythrocyte-megakaryocyte-monocyt
141 ult bone marrow contains the majority of the CFU-GM, a proportion of the CFU-Mix, and a minor populat
142 from AIDS BM patients are more inhibitory to CFU-GM than those from peripheral blood (p < 0.05).
143 it exerts varying degrees of suppression to CFU-GM, but minimal inhibition on erythroid colonies.
144 granulocyte-macrophage colony-forming unit (CFU-GM) (median slope per day, -0.57; P = .0008), and bu
145 granulocyte-macrophage colony-forming unit (CFU-GM) and erythroid burst-forming unit (BFU-E) colonie
146 or granulocyte-monocyte colony-forming unit (CFU-GM) and erythroid burst-forming unit (BFU-E) growth.
147 granulocyte macrophage colony-forming unit (CFU-GM) cell cycle and proliferation and have been impli
148 granulocyte-macrophage colony-forming unit (CFU-GM) colony growth in response to granulocyte-macroph
149 granulocyte-macrophage colony-forming unit (CFU-GM) compared with mPB were detected in the marrow of
150 granulocyte-macrophage colony-forming unit (CFU-GM) content were 7.73 x 10(4)/kg and 41.6 x 10(4)/kg
152 granulocyte macrophage-colony-forming unit (CFU-GM) growth, and elastase mutations cause cyclic and
153 granulocyte-macrophage colony-forming unit (CFU-GM) growth, macrophage progenitor proliferation, and
154 granulocyte macrophage-colony-forming unit (CFU-GM) progenitors from patients with chronic myelogeno
155 by granulocyte/monocyte-colony-forming unit (CFU-GM), complete blood count (CBC), and donor chimerism
157 granulocyte-macrophage colony-forming units (CFU-GM) and erythroid burst-forming units (BFU-E) were p
158 granulocyte macrophage-colony-forming units (CFU-GM) by 1.7- to 6.2-fold and the proportion of CFU-GM
159 granulocyte/macrophage colony-forming units (CFU-GM), responsive to stimulation by granulocyte/macrop
160 body weight (r = .7, P < .005) but not with CFU-GM per kilogram or nucleated cells per kilogram.
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