ライフサイエンスコーパス: thalassemia

1 eta(0)-thalassemia, and hemoglobin S/beta(+)-thalassemia).

2 ron overload in mice with nontransfused beta-thalassemia.

3 tivity contributes to the pathophysiology of thalassemia.

4 kle S trait associated to heterozygous alpha thalassemia.

5 ing and in distress, and he had a history of thalassemia.

6 n imbalance in cells from patients with beta-thalassemia.

7 CS-R2 alpha-globin enhancer and causes alpha-thalassemia.

8 es are a frequent finding in patients with b-thalassemia.

9 including sickle cell disease (SCD) and beta-thalassemia.

10 strategy for personalized treatment of beta-thalassemia.

11 in people with sickle cell disease and beta-thalassemia.

12 semia-free survival of class 3 patients with thalassemia.

13 disorders, including sickle cell disease and thalassemia.

14 lpha2beta2) production, the hallmark of beta-thalassemia.

15 all patients born each year with severe beta-thalassemia.

16 the severity of sickle cell disease and beta-thalassemia.

17 n those mice does not improve anemia of beta-thalassemia.

18 es to iron overload in a mouse model of beta-thalassemia.

19 patients with hereditary hemochromatosis or thalassemia.

20 ctor suppressing hepcidin production in beta-thalassemia.

21 hemoglobin (Hb) S heterozygotes, and alpha(+)thalassemia.

22 are a frequent finding in patients with beta-thalassemia.

23 tis) for the removal of cardiac iron in beta-thalassemia.

24 nthesis to treat sickle cell anemia and beta thalassemia.

25 e of an autocrine amplification loop in beta-thalassemia.

26 ythroblasts and sera from subjects with beta-thalassemia.

27 mplication is linked to improved outcomes of thalassemia.

28 cal severity of sickle cell disease and beta-thalassemia.

29 d transfusion independence for patients with thalassemia.

30 f patients with sickle cell disease and beta-thalassemia.

31 odifier of hemoglobin disorders such as beta-thalassemia.

32 JAK-2 pathway may reduce thrombotic risk in thalassemia.

33 and ineffective erythropoiesis, such as beta-thalassemia.

34 such as hereditary hemochromatosis and beta-thalassemia.

35 on chelation are all tools to prevent HCC in thalassemia.

36 med was to explore the heparanase profile in thalassemia.

37 bing how to manage HCC in patients with beta-thalassemia.

38 factors, HCC screening seems appropriate for thalassemia.

39 proach in sickle cell disease (SCD) and beta-thalassemia.

40 t schedules of transferrin treatment in beta-thalassemia.

41 uscular atrophy, alpha-thalassemia, and beta-thalassemia.

42 25 were heterozygous), and 6 had alpha-/beta-thalassemia.

43 tion modifying anemia for patients with beta-thalassemia.

44 ment with hepcidin mimetics ameliorates beta-thalassemia.

45 reat congenital blood disorders such as beta-thalassemia.

46 geting ferroportin for the treatment of beta-thalassemia.

47 disease complications in patients with beta-thalassemia.

48 , such as sickle cell disease (SCD) and beta-thalassemia.

49 pe in a heterozygous humanised model of beta-thalassemia.

50 the anemia and ineffective erythropoiesis in thalassemias.

51 e is still no universally available cure for thalassemias.

52 eases, including anemia, erythrocytosis, and thalassemias.

53 malaria risk (HbAS polymorphism, 6.3%; alpha-thalassemia, 0.3%; ABO group, 0.3%; and glucose-6-phosph

54 the severity of sickle cell disease and beta-thalassemia(1).

55 hemoglobin SS (58.7%), 14 SC (30.4%), 4 beta-thalassemia (8.7%), and 1 sickle trait (2.2%).

56 l trait (10/218 [4.6%]) and homozygous alpha+thalassemia (8/216 [3.7%]) were significantly lower amon

57 d nonmalignant homeostasis, we selected beta-thalassemia, a hemoglobin disorder, as a paradigm.

58 together with varying frequencies of alpha(+)thalassemia across Africa may explain the inconsistent r

59 tments in ameliorating IE and anemia in beta-thalassemia and could provide guidance to translate some

60 ncreased erythropoiesis but is pathologic in thalassemia and hemochromatosis.

61 ding to hemoglobin variants and all types of thalassemia and hemoglobinopathies.

62 beta-Thalassemia and HFE-related hemochromatosis are 2 of the

63 sease variation and pathogenesis in HbE beta-thalassemia and indicates that the epidemiology of beta-

64 step, the possible differences between beta-thalassemia and non beta-thalassemia patients.

65 In beta-thalassemia and polycythemia vera (PV), disordered eryth

66 as future therapeutics for untransfused beta-thalassemia and PV.

67 The most recent clinical trials for beta-thalassemia and SCD are showing promising outcomes: pati

68 levels can reduce the severity of both beta-thalassemia and SCD.

69 severity of hemoglobinopathies such as beta-thalassemia and sickle cell anemia.

70 beta-Thalassemia and sickle cell disease (SCD) are the most p

71 dvances include the hemoglobinopathies (beta-thalassemia and sickle cell disease); rare genetic disor

72 s give rise to the beta-globinopathies, beta-thalassemia and sickle cell disease, which begin to mani

73 jor disorders of adult beta-hemoglobin: beta-thalassemia and sickle cell disease.

74 bF inducers to be used in patients with beta-thalassemia and sickle cell disease.

75 The mechanisms by which alpha-thalassemia and sickle cell traits confer protection fro

76 with co-inheritance of heterozygous alpha + -thalassemia and sickle trait.

77 ns and 27 ethnic groups for alpha-, and beta-thalassemias and additional querying options in the HbVa

78 mozygous hemoglobin S or hemoglobin Sbeta(0)-thalassemia), and approximately two thirds were receivin

79 tic fibrosis, spinal muscular atrophy, alpha-thalassemia, and beta-thalassemia.

80 c conditions, including sickle cell disease, thalassemia, and G6PD deficiency, erythrocyte lifespan i

81 pression by erythropoietin, iron deficiency, thalassemia, and hemochromatosis.

82 lobin S (hemoglobin SC, hemoglobin S/beta(0)-thalassemia, and hemoglobin S/beta(+)-thalassemia).

83 ) of patients with sickle cell disease, beta-thalassemia, and hemophilia A/B or von Willebrand diseas

84 ameliorating clinically severe forms of beta-thalassemia, and in particular, the very common subgroup

85 r diseases such as hereditary spherocytosis, thalassemia, and malaria.

86 al in individuals with hemochromatosis, beta-thalassemia, and related disorders.

87 Sickle cell disease and beta-thalassemia are common genetic disorders caused by mutat

88 t to guidelines for the management of HCC in thalassemia are reported by an Italian panel of experts.

89 Thalassemias are a heterogeneous group of red blood cell

90 tic diseases, such as sickle cell anemia and thalassemia, are characterized by enhanced release of he

91 ron disorders, such as hemochromatosis, beta-thalassemia, atransferrinemia and anemia of inflammation

92 ), mainly sickle cell disease (SCD) and beta-thalassemia, become symptomatic postnatally as fetal gam

93 In beta-thalassemia, beta-globin synthesis is reduced causing al

94 oach for translation into a therapy for beta-thalassemia.beta-thalassemia is characterised by the pre

95 beta-thalassemia (betaT) is a genetic blood disorder causing

96 Beta thalassemias (betath) are the result of mutations in the

97 beta-Thalassemia (BT) is a hereditary disorder characterized

98 beta-Thalassemia (BT) is an inherited genetic disorder that i

99 on survey of Sri Lankan schoolchildren, beta-thalassemia (but not HbE) trait was associated with incr

100 pathies such as sickle cell disease and beta-thalassemia, but current gamma-globin-inducing drugs off

101 e response in asplenic individuals with beta-thalassemia, but previous PPSV23s affect the memory B-ce

102 disorders sickle cell disease (SCD) and beta-thalassemia by induction of fetal hemoglobin (HbF, alpha

103 artificially engineered model for human beta thalassemia by knocking down beta-globin gene and protei

104 traps may have therapeutic relevance in beta-thalassemia by suppressing the deleterious effects of GD

105 ealthy volunteers, and in patients with beta-thalassemia, by expanding late-stage erythroblasts throu

106 The effect of thalassemia carriage on hepcidin is also unknown, but it

107 All patients were registered at the Thalassemia Comprehensive Center affiliated with Shiraz

108 on of HbF to ameliorate sickle cell and beta-thalassemia disease severity.

109 with transfusion dependent hemoglobin E/beta-thalassemia disease was treated with hydroxyurea to indu

110 SCD, particularly hemoglobin SS and Sbeta(0)-thalassemia disease, is ethically sound.

111 ronic graft-vs-host disease; and sickle cell-thalassemia disease-free survival, immunologic recovery,

112 uction in patients with sickle cell and beta-thalassemia diseases because of its good efficacy and sa

113 alpha-thalassemia is co-inherited with beta-thalassemia, excess free alpha-globin chains are reduced

114 Patients with thalassemia exhibit an increased risk of thrombotic even

115 tion represents the curative treatment, with thalassemia-free survival exceeding 80%.

116 ailure/rejection and significantly increased thalassemia-free survival of class 3 patients with thala

117 The respective 5-year thalassemia-free survival rates were 73% (95% CI, 51-86%

118 Current thalassemia gene therapy protocols require the collectio

119 ions, thus representing an optimal graft for thalassemia gene therapy.

120 uld permit a broader clinical application of thalassemia gene therapy.

121 of normal, heterozygous, and homozygous beta thalassemia genetic disorders.

122 old) with HbSS and HbS variant (HbSC and HbS thalassemia) genotypes, and their age- and race-matched

123 Ad5/35++ vectors for in vivo gene therapy of thalassemia had a unique capsid that targeted primitive

124 More than 100 varieties of alpha-thalassemia have been identified.

125 with both nontransfused and transfused beta-thalassemia have very high serum ERFE levels, which decr

126 d sickle cell disease (Hb SS) or sickle beta thalassemia (Hb Sbeta), and underwent allogeneic haemato

127 n loading phenotype in a mouse model of beta-thalassemia [Hbb(th3/+) mice] and used these antibodies

128 We hypothesize that in beta-thalassemia heme oxygenase (HO) 1 could play a pathogeni

129 ocyte hydration include sickle cell disease, thalassemia, hemoglobin CC, and hereditary spherocytosis

130 ing altered hematocrit, sickle cell disease, thalassemia, hemolytic anemias, and malaria, with both a

131 history of hemophilia, sickle cell anemia or thalassemia, history of blood transfusion, cocaine and o

132 Hb S heterozygotes and alpha(+)thalassemia homozygotes were protected from severe malar

133 5% CI, 0.32-0.73, respectively), but alpha(+)thalassemia in combination with Hp2-2 was not protective

134 interaction between Hp genotype and alpha(+)thalassemia in predicting risk of severe malaria: Hp2-1

135 Our findings reveal a defect in HSCs in beta-thalassemia induced by an altered BM microenvironment an

136 Here we used a murine model of beta-thalassemia intermedia (Hbb(th1/th1) mice) to investigat

137 atment of mouse models of HH (Hfe(-/-)) and -thalassemia intermedia (Hbb(th3/+)) with Tmprss6 siRNA f

138 the bone marrow of animals affected by beta-thalassemia intermedia (Hbbth3/+).

139 ts with beta-thalassemia major (TM) and beta-thalassemia intermedia (TI) were consecutively recruited

140 lso activated to reduce the severity of beta-thalassemia intermedia in the Hbbth1/th1 murine model.

141 beta-Thalassemia intermedia is a disorder characterized by in

142 liver, spleen, heart, and kidney tissues of thalassemia intermedia mice (Hbb(th3/+)).

143 In contrast, in anemic beta-thalassemia intermedia mice, there is altered progressio

144 CD46-transgenic mice and in a mouse model of thalassemia intermedia that our in vivo approach resulte

145 pothesis, we exploited a mouse model of beta-thalassemia intermedia, Th3/(+) We observed that HO inhi

146 is greatly increased in Hbb(th3/+) mice with thalassemia intermedia, where it contributes to the supp

147 In beta-thalassemia intermedia, which does not require blood tra

148 of Hbb(Th3/+) mice (Th3/+), a mouse model of thalassemia intermedia.

149 mited iron overload in a mouse model of beta-thalassemia intermedia.

150 modifying disease-associated morbidities of -thalassemia intermedia.

151 eostasis in the Hbbth3/+ mouse model of beta-thalassemia intermedia.

152 may transform severe, transfusion-dependent thalassemia into relatively mild forms of anemia.

153 -thalassemia is a congenital anemia caused by partial or

154 beta-Thalassemia is a genetic anemia caused by partial or com

155 beta-thalassemia is a hereditary disorder with limited approv

156 Beta-thalassemia is a severe genetic blood disorder caused by

157 HbE/beta-thalassemia is a subtype of beta-thalassemia with extrem

158 In developed countries, treatment of thalassemia is also still far from ideal, requiring life

159 beta-Thalassemia is associated with several abnormalities of

160 B-thalassemia is caused by B-globin gene mutations resulti

161 nsplantation (BMT) for class 3 patients with thalassemia is challenging due to high rates of graft re

162 ion into a therapy for beta-thalassemia.beta-thalassemia is characterised by the presence of an exces

163 beta-Thalassemia is characterized by ineffective erythropoies

164 When alpha-thalassemia is co-inherited with beta-thalassemia, exces

165 alis syndrome (BHFS) resulting from alpha(0)-thalassemia is considered a universally fatal disorder.

166 However, since thalassemia is endemic in many under-developed countries

167 Clinical heterogeneity in HbE beta-thalassemia is incompletely explained by genotype, and t

168 donor hematopoietic cell transplantation in thalassemia is not well established.

169 beta-Thalassemia is one of the most common inherited anemias,

170 iology of ineffective erythropoiesis in beta-thalassemia is poorly understood.

171 Studying molecular defects behind beta-thalassemia is severely impeded by paucity of material f

172 Hemoglobin E (HbE) beta-thalassemia is the most common severe thalassemia syndro

173 chanism of increased iron absorption in beta-thalassemia is unclear.

174 transfusional iron-overload diseases, e.g., thalassemia, is overviewed.

175 roval and informed consent, 30 patients with thalassemia major (mean age +/- standard deviation, 34.6

176 Patients with thalassemia major (Thal) frequently have low plasma zinc

177 A total of 255 patients with beta-thalassemia major (TM) and beta-thalassemia intermedia (

178 PAH) remains a concern in patients with beta-thalassemia major (TM) and intermedia (TI); however, stu

179 e analyzed the outcomes of 485 patients with thalassemia major (TM) or sickle cell disease (SCD) rece

180 L)-6, and IL-8 in biofluids of patients with thalassemia major (TM) with or without gingivitis.

181 till a major cause of death in patients with thalassemia major (TM).

182 31 chronically transfused patients with beta-thalassemia major and collected samples immediately befo

183 Conclusion ECV is significantly increased in thalassemia major and is associated with myocardial iron

184 g cardiac magnetic resonance (MR) imaging in thalassemia major and to investigate the relationship be

185 A 34-year-old man with thalassemia major complained of nyctalopia and decreased

186 Hepcidin levels in patients with beta-thalassemia major dynamically reflect competing influenc

187 al incidence of melioidosis in children with thalassemia major from 2001 to 2010 was 140 per 100 000/

188 We studied 107 pediatric thalassemia major patients (61 boys, median age 14.4 yea

189 oietin levels were found in the plasma of 67 thalassemia major patients compared with 29 control subj

190 eek) for myocardial iron removal in 197 beta-thalassemia major patients with myocardial siderosis (T2

191 In spleen specimens of thalassemia major patients, a higher level of heparanase

192 (CMR) plays a key role in the management of thalassemia major patients, but few data are available i

193 tiparametric CMR approach can occur early in thalassemia major patients.

194 ction, and fibrosis in a cohort of pediatric thalassemia major patients.

195 Individuals with beta-thalassemia major require regular lifelong Red Blood Cel

196 Thalassemia major was a major risk factor for melioidosi

197 ron chelation therapy in 2010, no child with thalassemia major was diagnosed with melioidosis in 2011

198 n several of these disorders, including beta-thalassemia major, which is characterized by a defective

199 re reviewed including 11 (41%) children with thalassemia major.

200 progenitor cells (HPCs) in adults with beta-thalassemia major.

201 ents in the management of patients with beta-thalassemia major.

202 s between basic and clinical studies of beta-thalassemia major.

203 ith ineffective erythropoiesis, such as beta-thalassemia, manifest inappropriately low hepcidin produ

204 Ocular findings in beta-thalassemia may correlate to the disease itself, iron ov

205 Beta-thalassemia may present with various signs, both structu

206 Mutational inactivation of ATRX (alpha-thalassemia mental retardation X-linked) represents a de

207 ever, Sp100A cannot overcome Daxx- and alpha-thalassemia mental retardation, X-linked (ATRX)-mediated

208 characterize the Arabidopsis thaliana Alpha Thalassemia-mental Retardation X-linked (ATRX) ortholog

209 Alpha thalassemia/mental retardation syndrome X-linked (ATRX)

210 Alpha thalassemia/mental retardation syndrome X-linked chromat

211 he large N-terminal deletions of ATRX (Alpha Thalassemia/Mental Retardation, X-linked) that generate

212 ificantly higher than untreated heterozygous thalassemia mice suggesting that IUGT ameliorated poor c

213 which serve as a model of untransfused beta-thalassemia, minihepcidin ameliorates ineffective erythr

214 In older mice with untransfused beta-thalassemia, minihepcidin improves erythropoiesis and do

215 In the thalassemia model, a near-complete phenotypic correction

216 We used the Hbb(th3/+) beta-thalassemia mouse and hemoglobin E (HbE)/beta-thalassemi

217 Here, we reported that correction of beta-thalassemia mutations in patient-specific iPSCs using th

218 that CRISPR/Cas9 successfully corrects beta-thalassemia mutations in patient-specific iPSCs.

219 Naturally occurring alpha-thalassemia mutations that trigger aberrant splicing hav

220 vital process in pathologies, including beta-thalassemia, myelodysplastic syndrome, and viral infecti

221 Patients with transfusion-dependent beta-thalassemia need regular red-cell transfusions.

222 Beta-thalassemia ocular manifestations include ocular surface

223 ublished data suggest an incidence of HCC in thalassemia of about 2%.

224 beta-thalassemia, one of the most common genetic diseases wor

225 s with HCV infection and sickle cell anemia, thalassemia, or hemophilia A/B or von Willebrand disease

226 Co-inheritance of HPFH with beta-thalassemia- or SCD-associated gene mutations alleviates

227 parasitemia level at baseline (P = .02), and thalassemia (P = .027) influenced the initial decrease i

228 The underlying basis of thalassemia pathology is the premature apoptotic destruc

229 We further assessed whether thalassemia patient CD34(+) HPCs could be transduced wit

230 e procedure for beta-globin gene transfer in thalassemia patient CD34(+) HPCs, which we will implemen

231 of HbF have been studied in the past in beta-thalassemia patient populations, with limited success in

232 id progeny from sickle cell disease and beta-thalassemia patient-derived HSPCs, respectively.

233 om peripheral blood stem cells of a HbE/beta-thalassemia patient.

234 r cross-sectional study of 1309 Italian beta-thalassemia patients (mean age 36.4+/-9.3 years; 46% men

235 The prevalence of PAH in beta-thalassemia patients as confirmed on right heart cathete

236 ced pluripotent stem cells (iPSCs) from beta-thalassemia patients could offer an approach to cure thi

237 es were similar in diabetic and non-diabetic thalassemia patients indicating close monitoring and pro

238 g issue, the number of papers on HCC in beta-thalassemia patients is limited and based on anecdotal c

239 In this study, a high percentage of beta-thalassemia patients receiving luspatercept had hemoglob

240 halassemia mouse and hemoglobin E (HbE)/beta-thalassemia patients to investigate dysregulated neutrop

241 sed a new treatment protocol (Pc 26.1) in 16 thalassemia patients to perform BMT using phenotypically

242 that the Pc 26.1 preparative regimen allows thalassemia patients to safely undergo BMT from RDs who

243 r HSCT showed that the long-term HRQoL of ex-thalassemia patients was very similar to that of the gen

244 As beta-thalassemia patients' survival has increased over time,

245 into defective neutrophil maturation in beta-thalassemia patients, which contributes to deficiencies

246 plenectomized and nonsplenectomized HbE/beta-thalassemia patients.

247 rences between beta-thalassemia and non beta-thalassemia patients.

248 defective immune functions observed in beta-thalassemia patients.

249 rythropoiesis, such as in patients with beta-thalassemia, promotes the tissue iron accumulation that

250 s is the first human cellular model for beta-thalassemia providing a sustainable source of disease ce

251 between 5 and 16.7 years of age with class 3 thalassemia received HLA-matched sibling BMT following e

252 Beta-thalassemia represents a heterogeneous group of haemoglo

253 21 years old with hemoglobin SS or Sbeta(0) thalassemia requiring hospitalization for pain were elig

254 beta-thalassemia results from point mutations or small deleti

255 d ineffective erythropoiesis, for example in thalassemia, results in sustained elevations in iron abs

256 Here, we identify alpha-thalassemia retardation syndrome X-linked (ATRX) as a no

257 in C (SC) profile, 1 was sickle cell-beta(+) thalassemia (S beta(+)-thal), and 4 were sickle cell tra

258 a [Sbeta(0)], 495 SC, and 161 sickle beta(+)-thalassemia [Sbeta(+)]), aged 3 years old and over, were

259 07 SCD patients (1751 SS or sickle beta-zero-thalassemia [Sbeta(0)], 495 SC, and 161 sickle beta(+)-t

260 ring wild-type cells with hemoglobin H (HbH) thalassemia (shorter pathlength and reduced tortuosity)

261 Decisions in the management of HCC in thalassemia should follow a multidisciplinary effort.

262 diagnosis, and management suggest that alpha-thalassemias should have a higher priority on global pub

263 ickling, while those from patients with beta-thalassemia show restored globin chain balance.

264 isorders such as hereditary hemochromatosis, thalassemia, sickle cell disease, and myelodysplasia tha

265 is father is a carrier of heterozygous alpha-thalassemia status that it was unknown before.

266 Evidence from beta-thalassemia suggests that regulation of hepcidin by eryt

267 ) beta-thalassemia is the most common severe thalassemia syndrome across Asia, and millions of people

268 ligand trap as a novel therapeutic agent for thalassemia syndrome and other red cell disorders charac

269 The beta-thalassemia syndromes are the most prevalent genetic dis

270 hronic transfusions in transfusion-dependent thalassemia (TDT) and iron chelation impairs quality of

271 Transfusion-dependent beta-thalassemia (TDT) and sickle cell disease (SCD) are seve

272 in patients with transfusion-dependent beta-thalassemia (TDT) mainly chronic anemia, iron overload a

273 Sickle cell disease (SCD) and thalassemias (Thal) are common congenital disorders, whi

274 icantly more prevalent in patients with beta-thalassemia than previously recognized and correlate wit

275 subgroup of patients with hemoglobin E beta-thalassemia that makes up approximately half of all pati

276 th opioid use, HIV and transfusion-dependent thalassemia, the risk of fracture in these populations i

277 ntries, where the greatest demand for a beta-thalassemia therapy lies.

278 isorders such as sickle cell anemia and beta-thalassemia through activation of the fetal gamma-globin

279 atio, adults with transfusion-dependent beta-thalassemia to receive best supportive care plus luspate

280 sive review of observational studies on beta-thalassemia, to determine the prevalence and spectrum of

281 The thalassemias, together with sickle cell anemia and its v

282 In Southeast Asia, Thalassemia trait (TT) and iron deficiency anemia (IDA)

283 We also found that: (i) beta-thalassemia trait carriers displayed lower TC and were p

284 progression indicates that the lower IMF in thalassemia trait erythrocytes limits parasite density a

285 Reduction of IMFs in thalassemia trait erythrocytes was confirmed using clini

286 in control, HbAS, HbSS, and alpha- and beta-thalassemia trait erythrocytes, respectively.

287 s with erythrocyte indices and is reduced in thalassemia trait erythrocytes.

288 and indicates that the epidemiology of beta-thalassemia trait requires consideration when planning p

289 2, a marker used for the diagnosis of a beta-thalassemia trait.

290 In beta-thalassemia, unequal production of alpha- and beta-globi

291 tion with heterozygous or homozygous alpha(+)thalassemia was associated with protection from severe m

292 A humanised mouse model of beta-thalassemia was used, in which heterozygous animals are

293 of ineffective erythropoiesis in humans with thalassemia, was significantly increased in the culture

294 glucose-6-phosphate dehydrogenase, and alpha-thalassemia) were the only ones to be associated with al

295 ributes to iron-loading anemias such as beta-thalassemia, whereas excess hepcidin induction contribut

296 n summary, heparanase levels are elevated in thalassemia, which may contribute to thrombotic phenomen

297 of patients with transfusion-dependent beta-thalassemia who had a reduction in transfusion burden wa

298 s with sickle cell phenotype with or without thalassemia who underwent nonmyeloablative allogeneic HS

299 HbE/beta-thalassemia is a subtype of beta-thalassemia with extremely high frequency in Asia.

300 n 62 of 69 Sri Lankan patients with HbE beta-thalassemia with moderate or severe phenotype, hepcidin