ライフサイエンスコーパス: erythrocyte

1 to human Hsp70 chaperones endogenous to the erythrocyte.

2 vels on a human HAP-1 cell line and on sheep erythrocytes.

3 ated with cryopreserved P. malariae-infected erythrocytes.

4 were in the process of phagocytosing intact erythrocytes.

5 ytes through lysis and removal of uninfected erythrocytes.

6 t receptors on the cell surfaces of infected erythrocytes.

7 ll unilamellar vesicle liposomes, and rabbit erythrocytes.

8 ng and after P. falciparum invasion of human erythrocytes.

9 om exogenous sources such as the circulation/erythrocytes.

10 on commercial chips and similar to those on erythrocytes.

11 influenza A-mediated agglutination of human erythrocytes.

12 rn of O(2) modulation of ion transporters in erythrocytes.

13 ng leukocidins that kill leukocytes and lyse erythrocytes.

14 s incompatible with parasite growth in human erythrocytes.

15 rized by the loss of infected and uninfected erythrocytes.

16 gamete formation, and gametes egress out of erythrocytes.

17 ble self-tolerogenic potential of autologous erythrocytes.

18 an augmented clearance capacity of infected erythrocytes.

19 l parasites to infect both gorilla and human erythrocytes.

20 ay be derived from exogenous sources such as erythrocytes.

21 d interactions between the parasite and host erythrocytes.

22 owed a clear clustering of leukocytes versus erythrocytes.

23 r cells at the expense of lymphoid cells and erythrocytes.

24 ting global canonical microRNA expression in erythrocytes.

25 differences in the dynamics of once-infected erythrocytes.

26 host allows it to grow and multiply in human erythrocytes.

27 globin (Hb) leaked into the bloodstream from erythrocytes.

28 red for parasite development and invasion of erythrocytes.

29 aria by inducing the clearance of uninfected erythrocytes.

30 lobin expression and HbF production in adult erythrocytes.

31 support macrophage-mediated phagocytosis of erythrocytes.

32 patocytes or the invasion of and egress from erythrocytes.

33 er to P. vivax that is not present in mature erythrocytes?

34 gest family of surface proteins displayed by erythrocytes(1).

35 lines (gC) conjugates (MB-gCs) against human erythrocyte acetylcholinesterase (AChE), equine serum bu

36 In addition, we showed that erythrocyte adhesion molecules, which are specifically a

37 EGF)-like domains, was identified as a novel erythrocyte adhesive molecule.

38 ntibodies induce the clearance of uninfected erythrocytes after binding to PS exposed in their membra

39 leted in a mouse model of SAH, the degree of erythrocyte aggregation in CLNs is significantly lower,

40 rythrocyte-binding repeats of PfGARP induced erythrocyte aggregation reminiscent of the rosetting phe

41 Such erythrocyte-anchored systemic immunotherapy led to the i

42 The essential role of Raptor (mTORC1) in erythrocyte and B lineage commitment was confirmed in ad

43 Detailed characterization of erythrocyte and macrophage subpopulations from human spl

44 en monocytes and dendritic cells and between erythrocytes and basophils that suggest multiple pathway

45 ted that interleukin (IL)-33 associated with erythrocytes and co-cooperated with heme to promote the

46 vative caused no hemolytic effects in murine erythrocytes and could be considered promising for futur

47 panied by increased splenic sequestration of erythrocytes and fewer erythropoietic elements in the bo

48 cytes, B- lymphocytes, Monocytes, Leukocytes erythrocytes and human kidney cells HEK293), animal cell

49 also examined the variation of Sia forms on erythrocytes and in saliva from different animals.

50 nt for hematological analysis of leukocytes, erythrocytes and platelets.

51 of 17R-RvD1 involves (1) enhancement of SCD erythrocytes and polymorphonuclear leukocyte efferocytos

52 n causes a profound reduction in invasion of erythrocytes and rapid death of those merozoites that in

53 pore formation model, whereas in the case of erythrocytes and small unilamellar vesicles, Cyt1Aa's in

54 nked to the increase in rigidity of infected erythrocytes and their adhesion to endothelial receptors

55 Intact and lysed erythrocytes and their membrane fraction or specific ery

56 response able to recognize TEX1 in infected erythrocytes and to inhibit parasite growth through an a

57 for hemoglobin in blood plasma, in urine, in erythrocytes, and in full blood are obtained.

58 livered ICLs to the BM more efficiently than erythrocytes, and more selectively than PEGylated liposo

59 with complement component iC3b, agglutinates erythrocytes, and neutralizes influenza A virus.

60 en periodontitis and circulating leukocytes, erythrocytes, and platelets.

61 n cells (HeLa cells), chicken brain, chicken erythrocytes, and the protozoan Leishmania We used fluor

62 ood-stage merozoites of P. falciparum invade erythrocytes, and this requires interactions between mul

63 the distribution of HbF among HbF-containing erythrocytes; and (4) reactivation of HbF gene expressio

64 igand that recognizes an ectodomain of human erythrocyte anion-exchanger, band 3/AE1, as a host recep

65 to be a valuable tool for determining which erythrocyte antibodies would likely be candidates for cl

66 ere we show that a markedly higher number of erythrocytes are accumulated in the lymphatics of CLNs a

67 tions between Plasmodium parasites and human erythrocytes are prime targets of blood stage malaria va

68 tes in the cytosol of P. falciparum-infected erythrocytes as a cholesterol import system, likely betw

69 ng intravenous administration of Pf-infected erythrocytes as a model for early-clinical evaluation of

70 a substantial part of its life cycle inside erythrocytes as rings, trophozoites, and schizonts, befo

71 Plasmodium falciparum-infected erythrocytes bind to specific endothelial cell receptors

72 increased expression included members of the erythrocyte binding antigens (EBA), reticulocyte binding

73 uman antibodies to this protein also exhibit erythrocyte binding inhibition at physiologically releva

74 coding the immune response epitopes and core erythrocyte-binding activity.

75 Plasmodium falciparum erythrocyte-binding antigen 140 (EBA-140) plays a role i

76 The mAb functions were determined by erythrocyte-binding inhibition assay and invasion inhibi

77 Synthetic peptides derived from the erythrocyte-binding repeats of PfGARP induced erythrocyt

78 Entrapment and binding of adenovirus to erythrocytes, blood factors, and neutralising antibodies

79 n enhancing the adhesive properties of human erythrocytes by engaging band 3 as a host receptor.

80 Invasion of erythrocytes by merozoites is an essential step for the

81 arum malaria is extensive remodeling of host erythrocytes by the parasite, which facilitates the deve

82 es, which are specifically activated on aged erythrocytes, cause senescent erythrocytes to interact w

83 addition to the decreased hemolysis of human erythrocytes, CM14 impedes host cell rounding and lysis

84 ytes and their membrane fraction or specific erythrocyte components were examined in vitro using dive

85 one patient received a transfusion of three erythrocyte concentrates.

86 ns and show that both chicken and guinea pig erythrocytes contain complex sialylated N-glycans but th

87 kines suggest inflammation-induced damage to erythrocytes contributes to anemia and splenic retention

88 - for example, in echinoderm sperm and avian erythrocytes - could adopt a helical repeat of ~10 bp/tu

89 served associations between mLOY and reduced erythrocyte count (-0.009 [-0.014, -0.005] x 10(12) cell

90 FIKK4.1, mediates both rigidification of the erythrocyte cytoskeleton and trafficking of the adhesin

91 pment of RPMs as a response to physiological erythrocyte damage with important implications to iron r

92 s decreased as the percentage of parasitized erythrocytes decreased during tick acquisition feeding.

93 hich alters our current understanding of how erythrocyte degradation is regulated.

94 Presentation of erythrocyte-delivered nanoparticles to the spleen led to

95 Erythrocytes derived from gene-edited cells showed a mar

96 ated from patients carrying JAK2V617F and by erythrocyte-derived microvesicles from transgenic mice.

97 elial oxidative stress caused by circulating erythrocyte-derived microvesicles.

98 We used near-infrared erythrocyte-derived transducers (NETs), a contrast agent

99 mmune function of erythrocytes, we developed erythrocyte-driven immune targeting (EDIT), which presen

100 lglycerol effect showed dose-dependency with erythrocyte EPA + DHA (r = -0.15, P = 0.04), whereas HDL

101 mega-3 (n-3) fatty acids (EPA and DHA) raise erythrocyte EPA + DHA [omega-3 index (O3I)] concentratio

102 88, 2.62) fatty acid percentage-point higher erythrocyte EPA + DHA in the fish group (P < 0.001).

103 lected fasting blood samples for analysis of erythrocyte EPA [20:5n-3 (omega-3)] + DHA (22:6n-3) and

104 s could maximize liver exposure and minimize erythrocyte exposure to increase their therapeutic windo

105 ery of tests and questionnaires and analyzed erythrocyte fatty acid composition.

106 A high level of erythrocyte fetal hemoglobin (HbF) comprising alpha- and

107 re-injected to allow direct visualization of erythrocytes for in vivo measurement of speed.

108 38 control) matched individuals, as well as erythrocytes from 181 living participants, who comprised

109 the meningeal lymphatics drain extravasated erythrocytes from CSF into CLNs after SAH, while suggest

110 or to achieve highly efficient separation of erythrocytes from plasma within a short amount of time.

111 o intact senescent erythrocytes, the remnant erythrocyte ghost shells were prone to recognition and b

112 ndocyanine green (ICG) dye is sequestered in erythrocyte ghosts and autologously re-injected to allow

113 tes that are devoid of hemoglobin, so-called erythrocyte ghosts.

114 ere fabricated from hemoglobin-depleted mice erythrocyte-ghosts and doped with Indocyanine Green (ICG

115 In addition, shortened erythrocyte half-life, suppressed erythropoietin respons

116 he removal of dead parasites from their host erythrocyte, has been studied in patients with severe ma

117 ress potential in assuaging H(2)O(2) induced erythrocyte hemolysis and antioxidant activity by inhibi

118 ic red pulp macrophages (RPMs) contribute to erythrocyte homeostasis and are required for iron recycl

119 that regulates macrophage functions to link erythrocyte homeostasis with innate immunity.

120 and Asn-His-Ser motifs, which recognize both erythrocyte I/i self-antigens and commensal bacteria.

121 ysis of microvesicles derived from JAK2V617F erythrocytes identified increased expression of myeloper

122 ng pregnancy, Plasmodium falciparum-infected erythrocytes (IE) accumulate in the intervillous spaces

123 ined how mature-stage P. falciparum infected erythrocytes (IE) interact with tumor necrosis factor al

124 uestration of Plasmodium falciparum-infected erythrocytes (IEs) in the microvasculature contributes t

125 ing antibodies to antigens found on infected erythrocytes (IEs).

126 Leukocytes and erythrocytes, imaged with a laser beam of 4 mum and pixe

127 Mature erythrocytes, immature erythroid cells, and phagocytes a

128 Extravasated erythrocytes in cerebrospinal fluid (CSF) critically con

129 hatics are involved in clearing extravasated erythrocytes in CSF after SAH remains unclear.

130 ies against PfGARP kill trophozoite-infected erythrocytes in culture by inducing programmed cell deat

131 low haptoglobin, increased fragmentation of erythrocytes in peripheral blood smear, increased plasma

132 uction elements are activated in a-nucleated erythrocytes in response to infection with malaria paras

133 elets, the antibodies were used to sensitize erythrocytes in vitro and these were added to a platelet

134 tissues, on secreted mucus in saliva, and on erythrocytes, including those from IAV host species and

135 es; thus, P. vivax Sal I must invade Saimiri erythrocytes independent of DBP1.

136 at the plasma BDNF is more reliable than the erythrocyte index as biomarker for assessing the effecti

137 ex with the increases in plasma BDNF and the erythrocyte index were determined.

138 asma BDNF, it negatively correlated with the erythrocyte index.

139 hat is expressed on the exofacial surface of erythrocytes infected by early-to-late-trophozoite-stage

140 r SELEX to direct aptamers to the surface of erythrocytes infected with P. falciparum.

141 gene expression in Saimiri and Aotus monkey erythrocytes infected with P. vivax Salvador I (Sal I).

142 e steps leading to vascular cytoadherence of erythrocytes infected with the human parasite Plasmodium

143 ite's intravacuolar lifestyle for successful erythrocyte infection and provide perspectives for futur

144 against the compounds was highest for canine erythrocytes, intermediate for rat and human cells and l

145 Cell-free hemoglobin that is released from erythrocytes into the cerebrospinal fluid (CSF) is sugge

146 lates contain an inactivating mutation in an erythrocyte invasion associated gene, PfEBA165, the homo

147 on genotype, including the DBPbeta and NBPXa erythrocyte invasion genes.

148 oire of genes not previously associated with erythrocyte invasion phenotypes, suggesting the possibil

149 The central role that erythrocyte invasion plays in Plasmodium falciparum surv

150 onously through the 48 h lifecycle following erythrocyte invasion, such that at any one time there is

151 of cAMP and activity of PKA are critical for erythrocyte invasion, whilst key developmental steps tha

152 rect temporal activation of PKA required for erythrocyte invasion, whilst suppressing untimely PKA ac

153 possibly associated with the specificity of erythrocyte invasion.

154 n apical membrane antigen 1 (AMA1) regulates erythrocyte invasion.

155 nfections, and with parasites within 12 h of erythrocyte invasion.

156 described as a phenomenon where an infected erythrocyte (IRBC) is attached to uninfected erythrocyte

157 Moreover erythrocyte iron and lipid abnormally colocalized in the

158 The loss of uninfected erythrocytes is an important contributor to malarial ane

159 which P. falciparum merozoites invade human erythrocytes is complex, involving merozoite proteins as

160 an essential ligand for the invasion of host erythrocytes, is suspected to have played a critical rol

161 endothelial cells, rather than leukocytes or erythrocytes, is the critical target for lethality.

162 Erythrocytes isolated from endothelial NO synthase-defic

163 When a malaria parasite invades a host erythrocyte it pushes itself in and invaginates a portio

164 sks of traumatic lumbar puncture (>300 x 106 erythrocytes/L after excluding patients diagnosed with s

165 obacterial infection alters the formation of erythrocytes, leading to their accelerated removal from

166 ugh DR1, promotes the recruitment of LukD to erythrocytes, likely by facilitating LukED oligomer form

167 cells including BGC823 gastric cancer cells, erythrocytes, lymphocytes, and E. coli cells and quantif

168 timulated ex vivo with parasite schizont and erythrocyte lysates.

169 f high haemoglobin concentration released by erythrocyte lysis is likely to perturb Nf-L detection in

170 s used in adoptive cell transfers, including erythrocytes, macrophages, NK cells, T cells, etc.

171 ighly conserved in vertebrates and regulates erythrocyte maturation, where it becomes the most abunda

172 ge promotes atherosclerosis progression, and erythrocytes may contribute to this process.

173 Erythrocyte mediated velocimetry (EMV) is a novel techni

174 lungs, which is conventionally the target of erythrocyte-mediated delivery systems.

175 Erythrocyte-mediated systemic immunotherapy may represen

176 or surface antigen of P. falciparum-infected erythrocytes, mediates endothelial adhesion, and display

177 2 and blocks progenitor differentiation into erythrocytes, megakaryocytes, basophils, and granulocyte

178 Rh5 and Ripr are positioned parallel to the erythrocyte membrane before membrane insertion.

179 We demonstrate erythrocyte membrane cholesterol levels modulate the pre

180 bic acid, 25-hydroxyvitamin D [25(OH)D], and erythrocyte membrane fatty acids following birth until I

181 eous self-assembly of haemoglobin-containing erythrocyte membrane fragments on the surface of preform

182 also alters the mechanical properties of the erythrocyte membrane in a concentration-dependent manner

183 N, H(2)V(V)O(4)(-) and the ligands cross the erythrocyte membrane independently, with dhp the uptake

184 alcification model, and in vivo after murine erythrocyte membrane injection into neointimal lesions o

185 ified isolates and recombinant P. falciparum erythrocyte membrane protein 1 (PfEMP1) domains to quant

186 antigenically variant Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) family.

187 hese studies strongly suggest that extensive erythrocyte membrane protein phosphorylation and ubiquit

188 bellar ataxia-35; and loss of the structural erythrocyte membrane protein, protein 4.2, leads to here

189 ha-spectrin, which in turn leads to abnormal erythrocyte membrane structure and function.

190 mport system, likely between the PVM and the erythrocyte membrane, and that this transportation proce

191 ic constitutive model of the red blood cell (erythrocyte) membrane based on recently improved charact

192 Erythrocyte membranes (RMs) were used to coat the BPQDs,

193 Erythrocyte membranes dose-dependently enhanced calcific

194 Lysed erythrocyte membranes enhanced calcification to a simila

195 parum parasites and structurally investigate erythrocyte membranes, both during and after P. falcipar

196 d under analogous conditions on intact human erythrocyte membranes.

197 e study displays drastic changes in specific erythrocyte metabolite pools at different times during s

198 suggesting that phosphorylation may modulate erythrocyte modifications.

199 OAC patients had a three-fold increase in erythrocyte mutant frequency (EMF) compared to GORD pati

200 Using flow cytometry, GPI-anchor negative erythrocytes (mutants) were scored and compared amongst

201 .9, 2.6) fatty acid percentage points higher erythrocyte n-3 LCPUFA than in the poultry group.

202 Erythrocytes naturally capture certain bacterial pathoge

203 Erythrocyte(nex) can enhance the delivery of cargo prote

204 The interaction with erythrocytes of four [V(V)O(2)L(2)](-) complexes, with L

205 mation may be abnormal in both the brain and erythrocytes of those with schizophrenia, particularly i

206 rogressively lost the ability to agglutinate erythrocytes of various species and to replicate efficie

207 The commonly used erythrocyte omega-3 index is not suitable for brain beca

208 approximately 2800 P. falciparum parasitized erythrocytes on day 13.

209 rtic rings, and extravasated CD235a-positive erythrocytes or Perl iron-positive signals colocalized w

210 successful despite their ability to opsonize erythrocytes (or red blood cells, RBCs) and cause anemia

211 ike P. falciparum, which can invade all aged erythrocytes, P. vivax is restricted to reticulocytes.

212 en mediate turnover of billions of senescent erythrocytes per day.

213 iparum infections at less than 0.75 infected erythrocytes per microliter.

214 By killing trophozoite-infected erythrocytes, PfGARP could synergize with other vaccines

215 Antibodies which supported erythrocyte phagocytosis in vitro successfully ameliorat

216 ex vivo erythrocyte sickling, and increased erythrocyte phosphatidylserine exposure was also observe

217 to interrogate the activation status of host erythrocyte phospho-signaling pathways at three blood st

218 plex lipid bilayer that resembles the native erythrocyte plasma membrane.

219 a and tissue iron levels, the iron demand of erythrocyte precursors, and the presence of potential pa

220 Many erythrocyte processes and pathways, including glycolysis

221 n arrest in development at the megakaryocyte-erythrocyte progenitor stage.

222 tput as reflected by increased maturation of erythrocyte progenitors.

223 orm (EpoRm), which augments Epo signaling in erythrocyte progenitors.

224 rane fraction of lysed, but not intact human erythrocytes promoted mineralization of human arterial s

225 stantial species-specific phosphorylation of erythrocyte proteins by P. falciparum but not by Plasmod

226 Investigating the role that host erythrocyte proteins play in malaria infection is hamper

227 sites on parasite virulence factors and host erythrocyte proteins.

228 ion was primarily caused by MPs derived from erythrocytes, rather than from platelets, and that it wa

229 he malaria parasite interfaces with its host erythrocyte (RBC) using a unique organelle, the parasito

230 tes are contained within the infected host's erythrocytes (RBCs).

231 roup antigen (Duffy antigen), the only known erythrocyte receptor for the P. vivax merozoite invasion

232 he microvasculature has evolved from viewing erythrocytes (red blood cells [RBCs]) as passive carrier

233 used by Plasmodium falciparum-infected human erythrocytes/red blood cells are hallmarks of severe pat

234 ion as a regulator of cellular signaling and erythrocyte regeneration.

235 ignaling, erythroid progenitor function, and erythrocyte regeneration.

236 t of freeze-thaw cycles (0 or 1) and time to erythrocyte removal (30, 120, or 240 min) on the accurac

237 lently anchored onto the surface of injected erythrocytes results in local and systemic tumour suppre

238 vivax Duffy-binding protein (DBPII) with the erythrocyte's Duffy Ag receptor for chemokines (DARC) is

239 We analyzed metal levels in erythrocyte samples obtained at recruitment, as a biomar

240 hange in Disease Activity Score in 28 joints-Erythrocyte Sedimentation Rate (DAS28-ESR).

241 (adjusted OR, 2.71 [95% CI, 1.26-5.86]), and erythrocyte sedimentation rate (ESR) >40 mm/h (adjusted

242 ammation (C-reactive protein [CRP] level and erythrocyte sedimentation rate [ESR]), cardiac injury (t

243 respectively, of 0.54-0.78 and 0.46-0.95 for erythrocyte sedimentation rate and 0.73 and 0.78 for C-r

244 Erythrocyte sedimentation rate and C-reactive protein we

245 ch as HLA-B27 status, C-reactive protein and erythrocyte sedimentation rate have, at best, moderate d

246 % eosinophils [normal range, 1%-4%]), and an erythrocyte sedimentation rate of 31 mm per hour (normal

247 We evaluated the following tests: erythrocyte sedimentation rate, C-reactive protein, feca

248 pecially prominent in clots involving sickle erythrocytes (see figure), consistent with the increased

249 eveloping the High Efficiency Rapid Magnetic Erythrocyte Separator (H.E.R.M.E.S) sleeve, an apparatus

250 ted mucins in saliva and surface proteins of erythrocytes showed a high degree of variability in disp

251 Increased reticulocytosis, enhanced ex vivo erythrocyte sickling, and increased erythrocyte phosphat

252 Erythrocyte sickling, the primary pathologic event in SC

253 tory cells, we did not detect differences in erythrocyte sickling.

254 igating sickle hemoglobin polymerization and erythrocyte sickling.

255 comprehensive and dynamic assessment of host erythrocyte signaling during infection with Plasmodium f

256 Here, we examined 12 murine erythrocyte-specific antibodies of different specificity

257 rpose of this study is to determine the mean erythrocyte speed in the retinal microvasculature, as we

258 Inside erythrocytes stable V(IV)OL(2) complexes are formed, ind

259 ransportation process occurs during the live erythrocyte stages of P. falciparum.

260 of the cancer cells, leukocyte subtype, and erythrocyte status, respectively.

261 a proof of concept for capsules as adequate erythrocyte substitute.

262 tion in microvesicles derived from JAK2V617F erythrocytes suppressed their effect on oxidative stress

263 lex, involving merozoite proteins as well as erythrocyte surface proteins.

264 mbers of the PfEMP1 family exported onto the erythrocyte surface.

265 Antigenic nanoparticles were adsorbed on the erythrocyte surface.

266 n spleen tissue led to the identification of erythrocytes that are devoid of hemoglobin, so-called er

267 les are needed that can specifically bind to erythrocytes that are infected with P. falciparum for di

268 riments, we further confirmed that senescent erythrocytes that are retained in the spleen are subject

269 In contrast to intact senescent erythrocytes, the remnant erythrocyte ghost shells were

270 nisms involved in sequestration of senescent erythrocytes, their recognition, and their subsequent de

271 i.e., the number of nanoparticles loaded per erythrocyte), they were predominantly delivered to the s

272 separating all stages of Plasmodium-infected erythrocytes through lysis and removal of uninfected ery

273 nds other than DBP1 to invade Duffy-negative erythrocytes through other receptors.

274 BP1 binds Aotus but does not bind to Saimiri erythrocytes; thus, P. vivax Sal I must invade Saimiri e

275 of VAR2CSA expressing P. falciparum-infected erythrocytes to CSA in a standardized functional assay.

276 e glycome profiles of chicken and guinea pig erythrocytes to gain insights into reduced agglutination

277 human-liver-chimeric mice infused with human erythrocytes to generate hundreds of unique recombinant

278 ivated on aged erythrocytes, cause senescent erythrocytes to interact with extracellular matrix prote

279 (liposomes) and the plasma membrane of human erythrocytes to investigate the effect of DMSO when adde

280 rythropoiesis, which generates a wave of new erythrocytes to maintain erythroid homeostasis until ste

281 macrophages in the liver phagocytose damaged erythrocytes to prevent the toxic effects of cell-free h

282 erythropoiesis, which rapidly generates new erythrocytes to restore tissue oxygenation.

283 h presents nanoparticles from the surface of erythrocytes to the APCs in the spleen.

284 ciparum is the adhesion of parasite-infected erythrocytes to the vasculature or tissues of infected i

285 is of substantial importance in facilitating erythrocyte turnover through induction of hemolysis.

286 two cellular systems-the human platelet and erythrocyte under cold storage for use in transfusion me

287 esion molecule-driven retention of senescent erythrocytes under low shear conditions was found to res

288 d the cellular antioxidant activity on human erythrocytes under oxidative condition.

289 erythrocyte (IRBC) is attached to uninfected erythrocytes (URBC).

290 Presence of once-infected erythrocytes was assessed by flow cytometry in a sub-pop

291 ically, the osteoinductive activity of lysed erythrocytes was localized to their membrane fraction, d

292 By leveraging this innate immune function of erythrocytes, we developed erythrocyte-driven immune tar

293 influenza B-mediated agglutination of human erythrocytes when expressed in Chinese hamster ovary-K1,

294 r late-stage infections in Saimiri and Aotus erythrocytes when invasion ligands are expressed, we ide

295 as a key event in the turnover of senescent erythrocytes, which alters our current understanding of

296 igens on the surfaces of gametocyte-infected erythrocytes, which can potentially become a new group o

297 enables S. aureus to acquire iron by lysing erythrocytes, which depends on targeting the host recept

298 nic clearance of longer-circulating infected erythrocytes, which likely maintain parasitemias below c

299 colocalization of intravenously administered erythrocytes with metastases in the lungs, we show that

300 within each replicative cycle of parasitized erythrocytes without adhering to the vascular endotheliu