Relevant bibliographies by topics / Erythropoietin

Academic literature on the topic 'Erythropoietin'

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Published: 4 June 2021
Last updated: 28 July 2024

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Journal articles on the topic "Erythropoietin"

1

Rivera, Seth, Mihwa Pak, Miguel A. Lopez, Victoria Gabayan, and Tomas Ganz. "Hepcidin Suppression Following Phlebotomy Is Regulated by an Erythropoietic Regulator Found in Serum." Blood 108, no. 11 (November 16, 2006): 1554. http://dx.doi.org/10.1182/blood.v108.11.1554.1554.

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Abstract Increasing erythropoiesis requires a dramatic increase in iron absorption or the release of iron from tissue stores. Since the iron regulatory hormone hepcidin blocks both absorption and release from stores, it is suppressed during erythropoiesis. We have recently shown that hepcidin is primarily suppressed by an erythropoietic regulator rather then anemia, hypoxia, or erythropoietin (Pak et al, Blood, epub/in press). To further understand the regulation of hepcidin during erythropoiesis, we subjected groups of eight mice to phlebotomy and sacrificed them at various time points over 3 weeks. Hepcidin mRNA fell 25-fold by day 2 (p<0.001) and did not begin to rise until day 9. Hemoglobin rose well before hepcidin mRNA began to increase confirming that anemia was not the erythropoietic regulator. Serum iron never fell, excluding this as the erythropoietic regulator. Erythropoietin levels spiked early but returned to normal well before hepcidin. Reticulocyte counts increased shortly after the fall in hepcidin and remained elevated after hepcidin mRNA returned to normal. We therefore postulate that the erythropoietic iron regulator is either made by or in concert with early erythroid progenitor cells. Using primary hepatocytes treated with serum from erythropoietin stimulated or control mice, we also demonstrate that the erythropoietic regulator of hepcidin expression is present in the circulation. Experiments are underway to isolate the erythropoietic regulator of hepcidin from serum.
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Zangari, Maurizio, Federica Cavallo, Keshava Prasad, Louis Fink, Sharon Coon, Bart Barlogie, and Guido Tricot. "Erythropoietin Therapy and Venous Thromboembolic Events in Patients with Multiple Myeloma Receiving Chemotherapy with or without Thalidomide." Blood 108, no. 11 (November 16, 2006): 3572. http://dx.doi.org/10.1182/blood.v108.11.3572.3572.

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Abstract Background: The association between the use of recombinant human erythropoietin (rHUEPO) and venous thromboembolic events (VTE) has been described in cancer patients treated with chemotherapy. A higher risk of VTE has also been observed with the concurrent use of erythropoiesis-stimulating agents and chemotherapy. Methods: We retrospectively analyzed VTE incidence and concurrent use of erythropoiesis-stimulating agents in patients with multiple myeloma (MM) enrolled in our Total Therapy 2 (TT2) study. TT2 included 4 monthly cycles of induction chemotherapy followed by tandem transplant. Patients were randomly assigned to receive Thalidomide or not during the whole treatment. Both arms otherwise received identical chemotherapy. Results: The charts of 599 of a total of 668 patients enrolled (90%) were reviewed; 284 patients received Thalidomide, 315 did not. With median age was 57 years, 59% were male, 24% had IgA myeloma. 62% of patients received erythropoietin (erythropoietin alpha 40000 U SQ/week) during the first 4 months of treatment. In thalidomide treated patients, VTE occurred in 33 out of 166 (20%) patients who concomitantly received administration of erythropoietic agents and in 38 out of 118 (32%) patients who did not receive erythropoietin (p=.025). Among patients not receiving thalidomide, VTE occurred in 18 out of 203 (8%) patients who received concomitant administration of erythropoietic agents and in 17 out of 112 (15%) patients who did not receive erythropoietin (p=.10). Conclusions: The development of thrombosis in patients enrolled on TTII protocol was not increased by the concomitant use of erythropoiesis-stimulating agents and thalidomide. Similarly, erythropoiesis-stimulating therapy did not affect VTE incidence in newly diagnosed myeloma patients treated with intensive chemotherapy without thalidomide.
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Pak, Mihwa, Miguel A. Lopez, Victroia Gabayan, Tomas Ganz, and Seth Rivera. "Suppression of hepcidin during anemia requires erythropoietic activity." Blood 108, no. 12 (December 1, 2006): 3730–35. http://dx.doi.org/10.1182/blood-2006-06-028787.

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AbstractHepcidin, the principal iron regulatory hormone, regulates the absorption of iron from the diet and the mobilization of iron from stores. Previous studies indicated that hepcidin is suppressed during anemia, a response that would appropriately increase the absorption of iron and its release from stores. Indeed, in the mouse model, hepcidin-1 was suppressed after phlebotomy or erythropoietin administration but the suppression was reversed by inhibitors of erythropoiesis. The suppression of hepcidin necessary to match iron supply to erythropoietic demand thus requires increased erythropoiesis and is not directly mediated by anemia, tissue hypoxia, or erythropoietin.
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Verhoef, Hans, Clive E. West, Rob Kraaijenhagen, Silas M. Nzyuko, Rose King, Mary M. Mbandi, Susanne van Laatum, Roos Hogervorst, Carla Schep, and Frans J. Kok. "Malarial anemia leads to adequately increased erythropoiesis in asymptomatic Kenyan children." Blood 100, no. 10 (November 15, 2002): 3489–94. http://dx.doi.org/10.1182/blood-2001-12-0228.

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Malarial anemia is associated with a shift in iron distribution from functional to storage compartments. This suggests a relative deficit in erythropoietin production or action similar to that observed in other infections. Our study in Kenyan children with asymptomatic malaria aimed at investigating whether malaria causes increased erythropoiesis, and whether the erythropoietic response appeared appropriate for the degree of resulting anemia. Longitudinal and baseline data were used from a trial with a 2 × 2 factorial design, in which 328 anemic Kenyan children were randomly assigned to receive either iron or placebo, and sulfadoxine-pyrimethamine or placebo. Erythropoiesis was evaluated by serum concentrations of erythropoietin and soluble transferrin receptor. Prospectively collected data showed that malarial infection resulted in decreased hemoglobin concentrations, and increased serum concentrations of erythropoietin and transferrin receptor. Conversely, disappearance of malarial antigenemia resulted in increased hemoglobin concentrations, and decreased concentrations of these serum indicators. Additionally, our baseline data showed that current or recent malarial infection is associated with increased serum concentrations of erythropoietin and transferrin receptor, and that these were as high as or perhaps even higher than values of children without malarial infection and without inflammation. Our findings indicate that in asymptomatic malaria, the erythropoietic response is adequate for the degree of anemia, and that inflammation probably plays no or only a minor role in the pathogenesis of the resulting anemia. Further research is needed to demonstrate the role of deficient erythropoietin production or action in the pathogenesis of the anemia of symptomatic malaria.
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Dumitriu, Bogdan, Michael R. Patrick, Jane P. Petschek, Srujana Cherukuri, Ursula Klingmuller, Paul L. Fox, and Véronique Lefebvre. "Sox6 cell-autonomously stimulates erythroid cell survival, proliferation, and terminal maturation and is thereby an important enhancer of definitive erythropoiesis during mouse development." Blood 108, no. 4 (August 15, 2006): 1198–207. http://dx.doi.org/10.1182/blood-2006-02-004184.

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Abstract Erythropoiesis, the essential process of hematopoietic stem cell development into erythrocytes, is controlled by lineage-specific transcription factors that determine cell fate and differentiation and by the hormone erythropoietin that stimulates cell survival and proliferation. Here we identify the Sry-related high-mobility-group (HMG) box transcription factor Sox6 as an important enhancer of definitive erythropoiesis. Sox6 is highly expressed in proerythroblasts and erythroblasts in the fetal liver, neonatal spleen, and bone marrow. Mouse fetuses and pups lacking Sox6 develop erythroid cells slowly and feature misshapen, short-lived erythrocytes. They compensate for anemia by elevating the serum level of erythropoietin and progressively enlarging their erythropoietic tissues. Erythroid-specific inactivation of Sox6 causes the same phenotype, demonstrating cell-autonomous roles for Sox6 in erythroid cells. Sox6 potentiates the ability of erythropoietin signaling to promote proerythroblast survival and has an effect additive to that of erythropoietin in stimulating proerythroblast and erythroblast proliferation. Sox6 also critically facilitates erythroblast and reticulocyte maturation, including hemoglobinization, cell condensation, and enucleation, and ensures erythrocyte cytoskeleton long-term stability. It does not control adult globin and erythrocyte cytoskeleton genes but acts by stabilizing filamentous actin (F-actin) levels. Sox6 thus enhances erythroid cell development at multiple levels and thereby ensures adequate production and quality of red blood cells.
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Yu, Xiaobing, Chyuan-Sheng Lin, Frank Costantini, and Constance Tom Noguchi. "The human erythropoietin receptor gene rescues erythropoiesis and developmental defects in the erythropoietin receptor null mouse." Blood 98, no. 2 (July 15, 2001): 475–77. http://dx.doi.org/10.1182/blood.v98.2.475.

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Erythropoietin and its receptor are required for definitive erythropoiesis and maturation of erythroid progenitor cells. Mice lacking the erythropoietin receptor exhibit severe anemia and die at about embryonic day 13.5. This phenotype can be rescued by the human erythropoietin receptor transgene. Animals expressing only the human erythropoietin receptor survived through adulthood with normal hematologic parameters and appeared to respond appropriately to induced anemic stress. In addition to restoration of erythropoiesis during development, the cardiac defect associated with embryos lacking the erythropoietin receptor was corrected and the increased apoptosis in fetal liver, heart, and brain in the erythropoietin receptor null phenotype was markedly reduced. These studies indicate that no species barrier exists between mouse and human erythropoietin receptor and that the human erythropoietin receptor transgene is able to provide specific expression in hematopoietic and other selected tissues to rescue erythropoiesis and other organ defects observed in the erythropoietin receptor null mouse.
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Maekawa, Shun, and Takashi Kato. "Diverse of Erythropoiesis Responding to Hypoxia and Low Environmental Temperature in Vertebrates." BioMed Research International 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/747052.

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Erythrocytes are responsible for transporting oxygen to tissue and are essential for the survival of almost all vertebrate animals. Circulating erythrocyte counts are tightly regulated and respond to erythrocyte mass and oxygen tension. Since the discovery of erythropoietin, the erythropoietic responses to environment and tissue oxygen tension have been investigated in mice and human. Moreover, it has recently become increasingly clear that various environmental stresses could induce the erythropoiesis via various modulating systems, while all vertebrates live in various environments and habitually adapt to environmental stress. Therefore, it is considered that investigations of erythropoiesis in vertebrates provide a lead to the various erythropoietic responses to environmental stress. This paper comparatively introduces the present understanding of erythropoiesis in vertebrates. Indeed, there is a wide range of variations in vertebrates’ erythropoiesis. This paper also focused on erythropoietic responses to environmental stress, hypoxia, and lowered temperature in vertebrates.
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Baynes, RD, GK Reddy, YJ Shih, BS Skikne, and JD Cook. "Serum form of the erythropoietin receptor identified by a sequence- specific peptide antibody [see comments]." Blood 82, no. 7 (October 1, 1993): 2088–95. http://dx.doi.org/10.1182/blood.v82.7.2088.2088.

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Abstract The present investigation was undertaken to search for soluble forms of the erythropoietin receptor in human serum using polyclonal antibody against an amino terminal peptide sequence in the extracellular domain. This sequence was located adjacent to the amino terminus at residues 25- 38. When this antibody was used for Western blots of solubilized membranes from nucleated bone marrow cells, a protein consistent with native erythropoietin receptor was seen. Purified soluble ectodomain of the erythropoietin receptor displayed appropriate reactivity with this antibody. When sera from normal subjects and patients with a range of hematologic disorders were examined by Western blotting, a protein with a molecular mass of 34 Kd was detected in sera from patients with enhanced erythropoiesis including sickle cell anemia, thalassemia, and megaloblastic anemia. This protein was rarely detected in normal serum but appeared when normal subjects were treated with recombinant erythropoietin and disappeared after full treatment of patients with megaloblastic anemia due to vitamin B12 deficiency. The protein was not detected after myeloablation for bone marrow transplantation but appeared with marrow engraftment. Reactivity of this protein with the peptide antibody was competitively inhibited by the amino terminal peptide sequence. An additional 48 Kd protein was detected that showed minimal variation in intensity with differing degrees of erythropoietic activity. Detection of this protein could not be inhibited by the addition of synthetic peptide. Our findings indicate the presence of a soluble form of the erythropoietin receptor related to the extracellular domain that is highly correlated with enhanced erythropoiesis.
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Baynes, RD, GK Reddy, YJ Shih, BS Skikne, and JD Cook. "Serum form of the erythropoietin receptor identified by a sequence- specific peptide antibody [see comments]." Blood 82, no. 7 (October 1, 1993): 2088–95. http://dx.doi.org/10.1182/blood.v82.7.2088.bloodjournal8272088.

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The present investigation was undertaken to search for soluble forms of the erythropoietin receptor in human serum using polyclonal antibody against an amino terminal peptide sequence in the extracellular domain. This sequence was located adjacent to the amino terminus at residues 25- 38. When this antibody was used for Western blots of solubilized membranes from nucleated bone marrow cells, a protein consistent with native erythropoietin receptor was seen. Purified soluble ectodomain of the erythropoietin receptor displayed appropriate reactivity with this antibody. When sera from normal subjects and patients with a range of hematologic disorders were examined by Western blotting, a protein with a molecular mass of 34 Kd was detected in sera from patients with enhanced erythropoiesis including sickle cell anemia, thalassemia, and megaloblastic anemia. This protein was rarely detected in normal serum but appeared when normal subjects were treated with recombinant erythropoietin and disappeared after full treatment of patients with megaloblastic anemia due to vitamin B12 deficiency. The protein was not detected after myeloablation for bone marrow transplantation but appeared with marrow engraftment. Reactivity of this protein with the peptide antibody was competitively inhibited by the amino terminal peptide sequence. An additional 48 Kd protein was detected that showed minimal variation in intensity with differing degrees of erythropoietic activity. Detection of this protein could not be inhibited by the addition of synthetic peptide. Our findings indicate the presence of a soluble form of the erythropoietin receptor related to the extracellular domain that is highly correlated with enhanced erythropoiesis.
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Hankins, WD, J. Schooley, and C. Eastment. "Erythropoietin, an autocrine regulator? Serum-free production of erythropoietin by cloned erythroid cell lines." Blood 68, no. 1 (July 1, 1986): 263–68. http://dx.doi.org/10.1182/blood.v68.1.263.263.

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Abstract Production of lymphoid and myeloid growth regulatory factors by hematopoietic cells is well documented. On the other hand, the major site of production of erythropoietin (Epo), which regulates physiologic red blood cell development, is thought to be the kidney. Here we report the isolation of multiple erythroleukemia cell lines that produce erythropoietic factors and present extensive biological, immunologic, and biochemical evidence to document that the active agent is Epo. The erythropoietic activity was neutralized by Epo antiserum and exhibited physical properties indistinguishable from those of human and sheep Epo. Positive lines produced between 0.1 and 1.5 U/mL of Epo, which stimulated erythropoiesis in vivo and in vitro in nine biological assays. Twenty sublines derived from single cells were inducible for hemoglobin and spectrin synthesis. All the sublines produced Epo. Production of the hormone continued when the cells were seeded in the absence of serum. Our finding that multiple independent isolates produce Epo raises the possibility that Epo production by erythroid precursors may play a role in normal erythropoiesis or, alternatively, that Epo gene activation may be a relatively common occurrence that contributes to, or is associated with, certain forms of virus-induced leukemias.
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Dissertations / Theses on the topic "Erythropoietin"

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Leng, Henry Martin John. "The biogenesis of erythropoietin during inflammation." Doctoral thesis, University of Cape Town, 1995. http://hdl.handle.net/11427/27051.

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Anaemia frequently accompanies chronic inflammatory diseases like rheumatoid arthritis and cancer. It is postulated to result primarily from the suppression of erythropoiesis by inflammatory cytokines. A contributing factor could be the inhibition of erythropoietin synthesis which may also be mediated by cytokines. Erythropoietin is the hormone which regulates erythropoiesis. The aims of this project were to investigate whether cytokines can indeed suppress erythropoietin production, and to determine whether the erythropoietin response in experimental models of acute and chronic inflammation was appropriate for the associated anaemia. Macrophage-conditioned medium, interleukin-1β, interleukin-6, tumour necrosis factor-α, and neopterin were assayed for inhibition of erythropoietin synthesis by HepG2 cells in culture. All, except neopterin, effected dose-dependent reductions in the secretion of the hormone. Interleukin-1β and tumour necrosis factor-α down-regulated erythropoietin gene transcription, whereas interleukin-6 inhibited a post-transcriptional process. Rats with acute inflammation developed a mild anaemia which evoked an increase in their serum levels of erythropoietin. The serum erythropoietin levels were optimal, since rats with acute inflammation and severe phenylhydrazine-induced anaemia did not have lower levels of the hormone than controls with a similar degree of anaemia, but without acute inflammation. Erythropoietin is, therefore, not an acute phase reactant. Mice with cancer developed a progressive anaemia which was not due to bone marrow invasion by tumour cells. During the first fourteen days after inoculating them with cancer cells, the mice responded by increasing their serum levels of erythropoietin as the anaemia worsened. The erythropoietin response was appropriate when compared to mice with the same degree of phenylhydrazine-induced anaemia. Erythropoietin levels measured in mice with tumours older than fourteen days were significantly lower than those of control mice with the same degree of experimental anaemia. These animals were very cachectic, suggesting that a blunted erythropoietin response may depend on disease activity.
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Afrasiabi, Morteza. "Biochemical studies of erythropoietin and erythropoietin receptors." Thesis, Queen's University Belfast, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334533.

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McNamee, P. T. "A study of erythropoietin and factors regulating erythropoiesis in chronic renal failure." Thesis, Queen's University Belfast, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374226.

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Cervellini, Ilaria. "Neuroprotection by erythropoietin." Thesis, University of Brighton, 2012. https://research.brighton.ac.uk/en/studentTheses/1075c7e4-6f7d-4f53-b83e-42671edac8ca.

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Erythropoietin (EPO) is an erythropoietic cytokine that is also neuroprotective in vitro and in vivo. Neither the mechanism of action of EPO in neuroprotectio, nor the receptor involved is completely known. In fact, EPO regulates erythropoiesis by the homodimeric EPO receptor (EPOR)2. Variants of EPO, not binding (EPOR)2, are still neuroprotective, therefore another receptor may mediate this effect. In vivo, EPO is anti-inflammatory in several models of disease but, to date, a direct anti- inflammatory effect in vitro has not been clearly found. The focus of this thesis work was a twofold. Firstly, a direct anti-inflammatory effect of EPO was investigated in vitro. It was confirmed that EPO did not have any effect on production of cytokines induced by LPS. In addition, EPO did not reduce cytokines induced by alarmins and other inflammatory stimuli. EPO did not inhibit the pro-inflammatory receptor TREM-1. Finally, EPO did not act as anti-inflammatory by mobilization of endothelial precursor cells in vivo. The second focus of this thesis work was the study of a possible role of EPO on myelination by analysing the induction of myelin genes during differentiation of an oligodendrocyte cell line. EPO upregulated myelin gene expression (MaG and MBP), as studied by qPCR and Western Blot. EPOR was required for the effect of EPO, observed only in cells overexpressing EPOR. EPO induced high levels of the early growth response gene EGR2 that was however not involved in myelin gene induction. Finally, EPO was unable to induce myelin genes in an in vivo model of demyelination induced by cuprizone, neither at the peak of demyelination (3 and 5 weeks) nor during the recovery phase. Greater understanding of effects and mechanisms of action of EPO in the CNS would be useful to find new therapies promoting repair, for instance in diseases like MS in which no drug is available for that purpose.
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Krosl, Jana. "The role of erythropoietin and erythropoietin receptor in regulation of hemopoiesis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq25081.pdf.

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Zhang, Yingxin. "Symmetric signaling by an asymmetric 1 erythropoietin : 2 erythropoietin receptor complex." Thesis, Massachusetts Institute of Technology, 2008. http://hdl.handle.net/1721.1/45211.

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Thesis (M. Eng.)--Massachusetts Institute of Technology, Biological Engineering Division, 2008.
Includes bibliographical references (p. 43-46).
One erythropoietin molecule binds asymmetrically to two identical receptor monomers via erythropoietin site 1 and site 2, although it is unclear how asymmetry affects receptor activation and signaling. Here we report the computational design and experimental validation of two mutant erythropoietin receptors: one that binds only to erythropoietin site 1 but not site 2, and one that binds only to site 2 but not site 1. Expression of either mutant receptor alone in Ba/F3 cells cannot elicit a signal in response to erythropoietin, but when co-expressed, there is a proliferative response and activation of the JAK2 Stat5 signaling pathway. A truncated erythropoietin receptor with only one cytosolic tyrosine (Y343), on only one receptor monomer is sufficient for signaling in response to erythropoietin, regardless of the monomer on which it is located. The same results apply to having only one conserved juxtamembrane hydrophobic L253 or W258 residue, essential for JAK2 activation, in the full-length receptor dimer. We conclude that despite asymmetry in the ligand-receptor dimer interaction, both sides are competent for signaling, and we suggest that the receptors signal equally.
by Yingxin Zhang.
M.Eng.
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Yu, S. R. "Cytoprotective mechanisms of erythropoietin and erythropoietin derivatives in peripheral arterial disease." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1458006/.

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A third of patients with critical limb ischaemia (CLI) eventually require amputation. Inconsistencies between successful revascularisation and functional outcomes exist, and underlying musculopathy in CLI patients has been identified. Erythropoietin (EPO) has tissue-protective effects in response to ischaemic injury, but its clinical use is often precluded by thromboembolic side effects. Non-haematopoietic EPO-derivatives have been designed to retain only tissueprotective functions of EPO. We hypothesised that ARA-290 (EPO-derivative) may have tissue-protective potential that could represent a novel therapeutic adjunct in patients with CLI. The effect of EPO and ARA-290 in mediating cytoprotection in an in vitro simulated ischaemia model of skeletal muscle was assessed firstly in the immortalised murine C2C12 myoblast cell line and subsequently in skeletal myoblasts isolated from CLI and control donors. In human and murine cells, simulated ischaemia alone demonstrated a detrimental effect on cell function and survival. Addition of EPO or ARA-290 demonstrated significant improvements in function and survival and utilised JAK2/STAT3, PI3k/Akt and NF!B signalling molecules. Isolation of human skeletal myoblasts from CLI patients has not previously been described. Comparison of CLI and control myoblasts elucidated significant differences in their function and survival under both normoxic and simulated ischaemic conditions. CLI myoblasts and myotubes exhibited increased proliferative capacity but reduced migratory and contractile function and importantly a reduced susceptibility to a second ischaemic-insult compared with control myoblasts and myotubes. Evaluation of several variations in the hindlimb ischaemia model allowed the creation of a model which closely recapitulated the muscular pathology observed in human CLI patients. ARA-290 demonstrated improved functional, histological and perfusion outcomes compared to EPO or vehicle-control treated animals. These studies demonstrate the potential of ARA-290 to protect tissues and cells from ischaemic-injury and encourages the development of novel pharmacological therapies for use in patients with “no option” CLI or severe functional deficit.
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Chang, Kai-Hsin 1974. "Erythropoietin, erythropoiesis, and malarial anemia : the mechanisms and implications of insufficient erythropoiesis during murine blood-stage malaria." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84490.

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Severe anemia is a major life-threatening complication of malaria. Inappropriately low reticulocytosis in malaria patients with anemia suggests insufficient erythropoiesis, of which the mechanisms and implications are not clear. The principle growth factor that promotes erythropoiesis is erythropoietin (Epo). Studies determining the serum level of Epo in malaria infected patients have been inconclusive. Furthermore, the role of Epo and the erythropoietic response to Epo stimulation during malaria have never been examined. The purpose of the experiments performed in this thesis was, thus, to investigate the role of Epo and erythropoiesis in relation to anemia during blood-stage malaria using the murine model of Plasmodium chabaudi AS. A murine Epo specific ELISA, which was determined to be less biased by the presence of other cytokines in the samples as compared to the conventional Epo bioassay, was first developed to facilitate the research. The kinetics of Epo production in the kidney and the levels in the serum were characterized. It was demonstrated that Epo production during blood-stage malaria is mainly regulated by the degree of anemia and that renal cytokines may have only a minor effect on this response. Next, the roles of Epo and erythropoiesis during blood-stage malaria were investigated by neutralization of endogenous Epo or by administration of exogenous Epo. Timely onset of Epo-induced reticulocytosis was shown to be important for the alleviation of malarial anemia and survival. However, reticulocytosis in response to Epo stimulation is severely suppressed by infection with malaria. Dissection of the upstream events of erythropoiesis demonstrated that blood-stage malaria compromises the generation of reticulocytes by suppressing the proliferation, differentiation, and maturation of erythroid-lineage cells at various stages of erythroid development. Taken together, our data provide important insights for understanding the patho
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Rolfes, Simone [Verfasser]. "Einfluss von Erythropoietin und Erythropoietin-Isoformen auf die murine Neurogenese / Simone Rolfes." Berlin : Freie Universität Berlin, 2016. http://d-nb.info/108193543X/34.

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Barbeau, Paule. "Markers of the erythropoietin, erythropoietin receptor and RAD genes and cardiorespiratory endurance." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq25376.pdf.

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Books on the topic "Erythropoietin"

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Erythropoietins, erythropoietic factors, and erythropoiesis: Molecular, cellular, preclinical, and clinical biology. 2nd ed. Basel: Birkhäuser, 2009.

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Elliott, Steven G., Mary Ann Foote, and Graham Molineux, eds. Erythropoietins, Erythropoietic Factors, and Erythropoiesis. Basel: Birkhäuser Basel, 2009. http://dx.doi.org/10.1007/978-3-7643-8698-6.

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Jelkmann, Wolfgang, and Andreas J. Gross, eds. Erythropoietin. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83745-6.

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1949-, Jelkmann Wolfgang, and Gross Andreas J. 1958-, eds. Erythropoietin. Berlin: Springer-Verlag, 1989.

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Pavlov, A. D. Reguli͡a︡t͡s︡ii͡a︡ ėritropoėza: Fiziologicheskie i klinicheskie aspekty. Moskva: Medit͡s︡ina, 1987.

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Rich, Ivan N., ed. Molecular and Cellular Aspects of Erythropoietin and Erythropoiesis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72652-1.

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NATO Advanced Research Workshop on Molecular and Cellular Aspects of Erythropoiesis (1986 Bad Windsheim, Germany). Molecular and cellular aspects of erythropoietin and erythropoiesis. Berlin: Springer-Verlag, 1987.

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M, Schaefer R., Heidland August, and Hörl Walter H, eds. Erythropoietin in the 90s. Basel: Karger, 1990.

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Symposium, on Molecular Biology of Hemopoiesis (4th 1988 Reno Nev ). Molecular biology of erythropoiesis. New York: Plenum Press, 1989.

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Molineux, Graham, Mary Ann Foote, and Steven G. Elliott, eds. Erythropoietins and Erythropoiesis. Basel: Birkhäuser Basel, 2006. http://dx.doi.org/10.1007/3-7643-7543-4.

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Book chapters on the topic "Erythropoietin"

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Molineux, Graham, and Angus M. Sinclair. "Biology of erythropoietin." In Erythropoietins, Erythropoietic Factors, and Erythropoiesis, 41–60. Basel: Birkhäuser Basel, 2009. http://dx.doi.org/10.1007/978-3-7643-8698-6_3.

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Constantinescu, Stefan N. "Mechanism of erythropoietin receptor activation." In Erythropoietins, Erythropoietic Factors, and Erythropoiesis, 175–96. Basel: Birkhäuser Basel, 2009. http://dx.doi.org/10.1007/978-3-7643-8698-6_11.

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Mole, David R., and Peter J. Ratcliffe. "Regulation of endogenous erythropoietin production." In Erythropoietins, Erythropoietic Factors, and Erythropoiesis, 19–40. Basel: Birkhäuser Basel, 2009. http://dx.doi.org/10.1007/978-3-7643-8698-6_2.

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Lodish, Harvey F., Saghi Ghaffari, Merav Socolovsky, Wei Tong, and Jing Zhang. "Intracellular signaling by the erythropoietin receptor." In Erythropoietins, Erythropoietic Factors, and Erythropoiesis, 155–74. Basel: Birkhäuser Basel, 2009. http://dx.doi.org/10.1007/978-3-7643-8698-6_10.

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Osslund, Timothy D. "Structural basis for the signal transduction of erythropoietin." In Erythropoietins, Erythropoietic Factors, and Erythropoiesis, 143–53. Basel: Birkhäuser Basel, 2009. http://dx.doi.org/10.1007/978-3-7643-8698-6_9.

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Foote, Mary Ann. "Studies of erythropoiesis and the discovery and cloning of recombinant human erythropoietin." In Erythropoietins, Erythropoietic Factors, and Erythropoiesis, 77–85. Basel: Birkhäuser Basel, 2009. http://dx.doi.org/10.1007/978-3-7643-8698-6_5.

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Jelkmann, W., and A. J. Gross. "Introduction: Advances in Erythropoietin Research." In Erythropoietin, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83745-6_1.

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Grützmacher, P., and W. Schoeppe. "Renal Artery Stenosis and Renal Polyglobulia." In Erythropoietin, 111–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83745-6_10.

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Stockenhuber, F., K. Geissler, W. Hinterberger, and P. Balcke. "Erythrocytosis in Renal Graft Recipients." In Erythropoietin, 122–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83745-6_11.

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Battersby, R. V., and C. J. Holloway. "Recombinant Human Erythropoietin." In Erythropoietin, 133–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83745-6_12.

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Conference papers on the topic "Erythropoietin"

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Glukhova, Olga Yurievna. "Erythropoietin as a neuroprotector." In IX International Research-to-practice conference. TSNS Interaktiv Plus, 2016. http://dx.doi.org/10.21661/r-113774.

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Farha, S., K. Asosingh, J. Sharp, D. George, MA Aldred, R. Steinle, E. Hsi, et al. "Erythropoietin: Biomarker of Pulmonary Hypertension." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2662.

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Mora, Edna M., Chad V. Pecot, Alpa M. Nick, Lingegowda S. Mangala, Hee Dong Han, Martin A. Stein, Stephan Brock, et al. "Abstract 1618: Erythropoietin meets a new receptor." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1618.

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Petropoulos, Ioannis, Michael Brines, Ann Dunne, Monique Van Velzen, Paolo Proto, Claes-goren Ostenson, Rita Kirk, Albert Dahan, Anthony Cerami, and Rayaz Ahmed Malik. "Safety And Efficacy Of Ara 290, A Non-erythropoietic Peptide Engineered From Erythropoietin, In Patients With Painful Diabetic Neuropathy." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2014. http://dx.doi.org/10.5339/qfarc.2014.hbpp0801.

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Dyer, Edward, Philipp A. Pickerodt, Rachel Zarndt, and Erik R. Swenson. "ERYTHROPOIETIN MITIGATES VENTILATOR-INDUCED LUNG INJURY IN RATS." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1684.

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Kessler, U., S. Woelfer, N. Kukoc-Zivojnov, JP Kaltwasser, and B. Moeller. "FRI0033 Erythropoietin-receptor-expression in fibroblast-like synoviocytes." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.1162.

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Patel, Purvesh, Ali Sadoughi, Rebecca Miller, Rammohan Gumpeni, Nina Kohn, Mark Rosen, and Arunabh Talwar. "Erythropoietin Levels In Patients With Interstitial Lung Disease." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4382.

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Wenzel, F., M. Hauser, L. Saemann, and L. Toll. "Erythropoietin and thrombopoietin release kinetics in clinical settings." In GTH Congress 2024 – 68th Annual Meeting of the Society of Thrombosis and Haemostasis Research – Building Bridges in Coagulation. Georg Thieme Verlag, 2024. http://dx.doi.org/10.1055/s-0044-1779234.

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Ghanbari, Elmira, Atefeh Solouk, Rouhollah Mehdinavaz Aghdam, Masoumeh Haghbin Nazarpak, Seyed Hossein, and Ahmadi Tafti. "Erythropoietin-Loaded Nanofibrous Patch for Regeneration of Infarcted Myocardium." In 2017 24th National and 2nd International Iranian Conference on Biomedical Engineering (ICBME). IEEE, 2017. http://dx.doi.org/10.1109/icbme.2017.8430247.

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Khovaeva, Yaroslava, Dmitrii Sosnin, Tatyana Syromyatnikova, Larisa Ermachkova, Anna Podyanova, and Olga Nenasheva. "Erythropoietin in chronic obstructive pulmonary disease patients without anemia." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2583.

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Reports on the topic "Erythropoietin"

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Eliopoulos, Nicoletta. Soluble Erythropoietin Receptor for Gene Therapy of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada434585.

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Sytkowski, Arthur J. Functional Erythropoietin Receptors Expressed by Human Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, October 2006. http://dx.doi.org/10.21236/ada471524.

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Crowley, James P., Joseph A. Chazan, Jaclyn B. Metzger, Lucille Pono, and C. R. Valeri. Erythropoietin in Renal Failure: Blood Rheology and 2,3-DPG Levels. Fort Belvoir, VA: Defense Technical Information Center, December 1992. http://dx.doi.org/10.21236/ada360149.

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Feldman, Laurie. The Significance of Erythropoietin Receptor (EpoR) Acquisition by Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, November 2006. http://dx.doi.org/10.21236/ada459145.

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dong, bixuan, Xiaowei Fan, and Bin Li. Association between Erythropoietin Polymorphisms and Diabetic Retinopathy Risk: A Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2024. http://dx.doi.org/10.37766/inplasy2024.5.0130.

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Chuanhui, Dou. Erythropoietin combined with TCM for Chemotherapy-Induced Anemias: a protocol of systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2020. http://dx.doi.org/10.37766/inplasy2020.8.0041.

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Dou, Chuanhui. Erythropoietin for chemotherapy induced anaemia in patients with solid tumours: a protocol of systematic review and meta analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2020. http://dx.doi.org/10.37766/inplasy2020.6.0098.

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