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1 not be different from that indicated for non thalassemics.
2 a pathogenetic feature shared by parasitized thalassemic and G6PD-deficient RBCs, triggering abnormal
3 in the spleen, bone marrow, and liver of the thalassemic animals.
4                             As a result, the thalassemic beta-globin pre-mRNAs are spliced almost exc
5                                     For beta-thalassemic CD34(+) cells, similar gene transfer efficie
6                                              Thalassemic cells were associated with expression of cel
7                                  In isolated thalassemic cells, short-term proteasome inhibition bloc
8         This is the first reported case of a thalassemic condition that is maintained in a species as
9             These mice mimic the human alpha-thalassemic conditions and can be used as preclinical mo
10 n this locus such as sickle cell disease and thalassemic diseases.
11 icant overexpression of beta-globin in alpha-thalassemic disorders.
12 ate from the blood cells of one of four beta-thalassemic donors and 3H-alpha-chains or 3H-alpha-globi
13 ng effect on somatic recombination events in thalassemic embryos.
14 ins impose substantial oxidative stress on B-thalassemic erythroblasts and erythrocytes, impacting ce
15 s, with heme attached to them, accumulate in thalassemic erythroblasts causing oxidative stress and t
16                                      In beta-thalassemic erythrocyte precursors, free alpha-globin wa
17 rovide a framework for studying the enhanced thalassemic erythroid apoptosis.
18 vel of total endogenous alpha-globin mRNA in thalassemic erythroid cells resulted in improved red cel
19 ances translation of ATF4 mRNA in mouse beta-thalassemic erythroid precursors.
20 globin gene will be required to improve beta-thalassemic erythropoiesis?
21 larly effective in individuals carrying beta-thalassemic gene defects.
22 ilize the Erfe(-/-) mouse model as well as B-thalassemic (Hbb(th3/+)) mice with systemic loss of ERFE
23 t proteolysis pathway in unfractionated beta-thalassemic hemolysates.
24 s in mice with established predominant B0/B0-thalassemic hemopoiesis after in vivo injection of the H
25                  Mice transplanted with beta-thalassemic HSCs transduced with a gamma-globin/MGMT vec
26                 Using BALB/c donors and beta-thalassemic HW-80 recipients, we found significantly imp
27 experiments performed on blood from HbE/beta thalassemics in the temperature range 39 degrees C to 41
28 s substitutes for deficient adult globins in thalassemic individuals.
29 ls of thalassemia, aberrant splicing of beta-thalassemic IVS2-705 pre-mRNA was permanently corrected
30                       We report that HSCs in thalassemic mice (th3) have an impaired function, caused
31  was increased in splenic erythroblasts from thalassemic mice and in erythroblasts and sera from subj
32 imals was similar to that of normal non-beta-thalassemic mice but significantly higher than untreated
33                           Generation of beta-thalassemic mice chimeric for a minority proportion of g
34 r deferiprone (L1) intraperitoneally to beta-thalassemic mice for 4 wk and then studied RBC survival
35 Erfe and the consequences of its ablation in thalassemic mice from 3 to 12 weeks of age.
36      These cells were transplanted into beta-thalassemic mice given nonmyeloablative pretransplantati
37                      Serial analyses of beta-thalassemic mice indicate that while hemoglobin levels d
38                          The loss of ERFE in thalassemic mice led to full restoration of hepcidin mRN
39 e increase in expression of hepcidin in beta-thalassemic mice limits iron overload, decreases formati
40  in utero transplantation in nonanemic, beta-thalassemic mice to study chimerism, tolerance, and chan
41 eparate set of independent experiments, beta-thalassemic mice were bred with transgenic mice that exp
42                                    Moreover, thalassemic mice with established iron overload had sign
43                                 Injection of thalassemic mice with SCF plus nanoparticles containing
44 ontrast, prolonged in vivo treatment of beta-thalassemic mice with the proteasome inhibitor bortezomi
45 as been shown to be highly expressed in beta-thalassemic mice, restores hepcidin levels and corrects
46                                           In thalassemic mice, we observed that a greater than normal
47 s confirmed by up-regulation of TfR2 in beta-thalassemic mice, which, like hypotransferrinemic mice,
48 ated or did not improve splenomegaly in beta-thalassemic mice.
49 sg1 expression were performed in healthy and thalassemic mice.
50 d a Jak2 inhibitor, TG101209, to healthy and thalassemic mice.
51 xpression by 52%, yielding 9 g Hb/VC in beta-thalassemic mice.
52  production and correction of anemia in beta-thalassemic mice.
53 oxia during the recovery from anemia, and in thalassemic mice.
54  Transfection of HeLa cells expressing the 3 thalassemic mutants with modified U7 snRNA (U7.623), con
55 HbCS) is the most common nondeletional alpha-thalassemic mutation and is an important cause of HbH-li
56 rable populations of hemoglobin E (HbE)/beta thalassemics, one regularly transfused and one receiving
57 learance of rigid pathological cells such as thalassemic or sickle cells, and even to interactions of
58 t occurrences of benign clonal expansions in thalassemic patients and myelodysplastic syndrome in pat
59           In this study, CD34+ cells from 31 thalassemic patients mobilized with hydroxyurea+granuloc
60 rythropoietic cells from transgenic mice and thalassemic patients suggests the applicability of this
61 ta, thereby increasing the susceptibility of thalassemic patients to infection.
62   Mononuclear cells from peripheral blood of thalassemic patients were treated with morpholino oligon
63                                 Seventy-nine thalassemic patients without a history of chelation ther
64      Reduced HSC quiescence was confirmed in thalassemic patients, along with altered features of the
65        Our data indicate that in a number of thalassemic patients, subpopulations of red cells circul
66  the improvement of hemolytic anemia in beta-thalassemic patients.
67 tectable effect on the microbiome profile of thalassemic patients.
68  lentiviral vector successfully corrects the thalassemic phenotype in patient-derived hematopoietic a
69  Hamp modulation provides improvement of the thalassemic phenotype of the Hbb(th3/+) mouse.
70 bin in red blood cells without inducing beta-thalassemic phenotype.
71 s can result in severe and frequently lethal thalassemic phenotypes.
72 errant 5' or 3' splice sites in the IVS2-705 thalassemic pre-mRNA.
73 her gestational iron loading occurs in human thalassemic pregnancy, when blood transfusion can furthe
74            This premature destruction of the thalassemic RBC could in part be due to a loss of phosph
75 he presence of PS-exposing subpopulations of thalassemic RBC that are most likely physiologically imp
76 n deposits contribute to the pathobiology of thalassemic RBC.
77   Analysis by fluorescent microscopy of beta-thalassemic RBCs indicates that PS on the outer leaflet
78  The results indicate that in the context of thalassemic splicing mutations and possibly in other alt
79 of animals that received transplants of beta-thalassemic stem cells transduced with a new vector cont
80                    Without iron-deficient or thalassemic subjects, the difference had narrowed to 6.1
81 lobin genes in mice results in corresponding thalassemic syndromes that are uniformly fatal in utero.
82 osis of carriers and/or disease-states (i.e. thalassemic syndromes) in newly immigrated and undiagnos
83  the molecular abnormalities that led to the thalassemic syndromes, it still is not known how accumul
84 zed membranes from HbCS and deletional alpha-thalassemic variants and found that in addition to oxidi
85 s more severe when compared with other alpha-thalassemic variants.