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1 of Hbb(Th3/+) mice (Th3/+), a mouse model of thalassemia intermedia.
2 condition compared with other forms of beta thalassemia intermedia.
3 xhibited increased embryonic death and alpha-thalassemia intermedia.
4 mited iron overload in a mouse model of beta-thalassemia intermedia.
5 equently evaluated in a murine model of beta-thalassemia intermedia.
6 l hemoglobinuria, beta-thalassemia major, or thalassemia intermedia.
7 lable state reported to exist in severe beta-thalassemia intermedia.
8 two individuals of Greek Cypriot origin with thalassemia intermedia.
9 modifying disease-associated morbidities of -thalassemia intermedia.
10 s for this mutation, father and son, who had thalassemia intermedia and an apparent dominant mode of
11 ad in untransfused patients affected by beta-thalassemia intermedia and Hamp modulation provides impr
13 ot cover other hemoglobinopathies, including thalassemia intermedia and sickle cell anemia, in which
14 hydrops fetalis, hemoglobin H disease, beta-thalassemia intermedia, beta-thalassemia major/Cooley's
15 a(A)(2)) could be achieved in mice with beta-thalassemia intermedia following engraftment with bone m
17 atment of mouse models of HH (Hfe(-/-)) and -thalassemia intermedia (Hbb(th3/+)) with Tmprss6 siRNA f
19 rload in hereditary hemochromatosis and beta-thalassemia intermedia is caused by hepcidin deficiency.
21 se studies have shown correction of the beta-thalassemia intermedia phenotype and a partial, variable
23 pothesis, we exploited a mouse model of beta-thalassemia intermedia, Th3/(+) We observed that HO inhi
24 ts with beta-thalassemia major (TM) and beta-thalassemia intermedia (TI) were consecutively recruited
25 emoglobin (HbF) levels and morbidity in beta-thalassemia intermedia (TI), we analyzed data from 63 un
26 of beta-thalassemia, a model for human beta-thalassemia intermedia, we previously demonstrated that
27 is greatly increased in Hbb(th3/+) mice with thalassemia intermedia, where it contributes to the supp
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