ライフサイエンスコーパス: erythropoietic

1 These erythropoietic abnormalities are caused by translational

2 ly, and cases for both negative and positive erythropoietic actions of Lyn recently have been outline

3 EPO induction was associated with increased erythropoietic activity and elevated serum levels of gro

4 ore and after transfusion, in the context of erythropoietic activity and iron loading.

5 in anemias has now been linked to increased erythropoietic activity and is likely mediated by factor

6 e is advantageous in conditions of increased erythropoietic activity because of augmented iron mobili

7 zebrafish embryos, RAP-011 likely stimulates erythropoietic activity by sequestering lefty1 from eryt

8 uman alpha-globin gene cluster, migration of erythropoietic activity from the embryonic yolk sac to t

9 ression pattern coincides with the timing of erythropoietic activity in hematopoietic organs.

10 The immunomodulatory drugs show exciting erythropoietic activity in myelodysplastic syndrome that

11 abundant N-glycosylation, which enhances its erythropoietic activity in vivo by decreasing its metabo

12 regulation by the known stimuli (i.e., iron, erythropoietic activity, and inflammation) appears to be

13 sma iron and iron stores and is inhibited by erythropoietic activity, ensuring that extracellular pla

14 ate and affinity for EPOR, thereby enhancing erythropoietic activity.

15 y compensated by considerable enhancement in erythropoietic activity.

16 rkedly increased, an indication of increased erythropoietic activity.

17 n response to iron stores, inflammation, and erythropoietic activity.

18 iple factors including iron availability and erythropoietic activity.

19 pported enhanced erythroblast formation, and erythropoietic advantages due to DYRK3-deficiency also w

20 a on anemia (hemoglobin [Hb] <11 g/dL and/or erythropoietic agents and/or transfusion in the previous

21 Erythropoietic agents, a cornerstone of management, are

22 commonly titrated inputs, such as dosing of erythropoietic agents.

23 Based on these distinct erythropoietic and EPOR signaling properties, CNTO 530 h

24 vels eventually decline, consistent with the erythropoietic and hemoglobin deficits.

25 Erythropoietic and inflammatory markers were measured at

26 Erythropoietic and megakaryocytic programs are directed

27 Erythropoietic and megakaryocytic programs are specified

28 Erythropoietic and parasitic indicators were assessed at

29 the regulation of iron absorption involving erythropoietic and store regulators is discussed and a r

30 Here we examined whether erythropoietic and tissue-protective activities of rhEPO

31 arbamylated erythropoietin (CEPO) lacks both erythropoietic and vasoconstrictive actions.

32 Epo's erythropoietic capacity is ascribed largely to its antia

33 ific Sphk1 Sphk2-KO embryos were anemic, the erythropoietic capacity of hematopoietic stem cells (HSC

34 ea/fsn gene is required for iron uptake into erythropoietic cells and for kidney iron reabsorption.

35 is required for normal hemoglobinization of erythropoietic cells and protection against ischemia-rep

36 ct splicing of IVS2-654 pre-mRNA in cultured erythropoietic cells from transgenic mice and thalassemi

37 at this phenotypic response was reflected in erythropoietic cultures.

38 s "acute hepatic," "hepatic cutaneous," and "erythropoietic cutaneous" diseases.

39 er of E2f8, did not substantially worsen the erythropoietic defect resulted from Rb deficiency.

40 ermine if this difference was a result of an erythropoietic defect, competitive repopulation was perf

41 The erythropoietic defects in HIF-1alpha-deficient erythroid

42 ocitrate administration corrected anemia and erythropoietic defects in rats with ACDI.

43 link between ribosomal protein mutations and erythropoietic defects is not well understood.

44 Remarkably, inactivation of E2f2 rescued the erythropoietic defects resulting from Rb and E2f8 defici

45 in hematopoietic stem cells only led to mild erythropoietic defects, concomitant inactivation of both

46 -deficient embryos that die from anemia, the erythropoietic deficiency in RXR alpha(-/-) embryos is t

47 ay be required for optimal response to acute erythropoietic demand and that erythropoiesis in the spl

48 ations and iron stores remain stable and the erythropoietic demand for iron is met.

49 oncentrations in plasma and the liver and by erythropoietic demand for iron.

50 for erythropoiesis, the mechanisms by which erythropoietic demand modulates the iron supply ("erythr

51 f hepcidin necessary to match iron supply to erythropoietic demand thus requires increased erythropoi

52 din regulates iron metabolism in response to erythropoietic demand, iron stores and inflammation.

53 s and strongly modulated by inflammation and erythropoietic demand.

54 Porphyrias are classified as hepatic or erythropoietic, depending upon the site where the gene d

55 tanding of how molecular chaperones regulate erythropoietic development and hemoglobin homeostasis sh

56 essed and plays a significant role in normal erythropoietic differentiation and maturation, while its

57 However, Epo expression and erythropoietic differentiation become normalized in RXRa

58 pression and the initial phase of definitive erythropoietic differentiation in the fetal liver (E9-E1

59 cient level of expression to support further erythropoietic differentiation.

60 nitor cell proliferation and is required for erythropoietic differentiation.

61 nal and survival support niche for efficient erythropoietic differentiation.

62 e compartment may be a new strategy to treat erythropoietic disorders.

63 Enhanced erythropoietic drive and iron deficiency both influence

64 nt inflammation) and downregulating stimuli (erythropoietic drive) on hepcidin levels.

65 ss of function, we observed a strong in vivo erythropoietic effect for RBPMS but not for GTF2E2, supp

66 The erythropoietic effects of lenalidomide are cytokine depe

67 e sinusoids congested with blood; persistent erythropoietic elements and increased immature red blood

68 essential role in regulating the fetal liver erythropoietic environment and suggest that EBI formatio

69 PO-mediated signaling, but does not bind the erythropoietic EPO receptor homodimer, on the progressio

70 Abrogation of STAT5 blocked the erythropoietic expansion by epo mRNA, consistent with a

71 The expression of the erythropoietic factors erythropoietin and stem cell fact

72 ffling of the neural fold ridges, a yolk sac erythropoietic failure, and elevated alpha-ketoglutarate

73 ws donor bone marrow cells to adopt a stress erythropoietic fate and promotes the rapid expansion and

74 a durable drop in leukocyte counts, enhanced erythropoietic function, and markedly reduced spleen siz

75 When we assessed early expression of the erythropoietic gene gata-1 in transplant recipients, we

76 hrocyte-producing, notothenioids to discover erythropoietic genes via representational difference ana

77 o develop anemia during combination therapy, erythropoietic growth factors maintain higher drug treat

78 In conclusion, use of erythropoietic growth factors, specifically darbepoetin,

79 atient erythroblasts resulted in significant erythropoietic improvements.

80 ed, neither helix B nor the 11-aa peptide is erythropoietic in vitro or in vivo.

81 In this study, erythropoietic induction of iron absorption was further

82 , that Rb(-/-) macrophages are competent for erythropoietic island formation in the absence of exogen

83 Here we show that erythropoietic islands are disrupted by hypoxic stress,

84 of FGF in the specification of the embryonic erythropoietic lineage has remained unclear.

85 the role of FGF in the specification of the erythropoietic lineage in the Xenopus embryo.

86 nteract to regulate the specification of the erythropoietic lineage.

87 f the iron-regulating peptide hepcidin by an erythropoietic mechanism.

88 gh transplantation into vlad tepes (vlt), an erythropoietic mutant.

89 the bloodstream in the absence of increased erythropoietic needs and its toxic effects in parenchyma

90 ntly, Brm deficiency does not exacerbate the erythropoietic or vascular abnormalities found in Brg1(f

91 s sufficient to convert the placenta into an erythropoietic organ.

92 Congenital erythropoietic porphyria (CEP) is a rare autosomal reces

93 Congenital erythropoietic porphyria (CEP) is an autosomal recessive

94 families with autosomal recessive congenital erythropoietic porphyria (CEP) resulting from uroporphyr

95 Congenital erythropoietic porphyria (CEP), an autosomal recessive d

96 Congenital erythropoietic porphyria (CEP), an autosomal recessive i

97 ytopenia with thalassemia (XLTT), congenital erythropoietic porphyria (CEP), transient myeloprolifera

98 s who presented phenotypically as congenital erythropoietic porphyria (CEP).

99 Some other cases of late-onset erythropoietic porphyria may be explained by a similar m

100 Congenital erythropoietic porphyria, an autosomal recessive inborn

101 erythropoietic protoporphyria and congenital erythropoietic porphyria, result from germline mutations

102 biosynthetic enzyme defective in congenital erythropoietic porphyria.

103 ay and is the defective enzyme in congenital erythropoietic porphyria.

104 itivity: porphyria cutanea tarda; congenital erythropoietic porphyria; hepatoerythropoietic porphyria

105 The erythropoietic porphyrias, erythropoietic protoporphyria

106 ia cutanea tarda, and diagnose and treat the erythropoietic porphyrias, including chronic erythrocyte

107 and new and experimental treatments for the erythropoietic porphyrias.

108 e function of hematopoietic progenitors with erythropoietic potential and that its loss creates a pro

109 tyrosines have the capacity to restore full erythropoietic potential to the EPOR as determined in wh

110 s response also restricts the iron supply to erythropoietic precursors and may cause or contribute to

111 The cytokine erythropoietin (Epo) promotes erythropoietic progenitor cell proliferation and is requ

112 creased apoptosis of Ter119(-)/CD71(-) early erythropoietic progenitors, and loss of survivin express

113 d KLF2 regulate Myc to control the primitive erythropoietic program.

114 timulates erythropoiesis, with physiological erythropoietic proliferation, differentiation, and enucl

115 mouse models of human rbc disorders, namely erythropoietic protoporphyria (EPP) and beta-thalassemia

116 Autosomal recessive erythropoietic protoporphyria (EPP) and X-linked protopo

117 Erythrocytes from individuals with erythropoietic protoporphyria (EPP) have low levels of t

118 Amassing of PPIX in erythroid cells promotes erythropoietic protoporphyria (EPP) in the affected fami

119 Importance: Erythropoietic protoporphyria (EPP) is a rare hereditary

120 Erythropoietic protoporphyria (EPP) is a rare inherited

121 Erythropoietic protoporphyria (EPP) is a rare inherited

122 Erythropoietic protoporphyria (EPP) is an inherited cuta

123 Erythropoietic protoporphyria (EPP) is an inherited diso

124 Erythropoietic protoporphyria (EPP) is caused by a defec

125 Erythropoietic protoporphyria (EPP) is caused by mutatio

126 Erythropoietic protoporphyria (EPP) is characterized by

127 Erythropoietic protoporphyria (EPP) is marked by a defic

128 accumulation of protoporphyrin-IX (PP-IX) in erythropoietic protoporphyria (EPP) or X-linked-dominant

129 uppress the porphyric phenotype of mice with erythropoietic protoporphyria (EPP).

130 re a prerequisite for the inherited disorder erythropoietic protoporphyria (EPP).

131 ite of defect in the human inherited disease erythropoietic protoporphyria (EPP).

132 The erythropoietic porphyrias, erythropoietic protoporphyria and congenital erythropoie

133 ion analysis was performed for families with erythropoietic protoporphyria and four novel frameshift

134 minant fashion and that mutations underlying erythropoietic protoporphyria are heterogeneous.

135 Here we show that late-onset erythropoietic protoporphyria can be caused by deletion

136 etic studies have shown that the majority of erythropoietic protoporphyria cases are transmitted in d

137 a, the identification of an X-linked form of erythropoietic protoporphyria due to gain-of-function mu

138 Erythropoietic protoporphyria is a genetic disease in wh

139 Erythropoietic protoporphyria is a severe photodermatosi

140 Human erythropoietic protoporphyria is an inherited disorder o

141 Erythropoietic protoporphyria patients needing LT should

142 subjects and 30 individuals with manifested erythropoietic protoporphyria with or without a known mu

143 ease, is similar to that seen in humans with erythropoietic protoporphyria, a disorder of ferrochelat

144 1 donor site in four unrelated families with erythropoietic protoporphyria, and a G(- 1)-->A substitu

145 Using a mouse model of erythropoietic protoporphyria, we demonstrate here that

146 explain the sporadic hepatic consequences of erythropoietic protoporphyria.

147 patic injury occurring sporadically in human erythropoietic protoporphyria.

148 nd improved quality of life in patients with erythropoietic protoporphyria.

149 of the defect in the human inherited disease erythropoietic protoporphyria.

150 ailure or end-stage chronic liver disease in erythropoietic protoporphyria.

151 and stem cell gene therapies for congenital erythropoietic protoporphyria.

152 LAS2 are a cause of sideroblastic anemia and erythropoietic protoporphyria.

153 n, we report novel mutations associated with erythropoietic protoporphyria: g(+ 1)-->t transversion o

154 ria; hepatoerythropoietic porphyria and both erythropoietic protoporphyrias: autosomal dominant and X

155 we show that Stat5 is essential for the high erythropoietic rate during fetal development.

156 Erythropoietic rate is regulated at least in part throug

157 oblast Fas and FasL, consequently increasing erythropoietic rate.

158 lasts, suppressing erythroblast survival and erythropoietic rate.

159 atocrit but are deficient in generating high erythropoietic rates in response to stress.

160 Erythropoietic recovery began after 14 days but was iron

161 macrophage depletion significantly impaired erythropoietic recovery from hemolytic anemia, acute blo

162 n but is also required for activation of the erythropoietic regulators EKLF and GATA binding protein

163 matory inputs in a therapeutically tractable erythropoietic regulatory circuit.

164 opoietin-driven erythropoiesis and underlies erythropoietic repression in iron deficiency anemia.

165 In the mouse spleen, an erythropoietic reserve organ, early erythroblasts were p

166 .5%) of IV iron-treated patients achieved an erythropoietic response compared with 66.9% (95% CI, 59.

167 nflammation and oxidative stress and improve erythropoietic response in prevalent MHD patients.

168 With sufficient acclimatisation, the erythropoietic response increases red cell mass such tha

169 P1 plays a critical role in the differential erythropoietic response of CMS and non-CMS subjects: we

170 There was no difference in the erythropoietic response rate (ie, proportion of patients

171 etin (Epo) is the principal regulator of the erythropoietic response to hypoxic stress, through its r

172 iesis, the hormone erythropoietin drives the erythropoietic response to hypoxic stress.

173 necessary for approximately 50% of the acute erythropoietic response to hypoxic stress.

174 ence for reticulocytes we uncover an optimal erythropoietic response which minimizes disease severity

175 We hypothesized that absence of the erythropoietic response would be associated with greater

176 ted genetically such that many display a low erythropoietic response, resulting in near sea-level hae

177 n suggests that hemolysis, and the resultant erythropoietic response, results in the up-regulation of

178 er exercise capacity in Tibetans without the erythropoietic response, supported mostly by cardiac and

179 of inflammation and oxidative stress or the erythropoietic response.

180 with ACE-536 and EPO produced a synergistic erythropoietic response.

181 furan concentrations and did not improve the erythropoietic response.

182 transport, and (3) systemic inflammatory and erythropoietic responses.

183 hat hepcidin expression is not controlled by erythropoietic signals directly in this setting.

184 Erythropoietin (EPO) an erythropoietic stimulating agent also exerts effects on

185 y, and in monitoring therapeutic response to erythropoietic stimulating agents, while hyperchromic ce

186 le in negatively regulating inflammatory and erythropoietic stress and positively regulates the growt

187 not confer anemia, even under conditions of erythropoietic stress, and EBI formation is normal in th

188 We examined several mouse models of erythropoietic stress, including erythrocytosis and beta

189 were normal, as was their response to acute erythropoietic stress.

190 -) mice also exhibit superior recovery after erythropoietic stress.

191 s but are unable to rapidly respond to acute erythropoietic stress.

192 ression and aggravated anemia in response to erythropoietic stress.

193 se include preoperative autologous donation, erythropoietic support, acute normovolemic hemodilution,

194 concentrations >12 g/dl for 4 months without erythropoietic support.

195 restriction has been proposed as a cause of erythropoietic suppression in malarial anemia; however,

196 We then show that this in vitro erythropoietic system clearly signals exposure to genoto

197 ing cartilage, bone, muscle, kidney, and the erythropoietic system.

198 ated with renal disease and in resistance to erythropoietic therapies remains to be elucidated.

199 nd points further support equivalency of the erythropoietic therapies.

200 okines may account for hyporesponsiveness to erythropoietic therapy in patients with renal failure.

201 for patients with hemoglobin >12 g/dl and no erythropoietic therapy was lower than for the other pati

202 globin concentrations without transfusion or erythropoietic therapy.

203 ily of transporter proteins, identified from erythropoietic tissue (UT-B) and from kidney (UT-A).

204 ze Stat5 phosphorylation dynamics in primary erythropoietic tissue in vivo and in vitro, identifying

205 ite a marked compensatory expansion in their erythropoietic tissue.

206 ferrochelatase expression in iron-deficient erythropoietic tissues of mice lacking iron regulatory p

207 hropoietin and progressively enlarging their erythropoietic tissues.

208 , while the erythroid transcript was only in erythropoietic tissues.