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We then analyzed separately CFU-GM (Figures 4(c) and 4(d)) and BFU-E (Figures 4(e) and 4(f)) growth, observing a significant promotion of the CFU-GM growth in mPB [CD34.sup.+] cells after migration toward CXCL12 +IL-6 + TNF-[alpha] and CXCL12 + IL-6 + IL-1[beta] + TNF-[alpha] [+ or -] TIMP-1 as compared to CXCL12 alone (p [less than or equal to] 0.01, p [less than or equal to] 0.05 and p [less than or equal to] 0.01, resp.).
Supplementary Table 3: absolute numbers of CFU-C, CFU-GM, and BFU-E after incubation of [CD34.sup.+] cells from CB or mPB in methylcellulose-based medium for 14 days in the presence/absence of inflammatory stimuli.
The CFU-GM (c-d) and BFU-E (e-f) output was assessed.
The CFU-E and BFU-E training system was made into 0.2 ml cell suspension (2 x [10.sup.5]), 0.3 ml newborn calf (concentration: 20%), 0.2 ml mercaptoethanol (10mol/l), 0.05 ml EPO (CFU-E: 0.2 [micro]/ml, BFU-E:1 [micro]/ml) and 0.1ml methylcellulose (27g/1) by well mixing, after that the mixed solution was adjusted to 1.0 ml by using RPMI 1640 nutrient solution.
Blab/C mice in the model group that received [sup.60]Co exhibited changes in bone marrow nucleated cell count (BMNC), CFU-GM, CFU-E, BFU-E as compared to animals in the control group (Fig.
Similarly, DBT administered at middle dose group and high dose group could significantly increased the CFU-GM and BMNC of aplastic anemia mice bone marrow cell colonies, respectively (p < 0.05); furthermore, DBT administered at high dose group could very significantly increased the CFU-GM, CFU-E and BFU-E of aplastic anemia mice bone marrow cell colonies, respectively (p < 0.01) as compared to the model group.
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