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1 ment of their rodent orthologs but exhibited erythropoietic abnormalities and altered iron distributi
2                                        These erythropoietic abnormalities are caused by translational
3 ly, and cases for both negative and positive erythropoietic actions of Lyn recently have been outline
4  EPO induction was associated with increased erythropoietic activity and elevated serum levels of gro
5 ore and after transfusion, in the context of erythropoietic activity and iron loading.
6  in anemias has now been linked to increased erythropoietic activity and is likely mediated by factor
7 ciated with neonatal indicators of increased erythropoietic activity and poor iron status.
8 e is advantageous in conditions of increased erythropoietic activity because of augmented iron mobili
9 zebrafish embryos, RAP-011 likely stimulates erythropoietic activity by sequestering lefty1 from eryt
10 uman alpha-globin gene cluster, migration of erythropoietic activity from the embryonic yolk sac to t
11 ression pattern coincides with the timing of erythropoietic activity in hematopoietic organs.
12     The immunomodulatory drugs show exciting erythropoietic activity in myelodysplastic syndrome that
13 abundant N-glycosylation, which enhances its erythropoietic activity in vivo by decreasing its metabo
14 CV expansion is the result of an accelerated erythropoietic activity secondary to enhanced renal eryt
15 regulation by the known stimuli (i.e., iron, erythropoietic activity, and inflammation) appears to be
16 sma iron and iron stores and is inhibited by erythropoietic activity, ensuring that extracellular pla
17 iple factors including iron availability and erythropoietic activity.
18 ate and affinity for EPOR, thereby enhancing erythropoietic activity.
19 y compensated by considerable enhancement in erythropoietic activity.
20 rkedly increased, an indication of increased erythropoietic activity.
21 n response to iron stores, inflammation, and erythropoietic activity.
22 pported enhanced erythroblast formation, and erythropoietic advantages due to DYRK3-deficiency also w
23 a on anemia (hemoglobin [Hb] <11 g/dL and/or erythropoietic agents and/or transfusion in the previous
24                                              Erythropoietic agents, a cornerstone of management, are
25 ld be guided by the etiology and may include erythropoietic agents, folic acid, B12, and iron prepara
26  commonly titrated inputs, such as dosing of erythropoietic agents.
27                      Based on these distinct erythropoietic and EPOR signaling properties, CNTO 530 h
28 vels eventually decline, consistent with the erythropoietic and hemoglobin deficits.
29                                              Erythropoietic and inflammatory markers were measured at
30                                              Erythropoietic and megakaryocytic programs are directed
31                                              Erythropoietic and megakaryocytic programs are specified
32                                              Erythropoietic and parasitic indicators were assessed at
33  the regulation of iron absorption involving erythropoietic and store regulators is discussed and a r
34                     Here we examined whether erythropoietic and tissue-protective activities of rhEPO
35 arbamylated erythropoietin (CEPO) lacks both erythropoietic and vasoconstrictive actions.
36 progenitors induces microtubule collapse and erythropoietic blockade; conversely, enforced ferritin e
37                                        Epo's erythropoietic capacity is ascribed largely to its antia
38 ific Sphk1 Sphk2-KO embryos were anemic, the erythropoietic capacity of hematopoietic stem cells (HSC
39 ea/fsn gene is required for iron uptake into erythropoietic cells and for kidney iron reabsorption.
40  is required for normal hemoglobinization of erythropoietic cells and protection against ischemia-rep
41 ct splicing of IVS2-654 pre-mRNA in cultured erythropoietic cells from transgenic mice and thalassemi
42 (5h - 2d post IA LPS exposure) and increased erythropoietic clusters (at 8 and 15 days post IA LPS ex
43 stems had multiple beneficial effects in the erythropoietic compartment and beyond, providing a stron
44 r normal functioning in all human cells, the erythropoietic compartment consuming the majority in lig
45 at this phenotypic response was reflected in erythropoietic cultures.
46 s "acute hepatic," "hepatic cutaneous," and "erythropoietic cutaneous" diseases.
47 er of E2f8, did not substantially worsen the erythropoietic defect resulted from Rb deficiency.
48 ermine if this difference was a result of an erythropoietic defect, competitive repopulation was perf
49                                          The erythropoietic defects in HIF-1alpha-deficient erythroid
50 ocitrate administration corrected anemia and erythropoietic defects in rats with ACDI.
51 link between ribosomal protein mutations and erythropoietic defects is not well understood.
52 Remarkably, inactivation of E2f2 rescued the erythropoietic defects resulting from Rb and E2f8 defici
53 in hematopoietic stem cells only led to mild erythropoietic defects, concomitant inactivation of both
54 -deficient embryos that die from anemia, the erythropoietic deficiency in RXR alpha(-/-) embryos is t
55 ay be required for optimal response to acute erythropoietic demand and that erythropoiesis in the spl
56 ations and iron stores remain stable and the erythropoietic demand for iron is met.
57 oncentrations in plasma and the liver and by erythropoietic demand for iron.
58  for erythropoiesis, the mechanisms by which erythropoietic demand modulates the iron supply ("erythr
59 f hepcidin necessary to match iron supply to erythropoietic demand thus requires increased erythropoi
60 din regulates iron metabolism in response to erythropoietic demand, iron stores and inflammation.
61 s and strongly modulated by inflammation and erythropoietic demand.
62      Porphyrias are classified as hepatic or erythropoietic, depending upon the site where the gene d
63 tanding of how molecular chaperones regulate erythropoietic development and hemoglobin homeostasis sh
64 essed and plays a significant role in normal erythropoietic differentiation and maturation, while its
65                  However, Epo expression and erythropoietic differentiation become normalized in RXRa
66 pression and the initial phase of definitive erythropoietic differentiation in the fetal liver (E9-E1
67 -deficient embryonic stem cells are prone to erythropoietic differentiation.
68 cient level of expression to support further erythropoietic differentiation.
69 nitor cell proliferation and is required for erythropoietic differentiation.
70 nal and survival support niche for efficient erythropoietic differentiation.
71 e compartment may be a new strategy to treat erythropoietic disorders.
72                                     Enhanced erythropoietic drive and iron deficiency both influence
73 production is reduced by iron deficiency and erythropoietic drive to increase the iron supply when ne
74 nt inflammation) and downregulating stimuli (erythropoietic drive) on hepcidin levels.
75  hepcidin expression in response to iron and erythropoietic drive.
76 ndogenous hepcidin regulators, both iron and erythropoietic drives still regulate hepcidin in mice la
77 ss of function, we observed a strong in vivo erythropoietic effect for RBPMS but not for GTF2E2, supp
78                                          The erythropoietic effects of lenalidomide are cytokine depe
79 , glycemic, vascular, anti-inflammatory, and erythropoietic effects.
80 e sinusoids congested with blood; persistent erythropoietic elements and increased immature red blood
81 enic sequestration of erythrocytes and fewer erythropoietic elements in the bone marrow, despite sign
82 essential role in regulating the fetal liver erythropoietic environment and suggest that EBI formatio
83 PO-mediated signaling, but does not bind the erythropoietic EPO receptor homodimer, on the progressio
84              Abrogation of STAT5 blocked the erythropoietic expansion by epo mRNA, consistent with a
85                        The expression of the erythropoietic factors erythropoietin and stem cell fact
86 (EA/EA)) succumb to Tp53- and Chk2-dependent erythropoietic failure in utero, mirroring Lig1(-/-) mic
87 ffling of the neural fold ridges, a yolk sac erythropoietic failure, and elevated alpha-ketoglutarate
88 ws donor bone marrow cells to adopt a stress erythropoietic fate and promotes the rapid expansion and
89 a durable drop in leukocyte counts, enhanced erythropoietic function, and markedly reduced spleen siz
90 s is not expected in healthy adult mice, but erythropoietic gene expression was elevated in lineage-d
91     When we assessed early expression of the erythropoietic gene gata-1 in transplant recipients, we
92 hrocyte-producing, notothenioids to discover erythropoietic genes via representational difference ana
93 oss of red blood cells and downregulation of erythropoietic genes.
94 o develop anemia during combination therapy, erythropoietic growth factors maintain higher drug treat
95                        In conclusion, use of erythropoietic growth factors, specifically darbepoetin,
96      Erythropoietin (EPO), a kidney-produced erythropoietic hormone, exerts immunomodulatory effects
97 atient erythroblasts resulted in significant erythropoietic improvements.
98 ed, neither helix B nor the 11-aa peptide is erythropoietic in vitro or in vivo.
99                               In this study, erythropoietic induction of iron absorption was further
100 , that Rb(-/-) macrophages are competent for erythropoietic island formation in the absence of exogen
101                            Here we show that erythropoietic islands are disrupted by hypoxic stress,
102 disrupt transcriptional programs controlling erythropoietic lineage commitment, suggesting a role for
103 of FGF in the specification of the embryonic erythropoietic lineage has remained unclear.
104  the role of FGF in the specification of the erythropoietic lineage in the Xenopus embryo.
105 nteract to regulate the specification of the erythropoietic lineage.
106 ndance was associated with neonatal iron and erythropoietic markers (EPO: beta: 0.10; 95% confidence
107  that NEMP1 is essential for NE openings and erythropoietic maturation in vivo and provide the first
108 y hematopoietic precursors to rapidly elicit erythropoietic maturation upon need.
109 f the iron-regulating peptide hepcidin by an erythropoietic mechanism.
110 gh transplantation into vlad tepes (vlt), an erythropoietic mutant.
111  the bloodstream in the absence of increased erythropoietic needs and its toxic effects in parenchyma
112 cterization of host-parasite interactions in erythropoietic niches and define host cell maturation st
113 replication and gametocyte maturation in the erythropoietic niches of the bone marrow and spleen cont
114 itulate DBA phenotypes, although others lack erythropoietic or skeletal defects.
115 ntly, Brm deficiency does not exacerbate the erythropoietic or vascular abnormalities found in Brg1(f
116 s sufficient to convert the placenta into an erythropoietic organ.
117 eceptor, leading to substantial increases in erythropoietic output.
118 odel of the rare disease disorder congenital erythropoietic porphyria (CEP) as well as two well-known
119                                   Congenital erythropoietic porphyria (CEP) is a rare autosomal reces
120                                   Congenital erythropoietic porphyria (CEP) is a rare genetic disorde
121                                   Congenital erythropoietic porphyria (CEP) is an autosomal recessive
122                                   Congenital erythropoietic porphyria (CEP) is an inborn error of hem
123 families with autosomal recessive congenital erythropoietic porphyria (CEP) resulting from uroporphyr
124                                   Congenital erythropoietic porphyria (CEP), an autosomal recessive d
125                                   Congenital erythropoietic porphyria (CEP), an autosomal recessive i
126 ytopenia with thalassemia (XLTT), congenital erythropoietic porphyria (CEP), transient myeloprolifera
127 ribe studies in a murine model of congenital erythropoietic porphyria (CEP).
128 s who presented phenotypically as congenital erythropoietic porphyria (CEP).
129               Some other cases of late-onset erythropoietic porphyria may be explained by a similar m
130                                   Congenital erythropoietic porphyria, an autosomal recessive inborn
131 erythropoietic protoporphyria and congenital erythropoietic porphyria, result from germline mutations
132 nked protoporphyria, and the rare congenital erythropoietic porphyria.
133  biosynthetic enzyme defective in congenital erythropoietic porphyria.
134 ay and is the defective enzyme in congenital erythropoietic porphyria.
135 itivity: porphyria cutanea tarda; congenital erythropoietic porphyria; hepatoerythropoietic porphyria
136                                          The erythropoietic porphyrias, erythropoietic protoporphyria
137 ia cutanea tarda, and diagnose and treat the erythropoietic porphyrias, including chronic erythrocyte
138 tegories of acute vs non-acute or hepatic vs erythropoietic porphyrias.
139  and new and experimental treatments for the erythropoietic porphyrias.
140 e function of hematopoietic progenitors with erythropoietic potential and that its loss creates a pro
141  tyrosines have the capacity to restore full erythropoietic potential to the EPOR as determined in wh
142 L11 haploinsufficiency-induced inhibition of erythropoietic precursor differentiation and restores no
143 s response also restricts the iron supply to erythropoietic precursors and may cause or contribute to
144   The cytokine erythropoietin (Epo) promotes erythropoietic progenitor cell proliferation and is requ
145 creased apoptosis of Ter119(-)/CD71(-) early erythropoietic progenitors, and loss of survivin express
146 tomic states in committed transit-amplifying erythropoietic progenitors, which correlates with a cont
147 d KLF2 regulate Myc to control the primitive erythropoietic program.
148 timulates erythropoiesis, with physiological erythropoietic proliferation, differentiation, and enucl
149  mouse models of human rbc disorders, namely erythropoietic protoporphyria (EPP) and beta-thalassemia
150                          Autosomal recessive erythropoietic protoporphyria (EPP) and X-linked protopo
151           Erythrocytes from individuals with erythropoietic protoporphyria (EPP) have low levels of t
152 Amassing of PPIX in erythroid cells promotes erythropoietic protoporphyria (EPP) in the affected fami
153                                              Erythropoietic protoporphyria (EPP) is a genetic disease
154                                              Erythropoietic protoporphyria (EPP) is a rare and underd
155                                  Importance: Erythropoietic protoporphyria (EPP) is a rare hereditary
156                                              Erythropoietic protoporphyria (EPP) is a rare inherited
157                                              Erythropoietic protoporphyria (EPP) is a rare inherited
158                                              Erythropoietic protoporphyria (EPP) is an inherited cuta
159                                              Erythropoietic protoporphyria (EPP) is an inherited cuta
160                                              Erythropoietic protoporphyria (EPP) is an inherited diso
161                                              Erythropoietic protoporphyria (EPP) is caused by a defec
162                                              Erythropoietic protoporphyria (EPP) is caused by mutatio
163                                              Erythropoietic protoporphyria (EPP) is characterized by
164                                              Erythropoietic protoporphyria (EPP) is marked by a defic
165 accumulation of protoporphyrin-IX (PP-IX) in erythropoietic protoporphyria (EPP) or X-linked-dominant
166 uppress the porphyric phenotype of mice with erythropoietic protoporphyria (EPP).
167 re a prerequisite for the inherited disorder erythropoietic protoporphyria (EPP).
168 ite of defect in the human inherited disease erythropoietic protoporphyria (EPP).
169                 Of the 102 patients (93 with erythropoietic protoporphyria and 9 with X-linked protop
170               The erythropoietic porphyrias, erythropoietic protoporphyria and congenital erythropoie
171 ion analysis was performed for families with erythropoietic protoporphyria and four novel frameshift
172                                              Erythropoietic protoporphyria and X-linked protoporphyri
173 minant fashion and that mutations underlying erythropoietic protoporphyria are heterogeneous.
174                 Here we show that late-onset erythropoietic protoporphyria can be caused by deletion
175 etic studies have shown that the majority of erythropoietic protoporphyria cases are transmitted in d
176 a, the identification of an X-linked form of erythropoietic protoporphyria due to gain-of-function mu
177                                              Erythropoietic protoporphyria is a genetic disease in wh
178                                              Erythropoietic protoporphyria is a severe photodermatosi
179                                        Human erythropoietic protoporphyria is an inherited disorder o
180 ptom-free sunlight exposure in patients with erythropoietic protoporphyria or X-linked protoporphyria
181 ated with sunlight exposure in patients with erythropoietic protoporphyria or X-linked protoporphyria
182 reduce sunlight sensitivity in patients with erythropoietic protoporphyria or X-linked protoporphyria
183                                              Erythropoietic protoporphyria patients needing LT should
184  subjects and 30 individuals with manifested erythropoietic protoporphyria with or without a known mu
185 ease, is similar to that seen in humans with erythropoietic protoporphyria, a disorder of ferrochelat
186 1 donor site in four unrelated families with erythropoietic protoporphyria, and a G(- 1)-->A substitu
187 ading to functional iron deficiency, anemia, erythropoietic protoporphyria, and a neurodegenerative m
188                       Using a mouse model of erythropoietic protoporphyria, we demonstrate here that
189 cute porphyrias are porphyria cutanea tarda, erythropoietic protoporphyria, X-linked protoporphyria,
190 e sexual desire disorder (bremelanotide) and erythropoietic protoporphyria-associated phototoxicity (
191 explain the sporadic hepatic consequences of erythropoietic protoporphyria.
192 patic injury occurring sporadically in human erythropoietic protoporphyria.
193 of the defect in the human inherited disease erythropoietic protoporphyria.
194 al disorders but multiorgan diseases such as erythropoietic protoporphyria.
195 LAS2 are a cause of sideroblastic anemia and erythropoietic protoporphyria.
196 nd improved quality of life in patients with erythropoietic protoporphyria.
197 ailure or end-stage chronic liver disease in erythropoietic protoporphyria.
198  and stem cell gene therapies for congenital erythropoietic protoporphyria.
199 n, we report novel mutations associated with erythropoietic protoporphyria: g(+ 1)-->t transversion o
200 ria; hepatoerythropoietic porphyria and both erythropoietic protoporphyrias: autosomal dominant and X
201 we show that Stat5 is essential for the high erythropoietic rate during fetal development.
202                                              Erythropoietic rate is regulated at least in part throug
203 oblast Fas and FasL, consequently increasing erythropoietic rate.
204 lasts, suppressing erythroblast survival and erythropoietic rate.
205 oid progenitors that significantly increased erythropoietic rate.
206 atocrit but are deficient in generating high erythropoietic rates in response to stress.
207                                              Erythropoietic recovery began after 14 days but was iron
208  macrophage depletion significantly impaired erythropoietic recovery from hemolytic anemia, acute blo
209 e lncRNAs is hypoxia induced kinase-mediated erythropoietic regulator (HIKER)/LINC02228, which we sho
210 n but is also required for activation of the erythropoietic regulators EKLF and GATA binding protein
211 matory inputs in a therapeutically tractable erythropoietic regulatory circuit.
212 opoietin-driven erythropoiesis and underlies erythropoietic repression in iron deficiency anemia.
213                      In the mouse spleen, an erythropoietic reserve organ, early erythroblasts were p
214 .5%) of IV iron-treated patients achieved an erythropoietic response compared with 66.9% (95% CI, 59.
215 nflammation and oxidative stress and improve erythropoietic response in prevalent MHD patients.
216         With sufficient acclimatisation, the erythropoietic response increases red cell mass such tha
217 P1 plays a critical role in the differential erythropoietic response of CMS and non-CMS subjects: we
218    IL-17 administration also accelerated the erythropoietic response of mice to hypoxia.
219               There was no difference in the erythropoietic response rate (ie, proportion of patients
220             Genetic adaptations blunting the erythropoietic response to HA exposure have been propose
221  in Himalayan natives results from a blunted erythropoietic response to hypoxia (i.e., no increase in
222 etin (Epo) is the principal regulator of the erythropoietic response to hypoxic stress, through its r
223 necessary for approximately 50% of the acute erythropoietic response to hypoxic stress.
224 iesis, the hormone erythropoietin drives the erythropoietic response to hypoxic stress.
225 ence for reticulocytes we uncover an optimal erythropoietic response which minimizes disease severity
226          We hypothesized that absence of the erythropoietic response would be associated with greater
227 ted genetically such that many display a low erythropoietic response, resulting in near sea-level hae
228 n suggests that hemolysis, and the resultant erythropoietic response, results in the up-regulation of
229 er exercise capacity in Tibetans without the erythropoietic response, supported mostly by cardiac and
230 ptional changes associated with such altered erythropoietic response, thus highlighting the importanc
231 emia, where pan-HIF-P4H inhibitors induce an erythropoietic response.
232  of inflammation and oxidative stress or the erythropoietic response.
233  with ACE-536 and EPO produced a synergistic erythropoietic response.
234 furan concentrations and did not improve the erythropoietic response.
235 sociations levels of serum trace metals with erythropoietic responses and/or hematocrit generated mix
236 transport, and (3) systemic inflammatory and erythropoietic responses.
237 hat hepcidin expression is not controlled by erythropoietic signals directly in this setting.
238 mpacts hepcidin regulation by serum iron and erythropoietic signals, and its contribution to hepcidin
239                      Erythropoietin (EPO) an erythropoietic stimulating agent also exerts effects on
240 y, and in monitoring therapeutic response to erythropoietic stimulating agents, while hyperchromic ce
241 to drive postburn ACI and prevent meaningful erythropoietic stimulation through iron or erythropoieti
242 in response to hemorrhage, hypoxia, or other erythropoietic stimuli, and it suppresses the hepatic pr
243  studies of physiological responses to other erythropoietic stimuli, erythropoietin induced erythrobl
244 le in negatively regulating inflammatory and erythropoietic stress and positively regulates the growt
245 al erythroid differentiation when persistent erythropoietic stress was applied to CRISPR-edited human
246  not confer anemia, even under conditions of erythropoietic stress, and EBI formation is normal in th
247          We examined several mouse models of erythropoietic stress, including erythrocytosis and beta
248  were normal, as was their response to acute erythropoietic stress.
249 -) mice also exhibit superior recovery after erythropoietic stress.
250 s but are unable to rapidly respond to acute erythropoietic stress.
251 d inhibition of BMP signaling in response to erythropoietic stress.
252 ression and aggravated anemia in response to erythropoietic stress.
253          In response to hemorrhage and other erythropoietic stresses, increased erythropoietin stimul
254 se include preoperative autologous donation, erythropoietic support, acute normovolemic hemodilution,
255 concentrations >12 g/dl for 4 months without erythropoietic support.
256                                   Both fetal erythropoietic suppression and haemolysis contribute to
257  restriction has been proposed as a cause of erythropoietic suppression in malarial anemia; however,
258              We then show that this in vitro erythropoietic system clearly signals exposure to genoto
259 ing cartilage, bone, muscle, kidney, and the erythropoietic system.
260 ated with renal disease and in resistance to erythropoietic therapies remains to be elucidated.
261 nd points further support equivalency of the erythropoietic therapies.
262 okines may account for hyporesponsiveness to erythropoietic therapy in patients with renal failure.
263 for patients with hemoglobin >12 g/dl and no erythropoietic therapy was lower than for the other pati
264 globin concentrations without transfusion or erythropoietic therapy.
265 ily of transporter proteins, identified from erythropoietic tissue (UT-B) and from kidney (UT-A).
266 ze Stat5 phosphorylation dynamics in primary erythropoietic tissue in vivo and in vitro, identifying
267 ite a marked compensatory expansion in their erythropoietic tissue.
268  ferrochelatase expression in iron-deficient erythropoietic tissues of mice lacking iron regulatory p
269 hropoietin and progressively enlarging their erythropoietic tissues.
270 , while the erythroid transcript was only in erythropoietic tissues.
271 yte precursors (erythroblasts) developing in erythropoietic tissues.

 
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