ライフサイエンスコーパス: RBC

1 RBC deformability was also lower in older vs. young as i

2 RBC folate (RBF) is an indicator of folate status and ri

3 % RBC membrane docosahexaenoic acid (DHA) was reduced in F

4 RBC storage lesions are often assessed by microscopic ex

5 RBC tracking within the database demonstrated changes in

6 RBC transfusion correlates with increased mortality and

7 RBC transfusion is also an option.

8 RBC transfusions can increase oxygen availability to the

9 RBC-MVs directly activated factor XII (FXII) or prekalli

10 RBC-MVs initiated TG in normal pooled plasma and in FXII

11 RBCs from retinas deficient in GABA release also demonst

12 10 G6PD-deficient volunteers each donated 1 RBC unit.

13 3.89 x 10 RBC positions were tracked by the algorithm in real time

14 -TGN and TPMT levels were 953 pmol/8 x 10(5) RBC (IQR 145-1761) and 47 mu/L (IQR 34.5-96).

15 Using hydrodynamic simulations of a RBC and parasite, where both interact through discrete s

16 Thus, conversion of A, B, and AB RBCs to O-type RBCs should be achievable by removal of t

17 ypsin inhibitor was necessary for abolishing RBC-MV-induced TG in normal pooled plasma, whereas kalli

18 We analyzed RBC membrane TFA using GLC (in 2013-2014) and expressed

19 ons (P=0.044), major bleeding (P=0.041), and RBC transfusion (P=0.048) were independent correlates of

20 an unexpected improvement in hemoglobin and RBC transfusion-independence in patients with acute myel

21 mage processing, the nrLFA is identified and RBC fluid flow distances and rates are recorded in paral

22 ownstream consequences of polymerization and RBC sickling include vaso-occlusion, hemolytic anemia, a

23 g in intracellular Hb obtained from RBCs and RBC-derived microparticles (MPs) from the blood of 23 SC

24 n (AGP) and serum vitamin B-12 and serum and RBC folate among nonpregnant women of reproductive age (

25 itself, whereby SNO is released from Hb and RBCs during deoxygenation, in proportion to the degree o

26 dependent increase in haematocrit levels and RBCs over a 104 week period.

27 Tfr2 allele increased hemoglobin levels and RBCs.

28 andard, we quantify MCHC of healthy RBCs and RBCs infected with Plasmodium yoelii, a commonly studied

29 ncorrect absorption assumptions, anisotropic RBC scattering, and layered tissues may confound classic

30 Early onset disease correlates with anti-RBC antibodies, lower hematocrit, and reduced IL-7 signa

31 onal recommendations) to improve appropriate RBC utilization.

32 s Follow-Up Study participants with archived RBC specimens and no history of cancer at blood draw (19

33 technical framework of the state-of-the-art RBC-mediated delivery systems is explained in detail to

34 nce in many biomedical applications, such as RBC damage (hemolysis) and mechanoporation-based drug de

35 be used to routinely and objectively assess RBC storage lesions.

36 he stereotyped output synapse arrangement at RBC terminals.

37 is thus a key synapse organizing molecule at RBC terminals, where it regulates function of GABAergic

38 For homogeneous collisions between RBC pairs, a decrease in final displacement after a coll

39 eo microscopy, we find a strong link between RBC tension and merozoite invasion, and identify a tensi

40 Interaction testing between RBC transfusion and mortality was not statistically sign

41 e of RBC deformability on collisions between RBCs and platelets was found to be negligible due to the

42 RBCs and explore mechanical coupling between RBCs and LCs.

43 a major barrier to efficient gas handling by RBCs.

44 is the main driver of tissue oxygenation by RBCs.

45 Beyond this, the ex vivo CAA-RBC assay determined the cellular antioxidant activity o

46 based image acquisition method for capturing RBC images from the SCD patients in normoxia and hypoxia

47 apagliflozin on haematocrit, red blood cell (RBC) counts and reticulocyte levels in high-risk patient

48 ors are unneeded to maintain red blood cell (RBC) counts.

49 The influence of red blood cell (RBC) deformability in whole blood on platelet marginatio

50 Red blood cell (RBC) invasion by malaria merozoites involves formation o

51 disk shape of the mammalian red blood cell (RBC) is unique to the RBC and is vital for its circulato

52 The mature red blood cell (RBC) lacks a nucleus and organelles characteristic of mo

53 difications (PTMs) of Hb and red blood cell (RBC) membrane proteins of transgenic SCD mice.

54 mponent complex that affects red blood cell (RBC) membranes.

55 ng on their abundance in the red blood cell (RBC) or plasma; it is essential to preinvestigate the di

56 used for the manipulation of red blood cell (RBC) suspensions and analyses of flow-mediated biomechan

57 cer variants associated with red blood cell (RBC) traits map to enhancers that are co-bound by lineag

58 consensus on the benefit of red blood cell (RBC) transfusion after transcatheter aortic valve replac

59 guidelines advocate to limit red blood cell (RBC) transfusion during surgery, but the feasibility and

60 d IDA patients required less red blood cell (RBC) transfusion during the postoperative period (A 42.5

61 Evidence regarding red blood cell (RBC) transfusion practices and their impact on hematopoi

62 a that occurs in a subset of red blood cell (RBC) transfusion recipients is the development of alloan

63 omplications associated with red blood cell (RBC) transfusions.

64 we investigate the role that red blood cell (RBC) transport plays in establishing oxygen heterogeneit

65 h as hematocrit, hemoglobin, red blood cell (RBC), white blood cell (WBC), and platelet counts with a

66 abundant EVs of human blood, red blood cell (RBC)- and platelet (PLT)-derived EVs and studied their i

67 receptor 2 [Tfr2] to control red blood cell [RBC] synthesis).

68 f the Hb content in a single red blood cell, RBC, based on magnetophoretic mobility.

69 of HbS leads to sickling of red blood cells (RBC).

70 phosphoprotein in retinal rod bipolar cells (RBCs).

71 pses on axon terminals of rod bipolar cells (RBCs).

72 od flow, clearing senescent red blood cells (RBCs) and recycling iron from hemoglobin.

73 Stored red blood cells (RBCs) are needed for life-saving blood transfusions, but

74 ape, number, and content of red blood cells (RBCs) dramatically.

75 ia parasites invade healthy red blood cells (RBCs) during the blood stage of the disease.

76 y the transfusion of murine red blood cells (RBCs) expressing the human KEL glycoprotein.

77 r to distinguish the normal red blood cells (RBCs) from sickled cells.

78 for IgM and IgG binding to red blood cells (RBCs) from wild-type (WT), alpha1,3-galactosyltransferas

79 glycophorin A receptors on red blood cells (RBCs) improved the blood half-life.

80 ule that polymerizes inside red blood cells (RBCs) in reduced oxygen tension.

81 ids in the outer leaflet of red blood cells (RBCs) is reported.

82 the synchronous bursting of red blood cells (RBCs) on completion of the malaria parasite asexual cell

83 hat a 1-unit transfusion of red blood cells (RBCs) should yield a posttransfusion hemoglobin incremen

84 rately tracking the flow of red blood cells (RBCs) through a no-reaction lateral flow assay (nrLFA) d

85 into rigid fibers, causing red blood cells (RBCs) to sickle; leading to numerous adverse pathologica

86 creased adherence of sickle red blood cells (RBCs) to the vascular endothelium.

87 cy decreases the ability of red blood cells (RBCs) to withstand oxidative stress.

88 Red blood cells (RBCs) transport oxygen to tissues and remove carbon diox

89 ormation on the membrane of red blood cells (RBCs) under high mechanical tensions is of great importa

90 inefficient gas exchange by red blood cells (RBCs), a process that is poorly characterized yet assume

91 gical investigations on the red blood cells (RBCs), advanced strategies of RBC-mediated in vivo deliv

92 of blood, or more commonly red blood cells (RBCs), is integral to health care systems worldwide but

93 pecifically, we discuss how red blood cells (RBCs), platelets, neutrophils, mesenchymal stem cells (M

94 falciparum infection of the red blood cells (RBCs), the parasite replicates and consumes haemoglobin

95 ithin a group of individual red blood cells (RBCs), which is crucial for imaging cells in 3D.

96 FTIR) to detect B. bovis in red blood cells (RBCs).

97 modium falciparum to invade red blood cells (RBCs).

98 properties and behaviors of red blood cells (RBCs).

99 sociated with stiffening of red blood cells (RBCs; e.g., sickle cell anemia or malaria), the mechanic

100 from viewing erythrocytes (red blood cells [RBCs]) as passive carriers of oxygen to recognizing the

101 o opsonize erythrocytes (or red blood cells, RBCs) and cause anemia.

102 cytometry and deep learning to characterize RBC lesions.

103 Freshly collected RBCs were exposed to a mechanical stimulus known to dras

104 ilayer membrane have been assumed to control RBC shape, recent experiments reveal that RBC biconcave

105 nderlying mechanism for the counterintuitive RBC pattern.

106 ays.CONCLUSIONBased on current FDA criteria, RBCs from G6PD-deficient donors would not meet the requi

107 r patterns linked to deviations from current RBC transport theory, we calculated average vessel lengt

108 the absence of a transcellular cytoskeleton, RBC shape is determined by the membrane skeleton, a netw

109 Dantu RBCs have higher average tension than non-Dantu RBCs, me

110 s have higher average tension than non-Dantu RBCs, meaning that a greater proportion resist invasion.

111 ch invasion rarely occurs, even in non-Dantu RBCs.

112 dylserine on the surface of RBCs, decreasing RBC survival and resulting in anemia.

113 As expected, fresh G6PD-deficient RBCs demonstrated defects in the oxidative phase of the

114 During refrigerated storage, G6PD-deficient RBCs demonstrated increased glycolysis, impaired glutath

115 iorate the metabolic needs of G6PD-deficient RBCs.TRIAL REGISTRATIONClinicalTrials.gov NCT04081272.FU

116 hed-earth tactics, in which it both destroys RBCs and restricts their supply.

117 We detected RBC (GPA(+))-engulfed material in circulating PMos of pa

118 uter algorithm is developed to differentiate RBCs from the patient's blood before and after cell sick

119 Through experiments with dilute RBC suspensions, we find an off-center two-peak (OCTP) p

120 and classification may not optimally discern RBC quality, we went further and eliminated subjective h

121 We hypothesized that G6PD-deficient donor RBCs would have inferior storage quality for transfusion

122 FDA acceptability criterion for stored donor RBCs.

123 tion of several CYPs, demonstrated efficient RBC partitioning and high membrane permeability, and is

124 rasite interfaces with its host erythrocyte (RBC) using a unique organelle, the parasitophorous vacuo

125 nt for hemorrhagic shock; however, the exact RBC to fresh frozen plasma ratio is still unclear.

126 This study thus sought to explore RBC mechanical responses in shear flow using purpose-bui

127 rce distributions on the plasma membrane for RBC shape maintenance may also have implications for sha

128 However, current methods for RBC analysis and MCHC quantification rely on bulk measur

129 occurring in intracellular Hb obtained from RBCs and RBC-derived microparticles (MPs) from the blood

130 O(2) unloading from RBCs was considerably slower than previously estimated i

131 Furthermore, RBC exchange transiently reversed resistance of whole bl

132 Haematocrit, RBC and reticulocyte measurements were conducted during

133 ternal standard, we quantify MCHC of healthy RBCs and RBCs infected with Plasmodium yoelii, a commonl

134 Heating RBC-MVs at 60 degrees C for 15 minutes or pretreatment w

135 in older vs. young as indicated by a higher RBC transit time (RCTT) measured by blood filtrometry (R

136 lude that SUB2 activity is critical for host RBC membrane sealing following parasite internalisation

137 ablation of the substrate AMA1 produces host RBC lysis.

138 e distribution of O(2) unloading rates in HS RBCs identified a subpopulation of spherocytes with grea

139 ant P4-ATPase phospholipid flippase in human RBCs, whereas ATP11C and ATP8A1 are the major P4-ATPases

140 better understanding of factors that impact RBC alloantibody formation may allow general or targeted

141 Consequently, changes in RBC shape and hemoglobin concentration, which are common

142 mpaired Fe-S cluster biogenesis, a defect in RBC hemoglobinization, and the development of siderocyte

143 apeutic interventions to correct deficits in RBC-mediated vasodilation to improve oxygen delivery-ste

144 Cs in a donor, suggesting a variable rate in RBC production between donors, or variability in availab

145 pendent patients achieved >=20% reduction in RBC transfusion burden.

146 be attributed to the inherent variability in RBC mechanical properties, which is confirmed by a model

147 irmed by a model that takes the variation in RBC shear elasticity into account.

148 TPBG immunofluorescence in RBCs was strongly altered by the loss of TRPM1 in the ad

149 ynapses, and TPBG may play a similar role in RBCs.

150 thod to track the flow of O(2) in individual RBCs by combining ultrarapid solution switching (to mani

151 ermining the amount of polymer in individual RBCs under controlled oxygen.

152 ation, the ability of storage lesion-induced RBC-MVs to activate each zymogen of the intrinsic pathwa

153 dogma suggests that CM results from infected RBC (iRBC) sequestration in the brain microvasculature a

154 ct infected red blood cells (intact infected RBC, 77.3% and 79.2%).

155 study from the level of the single infected RBC using AFM-IR and confocal Raman to the detection of

156 The killer cells bound to infected RBCs and killed intracellular P. falciparum via the tran

157 Interestingly, RBC-MVs generated FIXa in a prekallikrein-dependent mann

158 finity and displays strong partitioning into RBCs.

159 O(2)) affinity of HbS, due to elevated intra-RBC concentrations of the natural Hb effector, 2,3-dipho

160 By using leukoreduced RBC units to isolate RBC microvesicles (RBC-MVs), they document that RBC-MVs

161 ough anti-KEL alloimmunization occurred, KEL RBC consumption by inflammatory monocytes and serum mono

162 < 70 g/L) or liberal (Hb threshold < 90 g/L) RBC transfusion strategy between day 0 and day 100.

163 Both antibodies labeled RBC dendrites in the outer plexiform layer and axon term

164 d from an isotropic aqueous phase into a LC, RBCs exhibit complex yet reversible shape transformation

165 By using leukoreduced RBC units to isolate RBC microvesicles (RBC-MVs), they d

166 safety of practice recommendations to limit RBC transfusion and tolerate anemia during and after hos

167 a massive GC in the Andromeda Galaxy (M31), RBC EXT8, that is extremely depleted in heavy elements.

168 Maternal RBC iron incorporation of an orally ingested tracer unde

169 Only 3 surveys measured RBC folate, and among them, correlations for WRA ranged

170 ion-induced, red cell-derived microvesicles (RBC-MVs) propagate coagulation by supporting the assembl

171 uced RBC units to isolate RBC microvesicles (RBC-MVs), they document that RBC-MVs activate factor IX

172 and ATP8A1 are the major P4-ATPases in mouse RBCs.

173 ignificantly lower than that for G6PD-normal RBCs (85.3% +/- 3.2%; P = 0.0009).

174 rine oxidation, as compared with G6PD-normal RBCs.

175 for transfusion as compared with G6PD-normal RBCs.METHODSMale volunteers were screened for G6PD defic

176 ed theranostic platforms taking advantage of RBC-delivery modalities.

177 Our approach of RBC labeling with the NPs also prevented reticuloendothe

178 nction of GABAergic synapses and assembly of RBC synaptic dyads.

179 odels corresponding to two distinct cases of RBC membrane conditions were employed, and they were der

180 alignment is governed by the combination of RBC membrane deformability and dynamics of adhesion bond

181 rovided an appreciation of the complexity of RBC membrane structure, while studies of the RBC membran

182 e current understanding of the complexity of RBC shapes and dynamics in microchannels is mainly based

183 e, aspects of the spatiotemporal dynamics of RBC suspensions flowing through a typical microchannel a

184 necessary insight into the heterogeneity of RBC health and improve therapeutic efficacy.

185 The influence of RBC deformability on collisions between RBCs and platele

186 oietic response and reduce the likelihood of RBC transfusion.

187 The number of RBC units transfused was lower in the restrictive-strate

188 inity for O(2) with subsequent prevention of RBC sickling.

189 del reveals the dynamic molecular process of RBC damage in biomedical devices and mechanoporation tha

190 baudi underlies the 24-hour-based rhythms of RBC bursting in mice.

191 To elucidate the mechanism(s) of RBC-MV-induced coagulation activation, the ability of st

192 Our massively parallel simulations of RBC flow in real-size microfluidic dimensions using the

193 d blood cells (RBCs), advanced strategies of RBC-mediated in vivo delivery have been developed rapidl

194 variability in available iron at the time of RBC formation.

195 t LC elasticity permits continuous tuning of RBC strains, and chemical cross-linking of RBCs, a model

196 imentation that led to this understanding of RBC function; from the foundational understanding of all

197 suggesting that the phenotypic variation of RBC traits could stem from altered responsiveness to ext

198 lete blood counts (CBC), antibody binding of RBCs, T cell numbers and activation, hematopoietic proge

199 paradoxically increases the deformability of RBCs when examined under low-shear conditions, despite o

200 distributions indicate that the fraction of RBCs that are below the bulk Hb concentration that defin

201 f RBC strains, and chemical cross-linking of RBCs, a model for diseased cells, leads to striking chan

202 Campylobacter megaplasmids mediates lysis of RBCs and likely contributes to survival on retail meats

203 vary across the heterogenous populations of RBCs found both within and between individuals.

204 Importantly, whereas the shapes of RBCs are similar in isotropic fluids, when strained by L

205 Refrigerated storage of RBCs induces oxidative stress.

206 rate that CR1 availability on the surface of RBCs modulates P. vivax invasion.

207 sure of phosphatidylserine on the surface of RBCs, decreasing RBC survival and resulting in anemia.

208 At present, judicious transfusion of RBCs is the primary strategy invoked in alloimmunization

209 nce, -0.87 g/dL; P = .022), as were units of RBCs transfused (median [interquartile range (IQR)], 1 [

210 y while preserving the beneficial effects on RBC production mediated by EPO or Tfr2 deletion.

211 nd signs of hemolytic anemia with a focus on RBC membrane disorders.

212 n association of low baseline CD35 levels on RBCs and of early inflammatory responses with the pathog

213 ing and disrupts presynaptic inhibition onto RBC terminals.

214 anges in functional capillary density and/or RBC velocity in septic shock, heart failure, hypovolemia

215 >= 1:2 and < 1:1) fresh frozen plasma:packed RBC ratio groups, respectively, compared with the low ra

216 Platelet:packed RBC ratio was not associated with mortality (adjusted re

217 eeding that required a transfusion of packed RBCs.

218 Among 2587 patients, RBC transfusion was administered in 421 cases (16%).

219 In the 842 propensity-matched patients, RBC transfusion was associated with increased mortality

220 Our aim was to evaluate plasma, RBCs, and hair CIR and NIR as biomarkers of fish, meat,

221 Postintervention RBC CIR and NIR had strong associations with baseline, s

222 tologous 51-chromium 24-hour posttransfusion RBC recovery (PTR) studies were performed.

223 red, or Brownian, nature of optically probed RBC dynamics typically assumed in classical DOF.

224 PSE RBCs had significantly decreased visualized and laser-de

225 nowledge, observations demonstrated that PSE RBCs had increased heterogeneity of direct visualized or

226 leads to either abortive invasion with rapid RBC lysis, or successful entry but developmental arrest.

227 MD genetic risk, but significantly reduced % RBC membrane omega-3 fatty acids and thinner foveas comp

228 Knockout of LRRTM4 reduces RBC axonal GABA(A) and GABA(C) receptor clustering and d

229 rts in classifying seven clinically relevant RBC morphologies associated with storage lesions, compar

230 njection, the Ter119-NPs achieved remarkable RBC labeling efficiencies (>95%), resulting in marked en

231 lated by native S-nitrosothiol (SNO)-replete RBCs and by SNO-Hb itself, whereby SNO is released from

232 output (p < 0.001), other bleeding requiring RBC transfusion (p = 0.01), activated clotting time (p =

233 output (p < 0.001), other bleeding requiring RBC transfusion (p = 0.03), and daily set platelet goal

234 leeding (p = 0.18), other bleeding requiring RBC transfusion (p = 0.75), fibrinogen level (p = 0.67),

235 nts undergoing HCT, the use of a restrictive RBC transfusion strategy threshold of 70 g/L was as effe

236 treatment with low-dose EPO triggered robust RBC production in both models.

237 veloped biochip to preconcentrate and rotate RBC clusters in 3D.

238 Senescent RBCs with reconstituted membranes were phagocytosed in s

239 marker, from the outer leaflet of senescent RBCs.

240 Single RBC measurements could provide necessary insight into th

241 To achieve single RBC trapping, we employ two parallel sidewall 3D electro

242 antifying hemoglobin concentration at single RBC resolution.

243 of invasion does not correlate with specific RBC-parasite receptor-ligand interactions.

244 geneous collisions between healthy and stiff RBC pairs, it is found that the stiffened RBC is displac

245 an blood containing varying healthy-to-stiff RBC fractions.

246 essel geometry with varying healthy-to-stiff RBC ratios, a decrease was observed in the red blood cel

247 ff RBC pairs, it is found that the stiffened RBC is displaced most.

248 margination due to an increase in stiffened RBCs present in flow.

249 at the wall due to the increase of stiffened RBCs in flow, suggesting a decrease of platelet marginat

250 order to resolve the influence of stiffened RBCs on platelet concentration at the channel wall, cell

251 on due to an increased fraction of stiffened RBCs present in the flow.

252 d stress-strain history can alter subsequent RBC behavior in physiologically relevant low-shear flows

253 In summary, RBC-MVs activate both FXII and prekallikrein, leading to

254 bat these pathologies, many therapies target RBCs and their contents directly.

255 ting serum dietary carotenoids and long-term RBC omega-3 fatty acid status, as well as common seconda

256 efficiently internalized by PC-3 cells than RBC-derived EVs.

257 microvesicles (RBC-MVs), they document that RBC-MVs activate factor IX (FIX) via 2 distinct pathways

258 Furthermore, we predict that RBC membrane tension and the orientation of the applied

259 It has also been reported that RBC-MVs initiate coagulation via the intrinsic pathway.

260 ol RBC shape, recent experiments reveal that RBC biconcave shape also depends on the contractile acti

261 deling of LC and cell mechanics reveals that RBC shape responses occur at constant cell membrane area

262 Previous studies have indicated that RBCs lose Hb during ex vivo storage; however, it is not

263 The RBC sickling is made worse by the low oxygen (O(2)) affi

264 embrane forces must be non-uniform along the RBC membrane and (b) the force density must be larger in

265 By analyzing the RBC migration and cell-free layer development within a h

266 e-like re-orientation of the parasite at the RBC membrane, while RBC deformation aids in the establis

267 the classical Helfrich-Canham model for the RBC membrane to test the role of heterogeneous force dis

268 RBC membrane structure, while studies of the RBC membrane disorders have offered valuable insights in

269 genotypic and phenotypic variability of the RBC membrane disorders in order to raise the index of su

270 Although disorders of the RBC membrane due to altered structural organization or a

271 and compression process that a patch of the RBC membrane usually experiences under high shear flow.

272 drastically with increasing rigidity of the RBC membrane.

273 Our results propose that the majority of the RBC-trait-associated variants that reside on transcripti

274 asm of the parasite and the cytoplasm of the RBC.

275 volume in the dimple and rim regions of the RBC.

276 s to the repertoire of proteins found on the RBC surface, but, unexpectedly, inhibition of invasion d

277 In this review, the RBC-mediated delivery of in vivo nanobiosensors for appl

278 the Helfrich-Canham energy, we find that the RBC biconcave shape depends on the ratio of forces per u

279 malian red blood cell (RBC) is unique to the RBC and is vital for its circulatory function.

280 mechanism, enclosing the parasite within the RBC.

281 were the most abundant phospholipids in the RBCs outer leaflet with PC 34:1 and SM 34:1 being the mo

282 f Hb content is a function of the age of the RBCs in a donor, suggesting a variable rate in RBC produ

283 o striking changes in shape responses of the RBCs.

284 Metabolomics analyses of these RBC units were also performed.RESULTSThe mean 24-hour PT

285 optical flowmetry (DOF) assesses deep tissue RBC dynamics by measuring coherent fluctuations of multi

286 that real-time targeting of therapeutics to RBC with NPs can potentially improve outcomes and reduce

287 Even though parasites initially adhere to RBCs with a random orientation, they need to align their

288 saturable and specific C-peptide binding to RBCs when delivered as part of a complex with albumin.

289 cytokines, and consumption of the transfused RBCs were evaluated longitudinally.

290 B and the first useful conversions of A-type RBCs, although under constrained conditions.

291 s, conversion of A, B, and AB RBCs to O-type RBCs should be achievable by removal of that sugar with

292 ively) on the core H-antigen found on O-type RBCs.

293 tion during pregnancy can be evaluated using RBC incorporation of orally administered stable iron iso

294 fer diffraction patterns and also visualized RBCs.

295 These data suggest novel mechanisms by which RBC transfusion mediates inflammatory and/or thrombotic

296 n of the parasite at the RBC membrane, while RBC deformation aids in the establishment of apex-membra

297 s (LCs) that are in osmotic equilibrium with RBCs and explore mechanical coupling between RBCs and LC

298 Interaction of SUB2-null merozoites with RBCs leads to either abortive invasion with rapid RBC ly

299 the distribution of Hb concentration within RBCs from a donor sample to be determined.

300 dentified pairs of patients with and without RBC transfusion.