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The major causes of anaemia in patients with diabetes and chronic kidney disease are iron deficiency, erythropoietin (EPO) deficiency, and impaired responsiveness to the actions of EPO 1.
The major causes of anaemia in patients with diabetes and chronic kidney disease, however, are deficiency of EPO and iron, as well as hyporesponsiveness to the actions of EPO 1.
When Epo (1 U/mL) was combined with SCF (100 ng/mL) cell growth was similar to that in the presence of Epo (1 U/mL) alone (Figure 1A), indicating that Epo and SCF did not cooperate for cell proliferation.
Stable transfectants were selected in growth medium containing 800 µg/mL G418 (Invitrogen, Cergy, France) and Epo (1 U/mL).
The cells were continously amplified in vitro in the presence of either Epo (1 U/mL) or SCF (100 ng/mL) [18].
663 and 812 cells cultured in the continuous presence of Epo (1 U/mL) were extensively washed and then switched to SCF (100 ng/mL).
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In zebrafish HREs are known for leg1a/b, birC5a/b, period1b, epo and igfbp1a.
%eGFR↓ at 120 hr: EPO -4 ± 3, placebo -13 ± 5 (p = 0.01) No significant difference in 1° outcome or 2° outcomes except AKI (AKIN UO).
More indirectly, Kit signaling contributes to the sustained expression of Stat5 protein which can then be activated by Epo [38].
To determine if Epo is able to signal through EpoR in HSCs, cells were cultured for 12h in vitro in the presence or absence of Epo [20].
When CD34+ cells were cultured on soft agar with minimal EPO (0.4 mU/mL) marked differences in the number and size of colonies were observed after 14 days.
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