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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.
70 /g liver phantom) to 5 mg Fe/g liver phantom iron overload (100X overdose).
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)
73 lu) in 6 unrelated patients with unexplained iron overload (9% of our cohort).
74                          Iron deficiency and iron overload affect over a billion people worldwide.
75 lation should be considered in patients with iron overload and a history of GBCA exposure.
76 te that additional novel tools for measuring iron overload and a molecular-mechanism-driven descripti
77        These data showed high sensitivity to iron overload and a strong relationship between quantita
78 t study to determine the association between iron overload and adult allogeneic hematopoietic cell tr
79          Here we investigated the effects of iron overload and age on cardiac hypertrophy using 1-, 5
80 e found no association between pretransplant iron overload and allogeneic HCT outcomes.
81 r iron exporter in mammals, leading to organ iron overload and associated morbidities.
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
84 o difference in ECV between patients without iron overload and control subjects (P = .647).
85                                              Iron overload and deficiency can adversely affect human
86 siologic cues underlies genetic disorders of iron overload and deficiency, including hereditary hemoc
87                                Transfusional iron overload and gonadal failure are addressed, followe
88 ia in mice with either genetic or iatrogenic iron overload and in human plasma.
89                       Conversely, organismal iron overload and increased adipocyte ferroportin expres
90 itions, hamp1 was upregulated in response to iron overload and infection and downregulated during ane
91 eta-thalassemia (TDT) mainly chronic anemia, iron overload and iron chelator toxicity.
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
99 nducing hepcidin expression in patients with iron overload and/or chronic liver diseases.
100  and survival have been shown to improve IE, iron overload, and anemia in animal models of BT.
101 was selected as the outer shell to eliminate iron overload, and BMSCs implantation with high-molecula
102 es including fibrosis, cirrhosis, steatosis, iron overload, and hepatocellular carcinoma.
103 munosuppression, anatomic barrier breakdown, iron overload, and hyperglycemia/acidosis.
104 taneous leg ulceration, renal insufficiency, iron overload, and liver dysfunction.
105  disease by lowering pulmonary inflammation, iron overload, and mortality.
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
109 protects against tissue iron accumulation in iron overload anemias.
110 A in circulating blood cells, and markers of iron overload are associated with high PlGF and early mo
111                           Chronic anemia and iron overload are believed to lie behind these abnormali
112             Hemochromatosis is a disorder of iron overload arising mostly from mutations in HFE.
113                         The complications of iron overload, arising from transfusions that represent
114 correlated to hepatic T2* times (ie, hepatic iron overload because of frequent blood transfusions; P<
115                     Complications, including iron overload, bilirubin gallstones, extramedullary hema
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
119                 In this study, the impact of iron overload by SPIONs was assessed on a mouse cirrhosi
120                                     However, iron overload can damage the organism through a variety
121                                              Iron overload can increase cellular oxidative stress lev
122  accumulating excessive iron in body organs (iron overload) can damage or even destroy an organ.
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
125 ated with iron dextran for 4 weeks to induce iron-overload cardiomyopathy.
126 ively reduce cellular ferritin expression in iron overloaded cells and regulate intracellular iron le
127                                              Iron-overloaded cells harboring a constitutively active
128 the suppression of hepcidin and the systemic iron overload characteristic of this disease.
129 ell hydrogel was fabricated for simultaneous iron overload clearance and bone marrow mesenchymal stem
130                  Fpn C326S mice had systemic iron overload compared to wild type and had the fastest
131  deficiency, serum iron overload, and tissue iron overload compared with single KO mice.
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
136                                              Iron overload damages many organs.
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
139                                      Because iron overload develops in some MDS patients who do not r
140 gside rapid decreases in LIC in this heavily iron-overloaded, difficult-to-treat population.
141               Hereditary hemochromatosis, an iron overload disease caused by a deficiency in the iron
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.
144  TFR2 function results in a rare form of the iron-overload disease hereditary hemochromatosis.
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
147 y hemochromatosis (HH) is a common inherited iron overload disorder.
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
151 te disease severity in mouse models of human iron overload disorders.
152 hepcidins may be useful for the treatment of iron overload disorders.
153  we report renal clearable nanochelators for iron overload disorders.
154 ion could be beneficial for the treatment of iron overload disorders.
155  broadly effective treatments for hereditary iron overload disorders.
156  cause of tissue-iron accumulation in anemic iron-overload disorders caused by hemolytic anemia.
157 a novel therapeutic target in several anemic iron-overload disorders.
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.
161 as effective and safe in inducing control of iron overload during 12 months of treatment.
162  mice developed microcytic anemia and tissue iron overload, especially in the spleen.
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
166                            Median LIC in the iron-overload group was 4.3 mg/g (range, 1.9-25.4).
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 (
169               Patients with prior myocardial iron overload had higher ECV than did patients without i
170   Humans with aceruloplasminemia causing RPE iron overload had increased RPE C3d deposition.
171  Moreover, thalassemic mice with established iron overload had significant improvement in tissue-iron
172                                        Brain iron overload has a detrimental role in brain injury aft
173 on, and its role in the mediation of hepatic iron overload has been dissected out.
174  age-dependent cardiac stress exacerbated by iron overload hemochromatosis.
175           Nevertheless, TFR2 mutations cause iron overload (hemochromatosis type 3) without overt ery
176                                Hemolysis and iron overload improved upon iron chelation with full cor
177          Our study indicates that preventing iron overload improves beta-thalassemia and strengthens
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.
180 ghly specific inhibitor successfully treated iron overload in a mouse model.
181 eficiency (A1ATD) is associated with hepatic iron overload in a subgroup of patients.
182 ssential for osteoclast differentiation, and iron overload in a variety of hematologic diseases is as
183                                    Transient iron overload in adult mice infected with E. coli result
184 lementation with 2,5-DHBA alleviates splenic iron overload in bdh2 null mice.
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
188 ed to embryonic lethality potentially due to iron overload in developing embryos.
189 nding is interesting in light of the role of iron overload in diabetes.
190 chanism, A1ATD could be a trigger of hepatic iron overload in genetically predisposed individuals or
191 epcidins for the prevention and treatment of iron overload in hepcidin-deficient mice.
192                                              Iron overload in hereditary hemochromatosis and beta-tha
193 amine (Dfx), which are already used to treat iron overload in humans, offer a new approach for treati
194 partially result from its ability to prevent iron overload in macrophages.
195 tes to pathological hepcidin suppression and iron overload in mice with nontransfused beta-thalassemi
196 cific deletion of either Alk2 or Alk3 causes iron overload in mice.
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
201 e(hi) iron handling coincides with adipocyte iron overload in obese mice.
202              Deferasirox was shown to reduce iron overload in patients with hemochromatosis and may b
203  inflammation, lung tissue inflammation, and iron overload in SCD.
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
206 ce of abnormal sideroblasts characterized by iron overload in the mitochondria, called RS.
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.
209            The most common complications are iron overload in transfused patients and syndrome-specif
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
213 dative stress and protected DKO mice against iron overload-induced retinal degeneration.
214  in this population should use LIC to define iron overload instead of ferritin.
215                                              Iron overload (IO) is a common complication in BT patien
216 prevalence of fatty liver diseases and liver iron overload is 42.2% (1082 of 2561) and 17.4% (447 of
217                                              Iron overload is a relatively common clinical condition
218            A strong recommendation to assess iron overload is accompanied by a moderate strength reco
219                                              Iron overload is associated with increased diabetes risk
220                                              Iron overload is the hallmark of hereditary hemochromato
221               Cardiac damage associated with iron overload is the most common cause of morbidity and
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
224 sfusions, a consequence of which is systemic iron overload leading to acute heart failure.
225                                              iron overload leads to increased levels of toxic non-tra
226 ere defined as no iron overload (N = 28) and iron overload (LIC >1.8 mg/g; N = 60).
227 itary liver diseases resulting in copper and iron overload may cause significant morbidity and mortal
228                                           An iron overload may induce pancreatic islet damage and inc
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
231            In addition, it removes iron from iron overloaded mice, including models of acquired (iron
232              In addition, AAV-ADIPOQ-treated iron-overload mice had lower expression of inflammatory
233                               RPE cells from iron-overloaded mice exhibit several features of tumor c
234  and intercellular adhesion molecule-1, than iron-overloaded mice not treated with AAV-ADIPOQ.
235  embryo iron endowment in iron-sufficient or iron-overloaded mice, we generated combinations of mothe
236  deposition and restored cardiac function in iron-overloaded mice.
237                  Patients were defined as no iron overload (N = 28) and iron overload (LIC >1.8 mg/g;
238 ed the efficacy and safety of deferasirox in iron-overloaded NTDT patients.
239 it of Fe-S cluster enzymes and mitochondrial iron overload occur in the myocardium of individuals wit
240                                              Iron overload occurs in many hemorrhagic injuries due to
241              Hamp2 did not respond to either iron overload or anemia but was highly upregulated durin
242 t in mouse models of these diseases prevents iron overload or decreases its potential toxicity, natur
243 utic target for the treatment of diseases of iron overload or deficiency.
244 he 'iron hypothesis' by showing that dietary iron overload or elevated non-transferrin bound iron (NT
245 erum of AN patients, without any evidence of iron overload or inflammation.
246 assemia may correlate to the disease itself, iron overload or the chelating agents used.
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
251                                          The iron overload phenotype was more marked in Alk3- than in
252          Recent data suggest that markers of iron overload portend a relatively poor prognosis, and r
253 the hereditary hemochromatosis, resulting in iron overload predominantly in the liver.
254 tion in iron-deficient, iron-sufficient, and iron-overloaded pregnant women and children.
255  cardiac isoprostane levels, suggesting that iron overload promotes oxidative stress and cardiac hype
256                            In mice, systemic iron overload protected against renal ischemia-reperfusi
257  of the most consistent findings in advanced iron overload resulting from hemochromatosis.
258 ered ROS landscape, we observed hemoglobin / iron overload, ROS production and lipid peroxidation in
259                      The Hemochromatosis and Iron Overload Screening (HEIRS) Study screened 99,711 pr
260                      The Hemochromatosis and Iron Overload Screening (HEIRS) Study was a multicenter
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
265  of these gene expression changes favored an iron-overloaded state.
266 ntify disease severity related to myocardial iron overload states or glycosphingolipid accumulation i
267                    In multivariate analyses, iron-overload status did not impact risks of overall mor
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
270                                 Dysmetabolic iron overload syndrome (DIOS) is a common cause of hyper
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
273 equently be developed into new therapies for iron overload syndromes.
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
276  whereas Smad158;Alb-Cre(+) mice had greater iron overload than Smad15;Alb-Cre(+) mice.
277 es a quantitative understanding of the liver iron overload that arises in this disease.
278          Transfused patients frequently show iron overload that negatively affects hematopoiesis.
279                              In all cases of iron overload, the expression of FLVCR and PCFT was upre
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
283       Magnetic resonance imaging showed that iron overload was absent in nine patients, mild in one p
284          A homogeneous pattern of myocardial iron overload was associated with a negative cardiac rem
285       Prevalence of fatty liver diseases and iron overload was calculated (weighted by probability of
286  transfused patients, hepatic and myocardial iron overload was measured by multi-breath-hold MRI T2*
287                                              Iron overload was mediated by decreased hepatic expressi
288                                              Iron overload was observed in 17.4% (447 of 2561 partici
289       The regulation of heme transporters by iron overload was studied in two genetic models of hemoc
290                         Myocardial and liver iron overload were measured by T2* multiecho technique.
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
296 inct congenital disorders can lead to tissue-iron overload with anemia.
297 d elevations in iron absorption, which cause iron overload with associated organ toxicities.
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
300 ble iron chelators is summarized for cardiac iron overload without overt cardiac dysfunction.

 
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