ライフサイエンスコーパス: sickle

1 ng, mediated by a pathway sometimes called P(sickle).

2 we did not detect differences in erythrocyte sickling.

3 despread catastrophic intravascular red-cell sickling.

4 clinical measures of anemia, hemolysis, and sickling.

5 om the patient's blood before and after cell sickling.

6 le hemoglobin polymerization and erythrocyte sickling.

7 y for O(2) with subsequent prevention of RBC sickling.

8 ents that reactivate fetal haemoglobin, anti-sickling agents, anti-adhesion agents, modulators of isc

9 c base edit of the BCL11A enhancer prevented sickling and ameliorated globin chain imbalance in eryth

10 eticulocytosis, enhanced ex vivo erythrocyte sickling, and increased erythrocyte phosphatidylserine e

11 lly confirmed sickle cell disease (Hb SS) or sickle beta thalassemia (Hb Sbeta), and underwent alloge

12 zero-thalassemia [Sbeta(0)], 495 SC, and 161 sickle beta(+)-thalassemia [Sbeta(+)]), aged 3 years old

13 d Ivory Coast, 2407 SCD patients (1751 SS or sickle beta-zero-thalassemia [Sbeta(0)], 495 SC, and 161

14 Numerous studies, however, have shown that sickle blood flow is affected even at high oxygen tensio

15 Our results suggest that sickle blood flow is altered systemically, from the arte

16 Overall, this study highlights that sickle blood flow is altered systemically, which can dri

17 ged an experimental platform that quantifies sickle blood velocity fields under a range of oxygen ten

18 ed by the platelet-free cellular fraction of sickle blood.

19 by PMos was specific to endothelial-attached sickle, but not control, RBCs and occurred mostly throug

20 esting findings including association of the sickle cell allele of betaglobin among non-Hispanic blac

21 His mother has Sickle cell anaemia (Hb SS) and his father is a carrier

22 We identified 51 (1%) children with sickle cell anaemia (HbSS), four (<1%) heterozygous for

23 st syndrome (ACS) is a major complication of sickle cell anaemia (SCA) and a leading cause for hospit

24 (PS) exposure is increased in red cells from sickle cell anaemia (SCA) patients.

25 The point mutation responsible for sickle cell anaemia codes for a variant hemoglobin, sick

26 biliary ultrasound findings in patients with sickle cell anaemia.

27 Most participants had sickle cell anemia (homozygous hemoglobin S or hemoglobi

28 ariate analysis showed that in patients with sickle cell anemia (SCA) genotypes, older age (95% confi

29 In children with sickle cell anemia (SCA), high transcranial Doppler (TCD

30 Sickle cell anemia (SCA)-related cardiomyopathy is chara

31 ory vaso-occlusive processes associated with sickle cell anemia (SCA).

32 T) prevents stroke in selected patients with sickle cell anemia (SCA).

33 is associated with diastolic dysfunction in sickle cell anemia (SCA).

34 at high concentration in the circulation of sickle cell anemia (SS) patients.

35 e validated in a cohort of 283 patients with sickle cell anemia and known pediatric cerebrovascular o

36 uld be present in about 10% of children with sickle cell anemia and represent a genetic risk factor t

37 enrolled children 1 to 10 years of age with sickle cell anemia in four sub-Saharan countries.

38 Among children with sickle cell anemia in sub-Saharan Africa, hydroxyurea wi

39 , feasibility, and efficacy in children with sickle cell anemia in sub-Saharan Africa, with studies s

40 Sickle cell anemia is a unique disease dominated by hemo

41 tment was feasible and safe in children with sickle cell anemia living in sub-Saharan Africa.

42 lls and enabled A*T-to-G*C base editing of a sickle cell anemia mutation using a previously inaccessi

43 h stiffening of red blood cells (RBCs; e.g., sickle cell anemia or malaria), the mechanical propertie

44 Hemolysis is a fundamental feature of sickle cell anemia that contributes to its pathophysiolo

45 Hydroxyurea is an effective treatment for sickle cell anemia, but few studies have been conducted

46 which occurs in diseases such as malaria and sickle cell anemia, or following blood transfusions.

47 iven disease processes in conditions such as sickle cell anemia, sepsis, transfusion reactions, medic

48 lotor (500-1000 mg per day) in patients with sickle cell anemia.

49 vestigations into cerebrovascular disease in sickle cell anemia.

50 lar transfusions to prevent complications of sickle cell anemia.

51 stating complication affecting children with sickle cell anemia.

52 readmission rate after hospitalization for a sickle cell crisis (SCC) is extremely high.

53 rvation, 95% CI 40-86) than in those without sickle cell disease (2.4 per 1000 person-years of observ

54 sickle cell disease than in children without sickle cell disease (210 per 1000 person-years of observ

55 Mortality was higher in children with sickle cell disease (58 per 1000 person-years of observa

56 ger than 50 years, had genetically confirmed sickle cell disease (Hb SS) or sickle beta thalassemia (

57 est expression in children with both SMA and sickle cell disease (HbSS), corresponding with elevated

58 ew byproducts, the primary genetic causes of sickle cell disease (requiring a transversion in HBB) an

59 e (ACS) is a common, serious complication of sickle cell disease (SCD) and a leading cause of hospita

60 ameliorate the severe beta-globin disorders sickle cell disease (SCD) and beta-thalassemia by induct

61 ta2) is an important therapeutic approach in sickle cell disease (SCD) and beta-thalassemia.

62 fully applied to hemoglobinopathies, such as sickle cell disease (SCD) and beta-thalassemia.

63 hemopexin deficiency, and kidney function in sickle cell disease (SCD) and report that (1) acute elev

64 sfusion-dependent beta-thalassemia (TDT) and sickle cell disease (SCD) are severe monogenic diseases

65 beta-Thalassemia and sickle cell disease (SCD) are the most prevalent monogen

66 n two patients admitted to the hospital with sickle cell disease (SCD) crisis.

67 issue of Blood, Matte et al demonstrate that sickle cell disease (SCD) disrupts inflammation-resoluti

68 Persons with sickle cell disease (SCD) exhibit subjective hypersensit

69 Children with sickle cell disease (SCD) experience cognitive deficits

70 Sickle cell disease (SCD) is a genetic disorder caused b

71 Sickle cell disease (SCD) is a genetic hemoglobinopathy

72 Sickle cell disease (SCD) is a highly complex genetic bl

73 Sickle cell disease (SCD) is a monogenic disorder that a

74 Sickle cell disease (SCD) is a worldwide hematological d

75 Sickle cell disease (SCD) is associated with chronic act

76 Pulmonary hypertension (PH) in adults with sickle cell disease (SCD) is associated with early morta

77 Sickle cell disease (SCD) is caused by a variant hemoglo

78 Sickle cell disease (SCD) is one of the most common here

79 Sickle cell disease (SCD) leads to significant morbidity

80 nd colleagues demonstrate that patients with sickle cell disease (SCD) on hydroxyurea have lower cere

81 on of sickle hemoglobin (HbS) play a role in sickle cell disease (SCD) pathogenesis.

82 gh hemoglobin-hyperviscous" subphenotypes of sickle cell disease (SCD) patients is based on North Ame

83 ating MPs on endothelial cells (ECs) from 60 sickle cell disease (SCD) patients.

84 Sickle cell disease (SCD) results from a hemoglobin (Hb)

85 Sickle cell disease (SCD) results in cardiopulmonary dys

86 openia are common clinical manifestations of sickle cell disease (SCD) with unclear mechanisms.

87 Pain is a characteristic feature of sickle cell disease (SCD), 1 of the most common inherite

88 Sickle cell disease (SCD), a genetic disorder of hemoglo

89 However, its function in sickle cell disease (SCD), a life-threatening hemolytic

90 he proximate event in the pathophysiology of sickle cell disease (SCD), are needed to address the sev

91 nificant cause of morbidity and mortality in sickle cell disease (SCD), but preventive, diagnostic, a

92 Altered mitochondrial function occurs in sickle cell disease (SCD), due in part to low nitric oxi

93 Certain populations, including people with sickle cell disease (SCD), exhibit a greater prevalence

94 hich leads to the systemic manifestations of sickle cell disease (SCD), including vaso-occlusion, ana

95 n these genes cause cystic fibrosis (CF) and sickle cell disease (SCD), respectively.

96 Sickle cell disease (SCD)-associated nephropathy is a ma

97 injury (AKI) is a major clinical concern in sickle cell disease (SCD).

98 ctivity correlates with heme levels in mouse sickle cell disease (SCD).

99 worsens symptoms and crises in patients with sickle cell disease (SCD).

100 evaluated for hemoglobin disorders including sickle cell disease (SCD).

101 lowering may also have beneficial effects in sickle cell disease (SCD).

102 sis (VOC) is the most common complication of sickle cell disease (SCD).

103 reportedly occurs in 10% of adolescents with sickle cell disease (SCD).

104 ies have hampered their development to treat sickle cell disease (SCD).

105 nts in the microvasculature of patients with sickle cell disease (SCD).

106 ry cause of morbidity and hospitalization in sickle cell disease (SCD); however, only 4 therapies (hy

107 mergent complication affecting patients with sickle cell disease (SCD); however, the molecular mechan

108 g inflammation, cancer, neuroprotection, and sickle cell disease among many others.

109 olled 17 consecutive patients: 12 (71%) with sickle cell disease and 5 (29%) with beta-thalassaemia m

110 in chain imbalance in erythroid progeny from sickle cell disease and beta-thalassemia patient-derived

111 oglobin (HbF) can ameliorate the severity of sickle cell disease and beta-thalassemia(1).

112 tical goal in the treatment of patients with sickle cell disease and beta-thalassemia.

113 Participants were tested for sickle cell disease and followed up for survival status

114 is simple risk score may guide patients with sickle cell disease and hematologists who are considerin

115 ase that manifests clinical complications in sickle cell disease and other chronic hereditary or acqu

116 a from patients with known oxidative stress (sickle cell disease and sepsis) and from a patient with

117 Of 996 patients with sickle cell disease and who underwent transplantation in

118 Sickle cell trait and sickle cell disease are thought to be independent risk f

119 ere, using vaso-occlusive episodes (VOEs) of sickle cell disease as a vascular disease model, we show

120 presented for immunisation were screened for sickle cell disease at five primary health-care centres

121 ian period 2: a missing beneficial factor in sickle cell disease by lowering pulmonary inflammation,

122 faster in patients with sickle cell trait or sickle cell disease compared with reference patients; it

123 We systematically screened for sickle cell disease consecutive newborn babies and infan

124 In Africa, 50-90% of children born with sickle cell disease die before they reach their fifth bi

125 Living with a long-term condition such as sickle cell disease during adolescence constitutes a sig

126 patient transition from paediatric to adult sickle cell disease health care is unlikely to address t

127 We enrolled patients with sickle cell disease in a single-center, open-label pilot

128 Increased longevity of patients with sickle cell disease in high-income, middle-income, and l

129 udy bodes well for the care of patients with sickle cell disease in resource-poor countries.

130 d mortality were high in young children with sickle cell disease in this Kenyan cohort, both were red

131 Sickle cell disease is a life-threatening inherited cond

132 The pathology of sickle cell disease is caused by polymerization of the a

133 Sickle cell disease is characterized by hemolytic anemia

134 Sickle cell disease is highly prevalent in sub-Saharan A

135 Sickle cell disease is one of the most common, life-thre

136 own for more than 60 years that the cause of sickle cell disease is polymerization of a hemoglobin mu

137 Sickle cell disease is the most common severe monogenic

138 Although the root cause of sickle cell disease is the polymerization of hemoglobin

139 one marrow transplantation for patients with sickle cell disease on a clinical trial that had a compa

140 children, pregnant women, and patients with sickle cell disease or AIDS.

141 Our study shows that outcome is impaired in sickle cell disease patients receiving extracorporeal li

142 from healthy donors and thrombocytopenic and sickle cell disease patients.

143 Over the 8-year period, 22 patients with sickle cell disease required extracorporeal life support

144 Sickle cell disease results from a homozygous missense m

145 ed to test the feasibility of implementing a sickle cell disease screening programme using innovative

146 to hospital was also higher in children with sickle cell disease than in children without sickle cell

147 clined significantly faster in patients with sickle cell disease than in patients with sickle cell tr

148 rities to consider for any young person with sickle cell disease transitioning from paediatric to adu

149 disease and sepsis) and from a patient with sickle cell disease treated with the antioxidant N-acety

150 n for admission to hospital among those with sickle cell disease was severe anaemia (incidence 48 per

151 Children with sickle cell disease were offered confirmatory testing an

152 Clinical manifestations of sickle cell disease were reduced or absent during the fo

153 so shows that neutrophils from patients with sickle cell disease were unresponsive to one of two majo

154 t-free survival is improved in patients with sickle cell disease who receive an allogenic transplanta

155 assess the visual function of patients with sickle cell disease with no visual symptoms despite temp

156 rom 60 participants (20 controls and 40 with sickle cell disease).

157 Of the 55 babies and infants with confirmed sickle cell disease, 41 (75%) were enrolled into a progr

158 In sickle cell disease, aberrant blood flow due to oxygen-d

159 51 patients with sickle cell trait, 230 with sickle cell disease, and 8729 reference patients, with a

160 the antiphospholipid syndrome, preeclampsia, sickle cell disease, and biomaterial-induced thromboinfl

161 as hereditary hemochromatosis, thalassemia, sickle cell disease, and myelodysplasia that can lead to

162 in animal models of diseases such as cancer, sickle cell disease, and renal fibrosis.

163 ul for severe acute chest syndrome in adults sickle cell disease, because of the frequent hemodynamic

164 f 41), and 89.4% (42 of 47) of patients with sickle cell disease, beta-thalassemia, and hemophilia A/

165 ation occurs in hemolytic disorders, such as sickle cell disease, but the pathological relevance and

166 QCT molecular counting to develop sgNIPTs of sickle cell disease, cystic fibrosis, spinal muscular at

167 In patients with sickle cell disease, donor and recipient red cell phenot

168 y be warranted when evaluating patients with sickle cell disease, even if asymptomatic with 20/20 vis

169 nts had beta-thalassaemia major, 27 (7%) had sickle cell disease, five (1%) had thalassodrepanocytosi

170 ess is thought to contribute to pathology in sickle cell disease, in this issue of Blood, Morris et a

171 from microcirculatory impairment, including sickle cell disease, ischemic heart disease, and heart f

172 Among children with sickle cell disease, mortality was lower in those who en

173 e KGBCS, and 128 (0.8%) of these infants had sickle cell disease, of whom 70 (54.7%) enrolled at the

174 y disorders of erythrocyte hydration include sickle cell disease, thalassemia, hemoglobin CC, and her

175 controlled trial involving participants with sickle cell disease, voxelotor significantly increased h

176 d between birth and 5 years with and without sickle cell disease, who were resident within the Kilifi

177 n offers a favorable risk-benefit profile in sickle cell disease.

178 liable and accurate in newborn screening for sickle cell disease.

179 us thromboembolism observed in patients with sickle cell disease.

180 polymerization drives the pathophysiology of sickle cell disease.

181 and prevention of long-term complications of sickle cell disease.

182 vent liver injury in hemolytic diseases like sickle cell disease.

183 transplantation outcomes of in patients with sickle cell disease.

184 ntage, as in the case of cystic fibrosis and sickle cell disease.

185 lly once daily) with placebo in persons with sickle cell disease.

186 and offer prospects for curative therapy of sickle cell disease.

187 ng the subcellular and cellular phenomena in sickle cell disease.

188 n a variety of diseases including cancer and sickle cell disease.

189 ne in black patients, with faster decline in sickle cell disease.

190 eneic hematopoietic cell transplantation for sickle cell disease.

191 he pathophysiology and many subphenotypes of sickle cell disease; (3) clinical implications of person

192 ssociation was observed between Sl genotype, sickle cell genotype, alpha+thalassaemia genotype, gende

193 Sickle cell genotypes included 27 patients with hemoglob

194 l homozygote (SS) genotype, 113 (28%) showed sickle cell hemoglobin C (SC) genotype, and 77 (19%) sho

195 nrollment with electrophoretically confirmed sickle cell hemoglobinopathies followed by the Universit

196 Peripapillary RNFL thinning in patients with sickle cell hemoglobinopathies occurred faster in patien

197 Children with sickle cell hemoglobinopathy (SCH) can demonstrate proli

198 enefit the development of therapies to treat sickle cell hepatic crisis.

199 e (SCD); however, the molecular mechanism of sickle cell hepatobiliary injury remains poorly understo

200 6 years; range 0-18 years), 208 (52%) showed sickle cell homozygote (SS) genotype, 113 (28%) showed s

201 at, relative to wild-type (WT) mice, Berkley sickle cell mice (BERK-SS) residing at sea level, mild (

202 emonstrate FnCas9-mediated correction of the sickle cell mutation in patient-derived induced pluripot

203 w robust bi-allelic correction of homozygous sickle cell mutations in a patient-derived induced PSC (

204 tan operation), for a kidney transplant 2.8 (sickle cell nephropathy as primary cause of end-stage re

205 P = .02) were associated with proliferative sickle cell retinopathy (PSR).

206 e at onset, and risk factors associated with sickle cell retinopathy (SCR) to inform development of s

207 The prevalence of both the sickle cell trait (10/218 [4.6%]) and homozygous alpha+t

208 ygous for HbS and HbC (HbSC), 740 (21%) with sickle cell trait (HbAS), 34 (1%) heterozygous for HbA a

209 's health in a case-control study, using the sickle cell trait (HbAS), a condition associated with a

210 rature regarding management of patients with sickle cell trait (SCT) undergoing cardiac surgery, sinc

211 Sickle cell trait and disease are associated with faster

212 duced compared with the number released from sickle cell trait and nonsickle clots in both mice and h

213 Sickle cell trait and sickle cell disease are thought to

214 S was associated with faster eGFR decline in sickle cell trait but may be confounded by concurrent he

215 2018) and included adult black patients with sickle cell trait or disease (exposures) or normal hemog

216 clined significantly faster in patients with sickle cell trait or sickle cell disease compared with r

217 We identified 1251 patients with sickle cell trait, 230 with sickle cell disease, and 872

218 In subjects with sickle cell trait, heterozygosity for PIEZO1 E756del did

219 In sickle cell trait, low hemoglobin S and elevated hemoglo

220 y cancer in patients of African descent with sickle cell trait.

221 th sickle cell disease than in patients with sickle cell trait.

222 ldren in the dose-escalation group had fewer sickle cell-related adverse events (incidence rate ratio

223 alaria), and benefits (laboratory variables, sickle cell-related events, transfusions, and survival).

224 on, with symptoms defining the acute painful sickle-cell crisis.

225 reacting with hydrogen peroxide (H(2)O(2)), sickle-cell hemoglobin (HbS, betaE6V) remains longer in

226 degree of protection to that afforded by the sickle-cell trait and considerably greater than that off

227 th many protective polymorphisms-such as the sickle-cell trait-having been selected to high frequenci

228 technique, we obtained similar percentage of sickle cells in blood samples as analyzed by conventiona

229 re consistent with the presence of PIEZO1 in sickle cells, able to mediate Ca(2+) entry but that PKC

230 ](i) is maintained at very low levels but in sickle cells, Ca(2+) permeability is increased, especial

231 ne-edited cells showed a marked reduction of sickle cells, with the level of normal hemoglobin (HbA)

232 n PIEZO1 agonist, to investigate its role in sickle cells.

233 guish the normal red blood cells (RBCs) from sickled cells.

234 t the structure, properties, and dynamics of sickle clot formation.

235 These properties of sickle clots may explain the increased risk of venous th

236 ansiently reversed resistance of whole blood sickle clots to fibrinolysis, in part by decreasing plat

237 , increased the number of RBCs released from sickle clots.

238 ce, 23 showed a 37.8% (+/-9.0%) reduction in sickling compared to vehicle treated mice.

239 esents many precipitating risk factors for a sickling crisis.

240 n is especially prominent in clots involving sickle erythrocytes (see figure), consistent with the in

241 reased erythrocyte S1P binds to deoxygenated sickle Hb (deoxyHbS), facilitates deoxyHbS anchoring to

242 > betaVal6 that changes normal Hb (HbA) into sickle Hb (HbS).

243 y-free paper-based test capable of detecting sickle hemoglobin (HbS) in newborn blood samples with a

244 idative stress and oxidative modification of sickle hemoglobin (HbS) play a role in sickle cell disea

245 Deoxygenated sickle hemoglobin (HbS) polymerization drives the pathop

246 intense interest given the HbF inhibition of sickle hemoglobin (HbS) polymerization.

247 atments directly targeting polymerization of sickle hemoglobin (HbS), the proximate event in the path

248 cell anaemia codes for a variant hemoglobin, sickle hemoglobin or HbS, whose presence drives the path

249 meliorate these manifestations by mitigating sickle hemoglobin polymerization and erythrocyte sicklin

250 in of adult hemoglobin (HbA) that results in sickled hemoglobin (HbS).

251 tream consequences of polymerization and RBC sickling include vaso-occlusion, hemolytic anemia, and s

252 ts on Hb modification, Hb-O(2) affinity, and sickling inhibition, with sustained pharmacological effe

253 The RBC sickling is made worse by the low oxygen (O(2)) affinity

254 The molecular identity of P(sickle) is also unclear but recent work has implicated t

255 id fibers, causing red blood cells (RBCs) to sickle; leading to numerous adverse pathological effects

256 ased, especially following deoxygenation and sickling, mediated by a pathway sometimes called P(sickl

257 Selective depletion of PMos in Townes sickle mice exacerbated vascular stasis and tissue damag

258 TF inhibition reduces lung vaso-occlusion in sickle mice mediated by arteriolar neutrophil-platelet m

259 ed that hemopexin deficiency promotes AKI in sickle mice under hemolytic stress.

260 AKI was blocked when hemopexin deficiency in sickle mice was corrected with infusions of purified hem

261 nhematopoietic cells, also reduces stasis in sickle mice.

262 on were observed in venous thrombi formed in sickle mice.

263 demonstrate efficient gene correction of the sickle mutation in both peripheral blood and bone marrow

264 nded oligonucleotide template to correct the sickle mutation in the beta-globin gene in hematopoietic

265 Sickling of RBCs and a significant increase in fibrin de

266 enated state, polymerization of HbS leads to sickling of red blood cells (RBC).

267 erived SCD HSPCs, a significant reduction in sickling of red blood cells, engraftment of gene-edited

268 systematization no doubt contributes to all sickle pathology.

269 a mouse model of SCD and blood samples from sickle patients to determine if these changes affect the

270 cant resistance to oxidative stress and anti-sickling properties to HbS and therefore could be potent

271 In addition, transfusions, by lowering sickle RBC uptake, improved PMo survival.

272 ar debris, could remove endothelial-adherent sickle RBCs and ameliorate VOC in SCD.

273 mechanisms that remove endothelial-attached sickle RBCs from the microvasculature are expected to be

274 echanism for removal of endothelial attached sickle RBCs mediated by PMos that can protect against VO

275 the morphologies and membrane stiffening of sickle RBCs.

276 Entrapment of sickled RBCs was largely factor XIIIa-independent and en

277 dult services, and evaluating readiness (the SICKLE recommendations).

278 usion is initiated by increased adherence of sickle red blood cells (RBCs) to the vascular endotheliu

279 phosphatidylserine exposed on the senescent sickle red cell membrane.

280 The entrapped sickle red cells make the attached fibrin more resistant

281 This is an unexpected way that sickle red cells modulate the clotting mechanism.

282 f vaso-occlusion by increasing entrapment of sickled red blood cells in the microvasculature.

283 and reduction in hemolysis and percentage of sickled red cells, supporting the potential of voxelotor

284 vaso-occlusion induced by integrin-dependent sickle-red blood cell-leukocyte adhesion.

285 Based on standard screening techniques, sickle retinopathy reportedly occurs in 10% of adolescen

286 eyes with adequate UWFA studies demonstrated sickle retinopathy.

287 parafoveal subfields of the deep plexus with sickle SC or proliferative retinopathy.

288 Abnormal sickle-shaped erythrocytes disrupt blood flow in small v

289 e optimal coil evolves from near-circular to sickle-shaped.

290 uman healthy (wild-type (WT)) and homozygous sickle (SS) red blood cells (RBCs) express a large numbe

291 t the precise time at which fibers distort ("sickle") the cells.

292 Erythrocyte sickling, the primary pathologic event in SCD, results i

293 Calculations of sickling times, based on a recently discovered universal

294 SC (30.4%), 4 beta-thalassemia (8.7%), and 1 sickle trait (2.2%).

295 is based on laser-induced polymerization in sickle trait cells and robust, automated image analysis

296 Sickle trait whole blood clots demonstrated an intermedi

297 lar hemoglobin composition also explains why sickle trait, the heterozygous condition, and the compou

298 shown to improve microvascular blood flow in sickle transgenic mice undergoing I/R, and we suggest ho

299 express therapeutic levels of HbF and resist sickling, while those from patients with beta-thalassemi

300 ontraction, the number of RBCs extruded from sickle whole blood clots was significantly reduced compa