ライフサイエンスコーパス: red cell

1 Components were typically whole blood and red cells.

2 modulus controlling the temporal response of red cells.

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

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

5 odel in preparation for production of mature red cells.

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

7 at proliferate and differentiate to generate red cells.

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

9 rization of the sickle hemoglobin within the red cells.

10 eived HLA selected or random units of packed red cells.

11 cells as progenitors do not generate viable red cells.

12 suscitation was started with crystalloid and red cells.

13 availability to allow maximal production of red cells.

14 ts only in circulating chorea-acanthocytosis red cells.

15 timate association with developing and dying red cells.

16 5 mins </=35 mm were more likely to receive red cell (46% vs. 17%, p < .001) and plasma (37% vs. 11%

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

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

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

20 Red cell and reticulocyte cellular indices are widely us

21 rrest in the normal expansion of circulating red cells and develop anemia, analogous to KLF1(-/-) KLF

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

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

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

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

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

27 cell surface protein from the Kell system on red cells, and subsequently demonstrated that Kell diffe

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

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

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

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

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

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

34 one marrow failure syndrome characterized by red cell aplasia and congenital anomalies.

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

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

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

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

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

40 However, interactions with the red cells are also found to cause an average wall-direct

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

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

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

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

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

46 othermic kidney perfusion with a plasma-free red cell-based solution is a feasible method of preserva

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

48 The red cell binding characteristics of these domains were s

49 ied from genome projects and from functional red cell-binding assays.

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

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

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

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

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

55 Red cell clearance is associated with a reduction in bot

56 oncentrates, fresh frozen plasma, and packed red cells collected using Fresenius Kabi bags.

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

58 ationship between HP CNV, HPR rs2000999, Hb, red cell count (RCC), LDL-C and TC in the British Women'

59 ated for antiplasmodial activity in in vitro red cell culture using SYBR Green I assay.

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

61 studies of hereditary diseases affecting the red cell cytoskeleton.

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

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

64 Relations between red cell density (assessed with phthalate density-distri

65 vent the anemia, suggesting that the bulk of red cell destruction was not due to the parasite.

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

67 In red cell development, the differentiation program direct

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

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

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

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

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

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

74 e study of altered erythropoiesis in various red cell disorders.

75 ts into disordered erythropoiesis in various red cell disorders.

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

77 5.8% (OR, 1.69; 95% CI, 1.52-1.86; p <.001); red cell distribution width >15.8% (OR, 2.61; 95% CI, 2.

78 .86; p <.001), all relative to patients with red cell distribution width </= 13.3%.

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

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

81 th quintiles after multivariable adjustment: red cell distribution width 13.3% to 14.0% (odds ratio [

82 nfidence interval [CI], 1.08-1.30; p <.001); red cell distribution width 14.0% to 14.7% (OR, 1.28; 95

83 4.7% (OR, 1.28; 95% CI, 1.16-1.42; p <.001); red cell distribution width 14.7% to 15.8% (OR, 1.69; 95

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

85 The prevalence of increased red cell distribution width and its significance in the

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

87 ents with blood cultures drawn (n = 18,525), red cell distribution width at critical care initiation

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

89 Elevated red cell distribution width at hospital discharge may id

90 y was to investigate the association between red cell distribution width at the initiation of critica

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

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

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

94 Red cell distribution width is a predictor of mortality

95 Red cell distribution width is a robust predictor of the

96 Red cell distribution width is associated with mortality

97 Red cell distribution width is commonly measured, inexpe

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

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

100 Increased discharge red cell distribution width likely reflects the presence

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

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

103 tion with a significant risk gradient across red cell distribution width quintiles after multivariabl

104 Red cell distribution width was a particularly strong pr

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

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

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

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

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

110 r, in patients with coronary artery disease, red cell eNOS expression and activity are both lower tha

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

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

113 Their red cells exhibit a panel of various shape abnormalities

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

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

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

117 . sex, gestation length, maternal and infant red cell folate, maternal and infant serum vitamin B(12)

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

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

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

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

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

123 1211 patients were assigned to receive fresh red cells (fresh-blood group) and 1219 patients were ass

124 ne the pressure required to eject individual red cells from a capillary-sized channel after the cell

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

126 Availability of cultured human red cells from haematopoietic stem cells in the quantiti

127 Red cells from P. chabaudi/P. berghei-infected animals h

128 by immunofluorescence microscopy showed that red cells from P. chabaudi/P. berghei-infected animals w

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

130 erythroblasts are specifically enriched for red cell functions.

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

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

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

134 failure syndrome characterised by selective red cell hypoplasia.

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

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

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

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

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

140 cusses the potential for generating cultured red cells in sufficient quantity for use in transfusion

141 utions will be required to generate cultured red cells in the large quantities required, and in this

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

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

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

145 Red cell indices continue to provide an essential suppor

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

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

148 Abnormal red cell indices, in particular increased reticulocyte c

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

150 ted hemoglobin chains has been implicated in red cell-induced vasodilation, although the mechanism fo

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

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

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

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

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

156 Tracking of red cells labeled ex vivo and in vivo and analysis of fr

157 known for more than 130 years that mammalian red cells lack a nucleus and, thus, differ fundamentally

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

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

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

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

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

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

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

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

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

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

168 ly changes in concentration and not absolute red cell mass of haemoglobin can be identified; and disa

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

170 cated PHD2 as the key PHD isoform regulating red cell mass.

171 Fresh red cells may improve outcomes in critically ill patient

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

173 The red cell membrane is stabilized by a spectrin/actin-base

174 All major red cell membrane proteins undergo dynamic changes durin

175 The red cell membrane skeleton is a pseudohexagonal meshwork

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

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

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

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

180 The red cell membranes were abnormal, most notably expressin

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

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

183 eus and, thus, differ fundamentally from the red cells of fish, birds, and reptiles that maintain the

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

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

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

187 A second RED cell pair increased RED stack potential and reduced

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

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

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

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

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

193 andidatus Mycoplasma haemolamae," an endemic red-cell pathogen of camelids.

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

195 Many red cell polymorphisms are a result of selective pressur

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

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

198 EpoR-HM mice prevents them from accelerating red cell production in response to stress, including a f

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

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

201 ession in adult animals, yet dispensable for red cell production.

202 nemias that are characterized by ineffective red cell production.

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

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

205 alance is a critical physiologic function of red cells (RBC) that can be perturbed in variety of RBC

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

207 51-Chromium posttransfusion red cell recovery studies were performed and laboratory

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

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

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

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

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

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

214 ythrocytes is almost solely dependent on the red cell's surface receptor, known as the Duffy blood-gr

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

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

217 Finally, we reveal that the biconcave red cell shape is highly stable under moderate shear str

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

219 t model demonstrated that sponges exposed to red cells showed an increase in mannose receptor-positiv

220 At these length scales, it is found that the red cells significantly augment the streamwise forces th

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

222 major discriminator of megakaryocyte versus red cell specification.

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

224 Lyn(up/up) mice were anemic, with dysmorphic red cells (spherocyte-like, acanthocytes) in their circu

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

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

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

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

229 derstanding the clinical impact of prolonged red cell storage.

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

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

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

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

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

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

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

237 large, multi-copy gene families that encode red cell surface antigens.

238 use that expresses the human KEL2 (Chellano) red cell surface protein from the Kell system on red cel

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

240 on relationship in the export of PfP2 to the red cell surface.

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

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

243 Red cells suspended in solutions much more viscous than

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

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

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

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

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

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

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

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

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

253 Restrictive red cell transfusion is recommended to minimize risk ass

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

255 rfarin resulted in faster reversal and lower red cell transfusion requirement with fewer adverse even

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

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

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

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

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

261 hemoglobin threshold at which postoperative red-cell transfusion is warranted is controversial.

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

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

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

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

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

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

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

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

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

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

272 ter); 3 of them were previously dependent on red-cell transfusions and no longer needed transfusions.

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

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

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

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

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

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

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

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

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 riteria remain JAK2 positivity and increased red cell volume, but Cr-51 RCM is mandatory for patients

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

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 A median of 2 units of red cells were transfused in the liberal-strategy group

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

297 localization of RASA3 to the cytosol in scat red cells where it is inactive, leading to increased GTP

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