ライフサイエンスコーパス: plasma iron

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1 obin, hematocrit, transferrin saturation, or plasma iron.

2 had excess fecal loss of isotopically tagged plasma iron.

3 Hepcidin synthesis is stimulated by plasma iron and iron stores and is inhibited by erythrop

4 bserved in the total KO mice, with increased plasma iron and massive parenchymal iron accumulation.

5 t on canine survival, multiple organ injury, plasma iron, and cell-free hemoglobin (CFH) levels depen

6 Plasma iron-binding antioxidant protection was negativel

7 Aberrant plasma iron chemistry (increased iron loading of transfe

8 th meningococcal septicemia exhibit abnormal plasma iron chemistry and decreased protection against i

9 Plasma iron circulates bound to transferrin (Trf), which

10 Hepcidin controls plasma iron concentration and tissue distribution of iro

11 oietic activity, ensuring that extracellular plasma iron concentrations and iron stores remain stable

12 High plasma iron concentrations with a lower level of transfe

13 Iron absorption, plasma iron concentrations, and tissue iron distribution

14 ly, transferrin injections normalized labile plasma iron concentrations, increased hepcidin expressio

15 he iron exporter ferroportin (Fpn) regulates plasma iron concentrations.

16 Hepcidin increased and plasma iron decreased during acute HIV-1 infection, as v

17 tter-based diets were associated with higher plasma iron in men (22.4 +/- 3.8 micro mol/L) than was t

18 Diet composition may affect plasma iron in men, but LDL oxidative susceptibility is

19 at apparently reflected implication of blood plasma iron in the inflammatory cell response to OPW-ind

20 y for Tf-iron uptake compensates for the low plasma iron levels associated with anemia in RA and help

21 the increased intestinal iron absorption and plasma iron levels characteristic of the juvenile hemoch

22 Labile plasma iron (LPI) was measured quarterly during the firs

23 tility preservation, whereas NTBI and labile plasma iron may be valuable for monitoring iron effect o

24 cin-chelatable iron, indicative of transient plasma iron-overload, was only found in one patient (6.5

25 anese exposure resulted in a 32% decrease in plasma iron (p<0.01) and no changes in plasma total iron

26 Iron status was estimated on the basis of plasma iron, soluble transferrin receptor (sTfR), ferrit

27 n sequestration in macrophages and decreased plasma iron; this is proposed to limit the replication o

28 with a periportal distribution and increased plasma iron, transferrin saturation, and non-transferrin

29 e primarily responsible on a daily basis for plasma iron turnover and are central in the pathogenesis

30 veal equivalent rates of iron absorption and plasma iron turnover, suggesting that iron accumulation

31 Plasma iron was negatively correlated with cytokine prod

32 These complications are caused by labile plasma iron, which is taken up by parenchymal cells in a

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