What's new for 'JKB_daily1' in PubMed
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Sender's message: Sepsis or genomics or altitude: JKB_daily1
Sent on Wednesday, 2013 June 05Search: (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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| PubMed Results |
| 1. | Nature. 2013 May 16;497(7449):317. doi: 10.1038/497317b.Archives: preserve our digital heritage.Milligan I.Comment on
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| PMID: 23676746 [PubMed - indexed for MEDLINE] | |
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| 2. | Nature. 2013 May 16;497(7449):297-9. doi: 10.1038/497297a.Chinese project probes the genetics of genius.Yong E. |
| PMID: 23676731 [PubMed - indexed for MEDLINE] | |
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| 3. | Nat Med. 2013 Apr;19(4):399-401. doi: 10.1038/nm.3156.Exploring the erythroblastic island.Socolovsky M. |
| PMID: 23558622 [PubMed - indexed for MEDLINE] | |
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| 4. | Nat Med. 2013 Apr;19(4):392. doi: 10.1038/nm0413-392.Natural-born scientists.Grushkin D. |
| PMID: 23558617 [PubMed - indexed for MEDLINE] | |
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| 5. | Nat Med. 2013 Apr;19(4):390-2. doi: 10.1038/nm0413-390.Natural products emergent.Grushkin D. |
| PMID: 23558616 [PubMed - indexed for MEDLINE] | |
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| 6. | Nat Med. 2013 Apr;19(4):429-36. doi: 10.1038/nm.3057. Epub 2013 Mar 17.CD169⁺ macrophages provide a niche promoting erythropoiesis under homeostasis and stress.Chow A, Huggins M, Ahmed J, Hashimoto D, Lucas D , Kunisaki Y, Pinho S, Leboeuf M, Noizat C, van Rooijen N, Tanaka M, Zhao ZJ, Bergman A, Merad M, Frenette PS.Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Albert Einstein College of Medicine, Bronx, New York, USA. Comment in
AbstractA role for macrophages in erythropoiesis was suggested several decades ago when erythroblastic islands in the bone marrow, composed of a central macrophage surrounded by developing erythroblasts, were described. However, the in vivo role of macrophages in erythropoiesis under homeostatic conditions or in disease remains unclear. We found that specific depletion of CD169(+) macrophages markedly reduced the number of erythroblasts in the bone marrow but did not result in overt anemia under homeostatic conditions, probably because of concomitant alterations in red blood cell clearance. However, CD169(+) macrophage depletion significantly impaired erythropoietic recovery from hemolytic anemia, acute blood loss and myeloablation. Furthermore, macrophage depletion normalized the erythroid compartment in a JAK2(V617F)-driven mouse model of polycythemia vera, suggesting that erythropoiesis in polycythemia vera remains under the control of macrophages in the bone marrow and splenic microenvironments. These results indicate that CD169(+) macrophages promote late erythroid maturation and that modulation of the macrophage compartment may be a new strategy to treat erythropoietic disorders. |
| PMID: 23502962 [PubMed - indexed for MEDLINE] | |
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| 7. | Nat Med. 2013 Apr;19(4):437-45. doi: 10.1038/nm.3126. Epub 2013 Mar 17.Macrophages support pathological erythropoiesis in polycythemia vera and β-thalassemia.Ramos P, Casu C, Gardenghi S, Breda L, Crielaard BJ, Guy E, Marongiu MF, Gupta R, Levine RL, Abdel-Wahab O, Ebert BL, Van Rooijen N, Ghaffari S, Grady RW, Giardina PJ, Rivella S.Department of Pediatrics, Division of Hematology-Oncology, Weill Cornell Medical College, New York, New York, USA. Comment in
AbstractRegulation of erythropoiesis is achieved by the integration of distinct signals. Among them, macrophages are emerging as erythropoietin-complementary regulators of erythroid development, particularly under stress conditions. We investigated the contribution of macrophages to physiological and pathological conditions of enhanced erythropoiesis. We used mouse models of induced anemia, polycythemia vera and β-thalassemia in which macrophages were chemically depleted. Our data indicate that macrophages contribute decisively to recovery from induced anemia, as well as the pathological progression of polycythemia vera and β-thalassemia, by modulating erythroid proliferation and differentiation. We validated these observations in primary human cultures, showing a direct impact of macrophages on the proliferation and enucleation of erythroblasts from healthy individuals and patients with polycythemia vera or β-thalassemia. The contribution of macrophages to stress and pathological erythropoiesis, which we have termed stress erythropoiesis macrophage-supporting activity, may have therapeutic implications. |
| PMID: 23502961 [PubMed - indexed for MEDLINE] | |
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