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1 present in vivo, e.g., under conditions of "iron overload".
2 d to serum ferritin (a traditional marker of iron overload).
3 netic disorders characterized by parenchymal iron overload.
4 ored red blood cells) and primary (Hfe(-/-)) iron overload.
5 usceptibility to mild-to-moderate late-onset iron overload.
6 emia major and is associated with myocardial iron overload.
7 ere negative for viral hepatitis B and C and iron overload.
8 the relationship between ECV and myocardial iron overload.
9 ates ineffective erythropoiesis, anemia, and iron overload.
10 l effect of the iron chelator deferiprone on iron overload.
11 n all erythroblast populations regardless of iron overload.
12 sis, many patients have unexplained signs of iron overload.
13 tations in BMP6 in patients with unexplained iron overload.
14 band was noted to have dyserythropoiesis and iron overload.
15 mice, restores hepcidin levels and corrects iron overload.
16 ssive absorption of dietary iron, leading to iron overload.
17 rried out in a family with A1ATD and hepatic iron overload.
18 uction is required, regardless of myocardial iron overload.
19 cidin levels indicate a significant risk for iron overload.
20 mary use of chelation has been transfusional iron overload.
21 sed intestinal iron absorption and therefore iron Overload.
22 urden generalizes to other human diseases of iron overload.
23 and serum hepcidin levels leading to severe iron overload.
24 nsfusion requirements resulting in secondary iron overload.
25 ing or treating the toxicity associated with iron overload.
26 and patients incur incremental transfusional iron overload.
27 opoiesis on hepcidin may also play a role in iron overload.
28 ecretion and prevented recurrence of hepatic iron overload.
29 olic dysfunction, and only rarely myocardial iron overload.
30 ganelles and protect mutant cells from acute iron overload.
31 th or causes diseases, including anaemia and iron overload.
32 e intravenous deferoxamine to treat systemic iron overload.
33 as only 1 patient had evidence of myocardial iron overload.
34 erabsorption of iron is the leading cause of iron overload.
35 n (NTBI), which appears in the plasma during iron overload.
36 influences from erythropoiesis, anemia, and iron overload.
37 decreased hepcidin production, and secondary iron overload.
38 sion or FPN responsiveness to HAMP result in iron overload.
39 observed and can significantly contribute to iron overload.
40 rs during mild oxidative stress triggered by iron overload.
41 causing ferritin synthesis in the absence of iron overload.
42 ic (Trf(hpx/hpx) ) mice that develop hepatic iron overload.
43 ions, such as hereditary hemochromatosis and iron overload.
44 gene has a well documented association with iron overload.
45 lebotomy) for children with SCA, stroke, and iron overload.
46 d can still develop serious complications of iron overload.
47 ed with excitotoxicity, but also in those of iron overload.
48 sis (IE), anemia, splenomegaly, and systemic iron overload.
49 dation (LPO) and steatosis in the absence of iron overload.
50 chelator for the treatment of transfusional iron overload.
51 oral chelator, in adults with transfusional iron overload.
52 es but have associated morbidities including iron overload.
53 way to manage children with SCA, stroke, and iron overload.
54 -stage erythroblasts that was independent of iron overload.
55 d absorption of dietary iron, and eventually iron overload.
56 opoiesis and iron dysregulation resulting in iron overload.
57 enic, and hemochromatosis is associated with iron overload.
58 pathway is perturbed in diseases that cause iron overload.
59 nted cell survival under the condition of an iron overload.
60 l HIF-2alpha in iron deficiency, anemia, and iron overload.
61 ive response to systemic iron deficiency and iron overload.
62 t of liver iron concentration and myocardial iron overload.
63 ence anemia and its complications, including iron overload.
64 itional posttranslational control to prevent iron overload.
65 cess toxic iron from patients with secondary iron overload.
66 ptake and drives iron hyperabsorption during iron overload.
67 ferroportin (Fpn), resulting in parenchymal iron overload.
68 on and transfusion therapy contribute to the iron overload.
69 iac-specific deletion leads to fatal cardiac iron overload.
71 neral density [BMD], 23.2%), serum ferritin (iron overload, 24.0%), and pulmonary function testing/ch
72 oad had higher ECV than did patients without iron overload (31.3% +/- 2.8 vs 28.2% +/- 3.4, P = .030)
76 te that additional novel tools for measuring iron overload and a molecular-mechanism-driven descripti
78 t study to determine the association between iron overload and adult allogeneic hematopoietic cell tr
82 repeated blood transfusions, which leads to iron overload and cellular damage, especially in the hea
83 rform the chronic phlebotomies to reduce the iron overload and clear the dermatologic lesions in porp
86 siologic cues underlies genetic disorders of iron overload and deficiency, including hereditary hemoc
90 itions, hamp1 was upregulated in response to iron overload and infection and downregulated during ane
92 dent thalassemia (NTDT) patients may develop iron overload and its associated complications despite r
93 hrocyte production, as well as to reduce the iron overload and organ toxicity in BT and in other diso
94 he iron distribution throughout the heart in iron overload and provide calibration in humans for card
95 cause of hyperferritinemia in the absence of iron overload and provides a possible diagnostic schema.
96 uced production of erythrocytes, anemia, and iron overload and PV by erythrocytosis and thrombosis.
97 expression under conditions of simultaneous iron overload and stress erythropoiesis, and impairing t
98 sociations for fatty liver disease and liver iron overload and their prevalence in a large-scale popu
101 was selected as the outer shell to eliminate iron overload, and BMSCs implantation with high-molecula
106 congestion, inflammatory cell infiltration, iron overload, and secretion of IL-6 in lavage fluid.
107 han in prior studies, the high penetrance of iron overload, and the frequency of at-risk genotypes, i
108 similar degree of hepcidin deficiency, serum iron overload, and tissue iron overload compared with si
110 A in circulating blood cells, and markers of iron overload are associated with high PlGF and early mo
114 correlated to hepatic T2* times (ie, hepatic iron overload because of frequent blood transfusions; P<
116 deposition occurs in pediatric patients with iron overload but normal renal and hepatic function who
117 rine beta-thalassemia not only mitigates the iron overload, but also the severity of the anemia.
118 best known as being associated with cellular iron overload, but the mechanism by which HFE H63D might
123 Using adiponectin for adjuvant therapies in iron-overload cardiac dysfunction may be an option in th
124 ortantly these changes preceded the onset of iron overload cardiomyopathy, providing an early biomark
126 ively reduce cellular ferritin expression in iron overloaded cells and regulate intracellular iron le
129 ell hydrogel was fabricated for simultaneous iron overload clearance and bone marrow mesenchymal stem
132 acute-phase response and the consequences of iron overload conditions on susceptibility to bacterial
133 loading in TM are directly relevant to other iron-overload conditions, including in particular Diamon
134 the patients showed a significant myocardial iron overload correlated with lower compliance to chelat
135 -null mouse) and in two nongenetic models of iron overload (cytomegalovirus infection and treatment w
137 neteen patients (63.3%) had prior myocardial iron overload (defined as midseptal T2* < 20 msec on any
138 Mice with a mosaic pattern of RPE-specific iron overload demonstrated co-localization of iron-induc
142 chelator currently used for the treatment of iron-overload disease and has been implemented as an alt
143 epithelium (RPE) and their regulation in the iron-overload disease hemochromatosis were examined.
145 rapeutics isa practical approach to treating iron overload diseases associated with diminished hepcid
146 active iron chelators to treat transfusional iron-overload diseases, e.g., thalassemia, is overviewed
148 epcidin-ferroportin axis are a main cause of iron overload disorders but can also cause iron-restrict
149 es that minihepcidins could be beneficial in iron overload disorders either used alone for prevention
150 ysiology of many of the genetically distinct iron overload disorders, collectively termed hereditary
158 is and chronic anemia and is associated with iron overload due to both transfused iron and increased
159 n and alpha-syn in exosomes, suggesting that iron overload due to impaired ferritinophagy or other ca
160 in human hemochromatosis protein (HFE) cause iron overload due to reduced hepatic hepcidin secretion.
163 Anemic patients affected by BT suffer from iron overload, even in the absence of chronic blood tran
164 ction of anemia, alloimmunization, and organ iron overload (for which the role of iron chelation rema
165 multiparametric CMR assessment of myocardial iron overload, function, and fibrosis in a cohort of ped
167 to hepcidin knockout mice with pre-existing iron overload had a more moderate effect and caused part
168 xteen of twenty-two participants with severe iron overload had glyceronephosphate O-acyltransferase (
171 Moreover, thalassemic mice with established iron overload had significant improvement in tissue-iron
178 erythropoiesis, corrected anemia and limited iron overload in a mouse model of beta-thalassemia inter
179 ates hepcidin suppression and contributes to iron overload in a mouse model of beta-thalassemia.
182 ssential for osteoclast differentiation, and iron overload in a variety of hematologic diseases is as
185 2alpha signaling is critical for progressive iron overload in beta-thalassemia and may be a novel the
186 10muM) pretreatment abrogates the effects of iron overload in brain endothelial cells protecting cell
187 tment to prevent recurrent stroke and manage iron overload in children chronically transfused over 7
190 chanism, A1ATD could be a trigger of hepatic iron overload in genetically predisposed individuals or
193 amine (Dfx), which are already used to treat iron overload in humans, offer a new approach for treati
195 tes to pathological hepcidin suppression and iron overload in mice with nontransfused beta-thalassemi
197 icient hepcidin synthesis is responsible for iron overload in minimally transfused patients with this
198 s that have been previously shown to prevent iron overload in murine models of hemochromatosis and in
199 and its tissue distribution, is the cause of iron overload in nearly all forms of hereditary hemochro
200 ation with deferasirox significantly reduces iron overload in NTDT patients with a frequency of overa
204 transfusions are one of the major causes of iron overload in several of these disorders, including b
205 p2(fl/fl) (Bmp2(LSECKO)) mice caused massive iron overload in the liver and increased serum iron leve
207 Central to early identification of cardiac iron overload in TM is the estimation of cardiac iron by
208 chelation strategies would reduce myocardial iron overload in TM patients compared with placebo.
210 he key iron regulator hepcidin (HAMP) causes iron overload in untransfused patients affected by beta-
211 mRNA levels are increased in mouse models of iron overload, indicating that TGF-beta1 may contribute
212 te hepatic porphyrias, identification of the iron overload-induced inhibitor of hepatic uroporphyrin
216 prevalence of fatty liver diseases and liver iron overload is 42.2% (1082 of 2561) and 17.4% (447 of
222 is associated with cognitive impairment, yet iron overload is thought to promote neurodegenerative di
223 wth retardation, aminoaciduria, cholestasis, iron overload, lactic acidosis and early death (GRACILE
227 itary liver diseases resulting in copper and iron overload may cause significant morbidity and mortal
229 injections of the nanochelator for 5 days to iron overload mice and rats decrease iron levels in seru
230 s detected in the visceral adipose tissue of iron overloaded mice, and gene expression analysis of vi
235 embryo iron endowment in iron-sufficient or iron-overloaded mice, we generated combinations of mothe
239 it of Fe-S cluster enzymes and mitochondrial iron overload occur in the myocardium of individuals wit
242 t in mouse models of these diseases prevents iron overload or decreases its potential toxicity, natur
244 he 'iron hypothesis' by showing that dietary iron overload or elevated non-transferrin bound iron (NT
247 anemias, GDF15 expression may contribute to iron overloading or other features of the disease phenot
248 the most significant association with severe iron overload (P = 3 x 10(-6) ; P = 0.033 by the likelih
249 as the best threshold for predicting cardiac iron overload (P=0.001 and P<0.0001, respectively).
250 ecific KO mice fully recapitulate the severe iron overload phenotype observed in the total KO mice, w
255 cardiac isoprostane levels, suggesting that iron overload promotes oxidative stress and cardiac hype
258 ered ROS landscape, we observed hemoglobin / iron overload, ROS production and lipid peroxidation in
261 polymorphisms associated with variability of iron overload severity in HFE-associated hemochromatosis
262 eading to red blood cell (RBC) transfusions, iron overload, shortened survival, and poor quality of l
263 eased hepatic Bmp6 mRNA levels, and systemic iron overload similar to mice deficient for Hjv alone.
264 gated disease complications of IE, including iron overload, splenomegaly, and bone pathology, while r
266 ntify disease severity related to myocardial iron overload states or glycosphingolipid accumulation i
268 ferroportin activity can lead to diseases of iron overload, such as haemochromatosis, or iron limitat
269 al cellular iron content under conditions of iron overload, suggesting that the stm3944-encoded prote
271 on, we characterized a model of dysmetabolic iron overload syndrome in which an iron-enriched diet in
272 is a potential drug target for patients with iron overload syndromes because its levels are inappropr
274 al HIF-2alpha plays an important role during iron overload, systemic iron deficiency, and anemia.
275 ntly lower in patients with prior myocardial iron overload than in control subjects (850.3 +/- 115.1
280 deficient mice in the presence or absence of iron overload to distinguish between the effects caused
281 ning for stroke risk, improved management of iron overload using oral chelators and non-invasive MRI
282 imary care participants in North America for iron overload using serum ferritin and transferrin satur
286 transfused patients, hepatic and myocardial iron overload was measured by multi-breath-hold MRI T2*
291 of Tmprss6 in Hfe(-/-) mice reduced systemic iron overload, whereas homozygous loss caused systemic i
292 90% transferrin saturation and massive liver iron overload, whereas Smad1(fl/fl);Smad5(fl/wt);Cre(+)
293 at it through blood transfusions, leading to iron overload, which is a quite harmful consequence.
294 patients affected by these disorders exhibit iron overload, which is the main cause of morbidity and
295 Observed familial clustering of hepatic iron overload with A1ATD suggests a genetic cause, but g
298 both Hfe and Tfr2 caused more severe hepatic iron overload with more advanced lipid peroxidation, inf
299 ignificantly reduces kidney damage caused by iron overload without demonstrating DFO's own nephrotoxi