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1 els of serum cholesterols and persistent low serum iron level.
2 hepcidin production and increased tissue and serum iron levels.
3 2 in Hfe-null mice had no effect on liver or serum iron levels.
4 erroportin downregulation and a reduction of serum iron levels.
5 e induces hepcidin and diminishes tissue and serum iron levels.
6 lted in reduced liver hepcidin and increased serum iron levels.
7 gue-Dawley rats resulted in no change in the serum iron level, a marked increase in the urinary excre
8 ions and inflammation, causing a decrease in serum iron levels and contributing to the development of
9 ive iron overload in the liver and increased serum iron levels and iron deposition in several organs
11 itionally, the Btbd9 mutant mice had altered serum iron levels and monoamine neurotransmitter systems
12 rpuscular volume, mean corpuscular Hb level, serum iron level, and Tfsat, and increased red blood cel
13 and 1200 ng/ml (reference 100 to 199 ng/ml), serum iron levels between 60 and 120 microg/ml (referenc
14 hich is secreted by the liver, and decreases serum iron levels by causing the down-regulation of the
15 decreased hepcidin expression and increased serum iron levels by mobilizing iron from splenic stores
17 eral or oral administration to mice, lowered serum iron levels comparably to those after parenteral n
19 nistic support for interventions that reduce serum iron levels in individuals at risk for hypertrigly
20 els of bioactive hepcidin and its effects on serum iron levels in mice infected with Borrelia burgdor
26 Iron loading was confirmed by increases in serum iron levels, percentages of transferrin saturation
27 independently associated with elevations in serum iron level, serum transferrin-iron saturation, ser
30 LFKO(-/-) mice on either diet, although the serum iron levels were slightly elevated in LFKO-/- mice
31 ped an anemia associated with abnormally low serum iron levels, yet accumulated hepatic and renal iro
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