ライフサイエンスコーパス: red cell

1 cells as progenitors do not generate viable red cells.

2 suscitation was started with crystalloid and red cells.

3 availability to allow maximal production of red cells.

4 ts only in circulating chorea-acanthocytosis red cells.

5 timate association with developing and dying red cells.

6 Components were typically whole blood and red cells.

7 modulus controlling the temporal response of red cells.

8 h results in a semi-dominant microcytosis of red cells.

9 n, which is a critical process in developing red cells.

10 odel in preparation for production of mature red cells.

11 at proliferate and differentiate to generate red cells.

12 h the altered cation content of DHSt patient red cells.

13 e allosteric activator of pyruvate kinase in red cells.

14 gs of others that venous fibrin clots entrap red cells.

15 pathic by exchange of whole blood for washed red cells.

16 vertebrates such as fish contains nucleated red cells.

17 line, which provides a continuous supply of red cells.

18 Clinical evidence suggests that red cell alarmins may cause AKI in SCD, however, the ste

19 nce: the development of a low cost, portable red cell analyzer to measure these parameters.

20 increase in the cytoskeletal tension of the red cell and a reduction in the bending modulus of the c

21 The cell-free plasma gap between the red cell and endothelial wall represents the ECG.

22 lving use and applications of genotyping for red cell and platelet blood group antigens affecting sev

23 Red cell and reticulocyte cellular indices are widely us

24 imported iron to mitochondria in developing red cells and of PCBP1 and NCOA4 in mediating iron flux

25 wo B mAb-Ds with 77-81% fucosylation cleared red cells and prevented D-immunisation but less effectiv

26 ibodies incompatible with donor or recipient red cells and three developed compatible antibodies.

27 cells (F-cells 58.9 to 93.6% of untransfused red cells) and HbF per F-cell of 9.0 to 18.6 pg per cell

28 lly had significant increases in neutrophil, red cell, and platelet lineages.

29 ely 270 billion hemoglobin molecules in each red cell, and roughly 2 million senescent red cells are

30 esent in erythroid precursors and peripheral red cells, and alleviated anemia by promoting differenti

31 lood cell traits (platelets, mature/immature red cells, and myeloid/lymphoid/compound white cells) an

32 e transporter) and then GLUT2 and GLUT4, the red cell anion exchange protein (Band 3), asialoglycopro

33 We assessed formation of new red cell antibodies after transplantation and red cell i

34 to donor antigens from the HPC graft and new red cell antibodies induced by transfusion can lead to i

35 After HPC transplantation, new red cell antibodies were seen in six patients (11 alloan

36 Pure red cell aplasia (PRCA) is a syndrome defined by a normo

37 lobulin (IVIG) therapy in patients with pure red cell aplasia (PRCA) related to human parvovirus B19

38 n and heme synthesis may be involved in pure red cell aplasia of DBA.

39 teins cause Diamond Blackfan Anemia (DBA), a red cell aplasia often associated with physical abnormal

40 graft-vs-host disease-like colitis, and pure red cell aplasia, different from the pattern observed in

41 Diamond Blackfan anemia (DBA), an inherited red cell aplasia, the bone marrow is characterized by a

42 isorders), the most common of which was pure red-cell aplasia.

43 d vorticity of the shear flow, tank-treading red cells appear as slender bodies.

44 or the first time that chorea-acanthocytosis red cells are characterized by impaired autophagy, with

45 ch red cell, and roughly 2 million senescent red cells are recycled each second.

46 Transfusion of fresh red cells, as compared with standard-issue red cells, di

47 Kidneys were perfused with a plasma free red-cell based solution at a mean temperature of 34.6 de

48 The first kidney was perfused with red cell-based perfusate at 37 degrees C for 75 min, mea

49 thermic machine perfusion with a plasma-free red cell-based perfusate.

50 hen underwent a 1-hour period of NMP using a red cell-based perfusate.

51 First: a new red-cell-based index, Joint Indicator A, to discriminate

52 cis-element alterations with importance for red cell biology and disease.

53 ny chromatin-modifying/remodeling enzymes in red cell biology remain enigmatic.

54 lood flow due to oxygen-dependent changes in red cell biomechanics is a key driver of pathology.

55 ys within the erythrocyte, which might alter red cell biophysical properties to facilitate invasion,

56 s mediated through phagocytosis of apoptotic red cells by dendritic cells.

57 nce of the motion of the membrane around the red cell called tank-treading.

58 oxygenation in the tissues to form fibers in red cells, causing them to deform and occlude the circul

59 safe features of mAb-Ds for mediating rapid red cell clearance at low doses, to enable effective, in

60 including all patients receiving 10 or more red cell concentrate transfusions in Sweden from 1987 an

61 tio (HR), 95% confidence interval (CI)] only red cell count (RCC) (p = 0.004), red cell distribution

62 ice, but, surprisingly, testosterone reduced red cell count in iron-deficient mice.

63 Testosterone treatment increased red cell count in iron-replete mice, but, surprisingly,

64 ipk1 to wild-type levels restores peripheral red cell counts as well as normal cytokine production.

65 alciparum protein translation; remodeling of red cell cytoskeletal components and transport of parasi

66 studies of hereditary diseases affecting the red cell cytoskeleton.

67 educed alpha-globin aggregates in peripheral red cells, decreased the elevated reactive oxygen specie

68 -day blood, the transfusion of 42-day packed red cells decreases acetylcholine-dependent forearm bloo

69 ave focused on the potential role of altered red cell deformability and blood rheology in precipitati

70 Storage lesion-induced, red cell-derived microvesicles (RBC-MVs) propagate coagu

71 KLF1) is a transcription factor crucial for red cell development that is directly involved in regula

72 NCOA4, and ferritin are critical for murine red cell development.

73 The age of transfused red cells did not affect 90-day mortality among critical

74 h red cells, as compared with standard-issue red cells, did not decrease the 90-day mortality among c

75 rminal domain of GATA1 is critical to normal red cell differentiation (erythropoiesis).

76 Here, we add another red cell disease to the panoply of erythrocytic changes

77 (SCD) is a worldwide distributed hereditary red cell disorder, characterized by severe organ complic

78 tic agent for thalassemia syndrome and other red cell disorders characterized by IE.

79 e findings not only improve understanding of red cell disorders, they are likely to impact many disci

80 r hemolysis after transfusion of aged stored red cells disrupt nitric oxide (NO) bioavailabity, via a

81 (CI)] only red cell count (RCC) (p = 0.004), red cell distribution width (RDW) (p < 0.001), percentag

82 red cell parameters: mean cell volume (MCV), red cell distribution width (RDW) and mean cell hemoglob

83 or Hgb, hematocrit (Hct), MCV, RBC count and red cell distribution width (RDW)] were each associated

84 -minute walk distance, disease duration, and red cell distribution width also predicted survival.

85 erms thought to plausibly interact with both red cell distribution width and mortality.

86 We hypothesized that an increase in red cell distribution width at hospital discharge in pat

87 Elevated red cell distribution width at hospital discharge may id

88 are who survive hospitalization, an elevated red cell distribution width at the time of discharge is

89 ts with critical illness, it is not known if red cell distribution width can predict subsequent risk

90 ic area under the curve shows that discharge red cell distribution width has moderate discriminative

91 Red cell distribution width is associated with mortality

92 y, all relative to patients with a discharge red cell distribution width less than or equal to 13.3%.

93 y, all relative to patients with a discharge red cell distribution width less than or equal to 13.3%.

94 Increased discharge red cell distribution width likely reflects the presence

95 Patients with a discharge red cell distribution width of 14.0-14.7%, 14.7-15.8%, a

96 riable adjustment, patients with a discharge red cell distribution width of 14.0-14.7%, 14.7-15.8%, a

97 and survived hospitalization, the discharge red cell distribution width was a robust predictor of al

98 The exposure of interest was red cell distribution width within 24 hours of hospital

99 iesis, as indicated by reduced spleen index, red cell distribution width, and mean corpuscular volume

100 n mean corpuscular hemoglobin concentration, red cell distribution width, hematocrit, or hemoglobin.

101 ng protein-2) and 5 clinical variables (age, red-cell distribution width, diabetes mellitus, hemoglob

102 thy individuals donated 1 U of leukopheresed red cells, divided and autologously transfused into the

103 These effects are likely to increase red cell entrapment in response to clinical triggers suc

104 patients showed abnormally low levels of the red cell enzyme pyruvate kinase, a known cause of CNSHA.

105 les, (2) plasma leakage persists well beyond red cell escape and mature thrombus formation, (3) the m

106 Their red cells exhibit a panel of various shape abnormalities

107 ell disease (SCD), the number of circulating red cells exposing PS on their surface is elevated.

108 4 to 41.3%), with HbF broadly distributed in red cells (F-cells 58.9 to 93.6% of untransfused red cel

109 SSNA (peroneal microneurography) and red cell flux (laser Doppler flowmetry; dorsum of foot)

110 SSNA (peroneal microneurography) and red cell flux (laser-Doppler flowmetry) in the innervate

111 ocol 1, SSNA (peroneal microneurography) and red cell flux in the affected dermatome (laser Doppler f

112 6 nmol/l p < 0.01 (95% CI - 2.54 to - 0.66), red cell folate 33.6 nmol/l p < 0.001 (95% CI - 43.64 to

113 te a feasible approach to the manufacture of red cells for clinical use from in vitro culture.

114 ires a drug that acts at an earlier stage of red cell formation and enhances the formation of Epo-sen

115 ntiation factors exert inhibitory effects on red cell formation by activating canonical SMAD2/3 pathw

116 bition of cathepsin B/L enhanced EPO-induced red cell formation in normal mice.

117 e molecular mechanism(s) by which TH affects red cell formation is still elusive.

118 reticulocyte-enriched chorea-acanthocytosis red cell fractions exhibited delayed clearance of mitoch

119 1211 patients were assigned to receive fresh red cells (fresh-blood group) and 1219 patients were ass

120 available methods for in vitro generation of red cells from adult and cord blood progenitors do not y

121 react with any test cells but did react with red cells from other patients with COVID-19 that were DA

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

123 culocytes are identical to those observed on red cells from splenectomized individuals and patients w

124 erythroblasts are specifically enriched for red cell functions.

125 t cell surface membrane proteins: GLUT1 (the red cell glucose transporter) and then GLUT2 and GLUT4,

126 Human mature red cells have a lifespan of 120 days before they become

127 in available serum iron leading to enhanced red cell hemoglobinization.

128 Using donor blood samples, we show that red cells heterozygous for PIEZO1 E756del are not dehydr

129 G6PD deficiency makes red cells highly vulnerable to oxidative damage, and the

130 failure syndrome characterised by selective red cell hypoplasia.

131 l to understanding and treating disorders of red cell imbalance such as anemia, myelodysplastic syndr

132 atients PS is present on the cell surface of red cells in large ( approximately 1.4 microm) discrete

133 d as an alternative oxygen carrier to packed red cells in NMP-L perfusion fluid.

134 The hemoglobin threshold for transfusion of red cells in patients with acute gastrointestinal bleedi

135 he donor bone marrow cells lacked FLVCR, all red cells in recipient mice were wild type.

136 expression of many genes required to build a red cell including those encoding globins, cytoskeletal

137 ed cell antibodies after transplantation and red cell incompatibility between donors and recipients.

138 Requirements for transfusion of red cells increased during pregnancy, from a mean of 0.1

139 Red cell indices continue to provide an essential suppor

140 The distributions of red cell indices differed by causal gene but not suffici

141 erritin index are more accurate than classic red cell indices in the diagnosis of iron deficiency ana

142 nships with anatomic attributes of PAVMs, or red cell indices often increased due to secondary polycy

143 Abnormal red cell indices, in particular increased reticulocyte c

144 fied several potential novel genes affecting red cell indices, which are not mediated by changes in i

145 vasion period during which dynamic merozoite-red-cell interactions align the merozoite apex in prepar

146 isms of the host-parasite interaction during red cell invasion by Plasmodium is important for develop

147 last decade that sub-cellular resolution of red cell invasion by the malaria parasite Plasmodium fal

148 ing involvement of both the receptors during red cell invasion.

149 e differential localizations within infected red cell (iRBC), suggesting different functional roles i

150 hemoglobin S (HbS) to form fibers that make red cells less flexible, most drugs currently being asse

151 e lesion" is increased hemolysis and reduced red cell lifespan after infusion.

152 e (oldest available), compatible, allogeneic red cells (long-term storage group).

153 esults show that protein loss persists after red cell loss has ceased.

154 states associated with unstable globins and red cell lysis and also insights into the factors govern

155 emoglobin is diluted into blood plasma after red cell lysis, the disassembly pathway appears to be do

156 luding anemia due to protein instability and red cell lysis.

157 The entrapped sickle red cells make the attached fibrin more resistant to fib

158 y analysis of the INforming Fresh versus Old Red cell Management (INFORM) trial, a pragmatic, multice

159 e diagnosed as PV owing to an elevated Cr-51 red cell mass (RCM), JAK2 positivity, and at least 1 min

160 ency, and point to multifactorial control of red cell mass by PHD2.

161 The central pathway for controlling red cell mass is the PHD (prolyl hydroxylase domain prot

162 tral pathway for oxygen-dependent control of red cell mass is the prolyl hydroxylase domain protein (

163 ation, the erythropoietic response increases red cell mass such that arterial O2 content (C(aO2)) is

164 me synthesis, GATA1 and heme together direct red cell maturation, and heme stops GATA1 synthesis, our

165 Fresh red cells may improve outcomes in critically ill patient

166 This suggests that COVID-19 may modulate the red cell membrane and present novel antigenic epitopes.

167 provide new insights into the genesis of the red cell membrane during human terminal erythroid differ

168 rstanding of the structural basis for normal red cell membrane function and allowed definition of the

169 The red cell membrane skeleton is a pseudohexagonal meshwork

170 This knowledge is important because the red cell membrane skeleton is the model for spectrin-bas

171 ons in all cells, and because defects in the red cell membrane skeleton underlie multiple hemolytic a

172 seful in studying diseases which involve the red cell membrane, such as malaria.

173 ntributes critically to the stability of the red cell membrane.

174 atidylserine exposed on the senescent sickle red cell membrane.

175 The red cell membranes were abnormal, most notably expressin

176 d effects of a common mutation that disrupts red cell membranes were elucidated using chemical cross-

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

178 d analyzed by CellaVision and microscopy for red cell morphology scans.

179 thrombosis, and concomitant cytoreduction of red cells, neutrophils, and eosinophils may be required

180 ccumulate into insoluble Heinz bodies in the red cells of patients with unstable hemoglobinopathies.

181 ificantly increased the primary outcome, the red cell omega-3 index (mean difference [98.75% confiden

182 Growing of red cells or platelets in large quantities from stem cel

183 hen adjusted for transfusion rates of packed red cells (p = 0.66).

184 We show here that using only a single RED cell pair (CP), created by operating the cathode in

185 nium bicarbonate (AmB) solutions in multiple RED cell pair stacks and the cathode chamber.

186 t1(-/-) double transgenic mice showed higher red cell parameters and lower platelet counts compared w

187 This study investigated association of red cell parameters and mortality in liver transplant ca

188 Ex12 mice induced no changes in platelet or red cell parameters, indicating that Stat1 does not play

189 This result is achieved using only three red cell parameters: mean cell volume (MCV), red cell di

190 ith sickle cell disease, donor and recipient red cell phenotypes should be carefully assessed before

191 Many red cell polymorphisms are a result of selective pressur

192 rtments at the expense of thrombopoietic and red cell precursors.

193 he anticipated effect of iron restriction on red cell production (ie, no increase in red blood cell [

194 The results confirm a reciprocal model of red cell production and destruction, show that anemia ca

195 n is a potentially novel pathway of inducing red cell production under stress.

196 As essential mediators of red cell production, erythropoietin (EPO) and its cell s

197 nemias that are characterized by ineffective red cell production.

198 The unique sensitivity of early red cell progenitors to iron deprivation, known as the e

199 e PKLR mutation and were associated with the red-cell pyruvate kinase protein level at baseline.

200 Washing red cells (RBC) before transfusion had a significantly d

201 s associated with decreasing posttransfusion red cell recovery (P = 0.002), decreasing elevations in

202 51-Chromium posttransfusion red cell recovery studies were performed and laboratory

203 esults suggest that a reduction in volume of red cell requirements may be achievable.

204 fferentiation of hematopoietic stem cells to red cells requires coordinated expression of numerous er

205 In addition, in many cases, the red cells resembled those seen in patients with membrane

206 aling and high-definition imaging to explore red cell responses during invasion.

207 oantibodies fix complement on the surface of red cells, resulting in extravascular hemolysis by the r

208 upture with exposure of highly thrombogenic, red cell-rich necrotic core material.

209 variants, including an innate variant in the red cell's major Ca(2)(+) pump and the acquired state of

210 Approximately one third of the red-cell samples from PCR-positive or high-titer AFIA-po

211 nd tetramers plays a key role in maintaining red cell shape and membrane integrity, and spectrins in

212 e freshest available, compatible, allogeneic red cells (short-term storage group) or standard-issue (

213 nce of widespread catastrophic intravascular red-cell sickling.

214 years since the first primitive model of the red cell skeleton was proposed, many additional proteins

215 onal changes of the highly flexible, dynamic red cell spectrin and effects of a common mutation that

216 among different species, in contrast to Nile red cell staining procedures.

217 aphy and mass spectrometry (GC-MS), and Nile red cell staining suffer drawbacks, including poor quant

218 ents were assigned to receive standard-issue red cells (standard-blood group).

219 provide evidence that the maximal allowable red cell storage duration should be reduced to the minim

220 derstanding the clinical impact of prolonged red cell storage.

221 It is uncertain whether the duration of red-cell storage affects mortality after transfusion amo

222 The duration of red-cell storage was not associated with significant dif

223 A major abnormality that characterizes the red cell "storage lesion" is increased hemolysis and red

224 ndomly assigned to receive leukocyte-reduced red cells stored for 10 days or less (shorter-term stora

225 We did not find that the transfusion of red cells stored for 10 days or less was superior to the

226 s or less was superior to the transfusion of red cells stored for 21 days or more among patients 12 y

227 can protect against failure in the case of a red cell subjected to an applied strain.

228 ction in hemolysis and percentage of sickled red cells, supporting the potential of voxelotor to serv

229 ole by binding to glycophorin A (GPA) on the red cell surface, although the function of this binding

230 and the identity of binding receptors on the red cell surface.

231 ts and transport of parasite proteins to the red cell surface; and chronic activation of the human in

232 Red cells suspended in solutions much more viscous than

233 t patients, there was no association between red cell TGN levels and taking 6-MP with food versus wit

234 gned critically ill adults to receive either red cells that had been stored for less than 8 days or s

235 d selection criteria, we identified infected red cells that were likely to rupture imminently, and re

236 tored for less than 8 days or standard-issue red cells (the oldest compatible units available in the

237 en 6-MP ingestion habits and 6-MP adherence, red cell thioguanine nucleotide (TGN) levels, and risk o

238 d the maximum allowable storage duration for red cells to 5 weeks before transfusion.

239 rigerated storage, transfusion of autologous red cells to healthy human volunteers increased extravas

240 combination also increased the need for any red cell transfusion (87 of 9,152 [1.0%] vs. 44 of 9,126

241 e standard, autologous, leukoreduced, packed red cell transfusion after 1, 2, 3, 4, 5, or 6 weeks of

242 verse event rates associated with IV iron vs red cell transfusion and discuss using first-line IV iro

243 ent revision include stricter definitions of red cell transfusion dependency and independency and con

244 Restrictive red cell transfusion is recommended to minimize risk ass

245 e criteria do not include treatments such as red cell transfusion or surgical interventions performed

246 reutzfeldt-Jakob disease and an asymptomatic red cell transfusion recipient, who did not die of varia

247 mpare outcomes of a restrictive to a liberal red cell transfusion strategy in 20% or more total body

248 Mean red cell transfusion was 3.2 with frozen plasma and 1.4

249 plasma hemoglobin increase immediately after red cell transfusion, with more significant increases ob

250 cause of transfusion-related mortality with red cell transfusion.

251 Secondary outcomes included red-cell transfusion and other clinical outcomes.

252 t infants, a higher hemoglobin threshold for red-cell transfusion did not improve survival without ne

253 Red-cell transfusion occurred in 52.3% of the patients i

254 The effect of a restrictive versus liberal red-cell transfusion strategy on clinical outcomes in pa

255 eath after cardiac surgery) to a restrictive red-cell transfusion threshold (transfuse if hemoglobin

256 g from induction of anesthesia) or a liberal red-cell transfusion threshold (transfuse if hemoglobin

257 we randomly assigned patients who required a red-cell transfusion to receive blood that had been stor

258 ovided to the 1098 participants who received red-cell transfusion was 7 days in the shorter-term stor

259 for death, a restrictive strategy regarding red-cell transfusion was noninferior to a liberal strate

260 Jakob disease have been identified following red cell transfusions from donors who subsequently devel

261 ty and compliance with each of inotropes and red cell transfusions, glucocorticoids, and lung-protect

262 ive vasopressor infusions (66.6% vs. 57.8%), red-cell transfusions (13.6% vs. 7.0%), and dobutamine (

263 of intravenous fluids, vasoactive drugs, and red-cell transfusions and reflected by significantly wor

264 sideroblasts who had been receiving regular red-cell transfusions and who had disease that was refra

265 ed within 48 hours after delivery to receive red-cell transfusions at higher or lower hemoglobin thre

266 uggest that higher hemoglobin thresholds for red-cell transfusions may reduce the risk of cognitive d

267 sideroblasts who had been receiving regular red-cell transfusions to receive either luspatercept (at

268 estrictive threshold for hemoglobin level in red-cell transfusions, as compared with a liberal thresh

269 not effective generally become dependent on red-cell transfusions.

270 ents, spleen response, and independence from red-cell transfusions.

271 ate kinase deficiency who were not receiving red-cell transfusions.

272 sion-dependent beta-thalassemia need regular red-cell transfusions.

273 thermore, spatial heterogeneity in capillary red cell transit was highly constrained, and red blood c

274 ls to ensure the proper generation of mature red cells under multiple physiological conditions.

275 Just before PVM breakdown, the host red cell undergoes an abrupt, dramatic shape change due

276 13 through 24 plus a reduction of at least 2 red-cell units over this 12-week interval was significan

277 13 through 24 plus a reduction of at least 2 red-cell units over this 12-week interval.

278 The median storage time of red-cell units provided to the 1098 participants who rec

279 al studies have reported that transfusion of red-cell units that have been stored for more than 2 to

280 the transfusion burden (the total number of red-cell units transfused) in such patients.

281 the plasma protein binding (71% +/- 5%) and red cell uptake (16% +/- 2%) of (131)I-OIH (P < 0.001).

282 The plasma protein binding and red cell uptake of (99m)Tc(CO)3(NTA) were 35% +/- 7% and

283 Plasma protein binding, red cell uptake, and percentage injected dose in the uri

284 Multiple red cell variants are known to confer protection from ma

285 Red cell variants that modulate malaria risk can serve a

286 New red cell variants, including an innate variant in the re

287 Hypoxia promptly increased red cell velocity and flux in control capillaries, but i

288 he most reliable for demonstrating increased red cell volume and for monitoring response to therapy;

289 Measurements of red cell volume, hemoglobin (Hb) concentration and Hb co

290 t land plants, have been reported to produce red cell wall-bound riccionidin pigments in response to

291 In most cases, the red cells were hypochromic and microcytic, consistent wi

292 ing units in spleen, and more differentiated red cells were partially restored by reducing Id2 levels

293 ry and were likely to undergo transfusion of red cells were randomly assigned to receive leukocyte-re

294 Red cells were stored a mean (+/-SD) of 6.1+/-4.9 days i

295 Fresh frozen plasma and packed red cells were the most frequently transfused blood prod

296 er or less to receive 1 unit of leukoreduced red cells when the hemoglobin level was 7 g per decilite

297 s occur along the disassembly pathway inside red cells, where the hemoglobin concentration is very hi

298 e stability, and (3) release of ATP from the red cell which has been linked to vasodilation.

299 ion genetic variants for association with 36 red cell, white cell, and platelet properties in 173,480

300 DHSt patient red cells with the R2456H mutation exhibit increased ion