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1 obin, hematocrit, transferrin saturation, or plasma iron.
2 his process consumes most of the circulating plasma iron.
3 had excess fecal loss of isotopically tagged plasma iron.
4 scent, is strongly associated with increased plasma iron.
5          Hepcidin synthesis is stimulated by plasma iron and iron stores and is inhibited by erythrop
6 bserved in the total KO mice, with increased plasma iron and massive parenchymal iron accumulation.
7                     In summary, low and high plasma iron and transferrin saturation were independentl
8 t on canine survival, multiple organ injury, plasma iron, and cell-free hemoglobin (CFH) levels depen
9                                              Plasma iron-binding antioxidant protection was negativel
10                       Transferrin, the major plasma iron-binding molecule, interacts with cell-surfac
11                                     Aberrant plasma iron chemistry (increased iron loading of transfe
12 th meningococcal septicemia exhibit abnormal plasma iron chemistry and decreased protection against i
13                                              Plasma iron circulates bound to transferrin (Trf), which
14                            Hepcidin controls plasma iron concentration and tissue distribution of iro
15 oietic activity, ensuring that extracellular plasma iron concentrations and iron stores remain stable
16                                         High plasma iron concentrations with a lower level of transfe
17                             Iron absorption, plasma iron concentrations, and tissue iron distribution
18 ly, transferrin injections normalized labile plasma iron concentrations, increased hepcidin expressio
19 he iron exporter ferroportin (Fpn) regulates plasma iron concentrations.
20                       Hepcidin increased and plasma iron decreased during acute HIV-1 infection, as v
21                                          Low plasma iron (hypoferremia) induced by hepcidin is a cons
22 tter-based diets were associated with higher plasma iron in men (22.4 +/- 3.8 micro mol/L) than was t
23                  Diet composition may affect plasma iron in men, but LDL oxidative susceptibility is
24 at apparently reflected implication of blood plasma iron in the inflammatory cell response to OPW-ind
25                                           In plasma, iron is normally bound to transferrin, the princ
26 n of anemia but correlating with rather high plasma iron level.
27 ver and splenic macrophages, thus decreasing plasma iron levels and restricting iron availability for
28 y for Tf-iron uptake compensates for the low plasma iron levels associated with anemia in RA and help
29 the increased intestinal iron absorption and plasma iron levels characteristic of the juvenile hemoch
30 ether intestinal hepcidin may play a role in plasma iron lowering, we generated transgenic mice overe
31                                       Labile plasma iron (LPI) was measured quarterly during the firs
32 1.14 (95% CI, 1.07-1.22) in individuals with plasma iron <=5th or >=95th percentile compared with ind
33 iver magnetic resonance relaxation times and plasma iron markers were collected longitudinally.
34 tility preservation, whereas NTBI and labile plasma iron may be valuable for monitoring iron effect o
35 pid and convenient alternative for serum and plasma iron measurements, which can substantially reduce
36 cluding a mild decrease in hemoglobin, lower plasma iron, microcytosis, and an increased red blood ce
37                                   We propose plasma iron modulates the profile of innate immunity by
38 cin-chelatable iron, indicative of transient plasma iron-overload, was only found in one patient (6.5
39 anese exposure resulted in a 32% decrease in plasma iron (p<0.01) and no changes in plasma total iron
40    Iron status was estimated on the basis of plasma iron, soluble transferrin receptor (sTfR), ferrit
41 n sequestration in macrophages and decreased plasma iron; this is proposed to limit the replication o
42 with a periportal distribution and increased plasma iron, transferrin saturation, and non-transferrin
43 s increased in C282Y homozygotes with normal plasma iron, transferrin saturation, or ferritin, and in
44 omatosis and in individuals with low or high plasma iron, transferrin saturation, or ferritin.
45 e primarily responsible on a daily basis for plasma iron turnover and are central in the pathogenesis
46 veal equivalent rates of iron absorption and plasma iron turnover, suggesting that iron accumulation
47                                              Plasma iron was negatively correlated with cytokine prod
48     These complications are caused by labile plasma iron, which is taken up by parenchymal cells in a