What's new for 'JKB_daily1' in PubMed

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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Thursday, 2013 December 19
Search: (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

Items 1 - 8 of 8

1.	Science. 2013 Nov 29;342(6162):1059. doi: 10.1126/science.1248055. Retrospective. Fred Sherman (1932-2013). Liebman SW, Haber JE. Author information: University of Illinois at Chicago, Chicago, IL, USA.
	PMID: 24288325 [PubMed - indexed for MEDLINE]
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2.	Science. 2013 Nov 29;342(6162):1057-8. doi: 10.1126/science.1247023. Microbiology. Genomes from metagenomics. Sharon I, Banfield JF. Author information: Department of Earth and Planetary Science, University of California, Berkeley, CA 94720, USA.
	PMID: 24288324 [PubMed - indexed for MEDLINE]
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3.	Science. 2013 Nov 22;342(6161):1242974. doi: 10.1126/science.1242974. Beyond stem cells: self-renewal of differentiated macrophages. Sieweke MH, Allen JE. Author information: Centre d'Immunologie de Marseille-Luminy (CIML), Aix-Marseille Université, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. Abstract In many mammalian tissues, mature differentiated cells are replaced by self-renewing stem cells, either continuously during homeostasis or in response to challenge and injury. For example, hematopoietic stem cells generate all mature blood cells, including monocytes, which have long been thought to be the major source of tissue macrophages. Recently, however, major macrophage populations were found to be derived from embryonic progenitors and to renew independently of hematopoietic stem cells. This process may not require progenitors, as mature macrophages can proliferate in response to specific stimuli indefinitely and without transformation or loss of functional differentiation. These findings suggest that macrophages are mature differentiated cells that may have a self-renewal potential similar to that of stem cells.
	PMID: 24264994 [PubMed - indexed for MEDLINE]
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4.	Nature. 2013 Nov 7;503(7474):18-9. doi: 10.1038/503018a. Proteins help solve taxonomy riddle. Callaway E.
	PMID: 24201261 [PubMed - indexed for MEDLINE]
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5.	J Exp Med. 2013 Oct 21;210(11):2477-91. doi: 10.1084/jem.20121999. Epub 2013 Oct 7. IL-4 directly signals tissue-resident macrophages to proliferate beyond homeostatic levels controlled by CSF-1. Jenkins SJ, Ruckerl D, Thomas GD, Hewitson JP, Duncan S, Brombacher F, Maizels RM, Hume DA, Allen JE. Author information: Institute of Immunology and Infection Research, School of Biological Sciences; and 2 Medical Research Council Centre for Inflammation Research and 3 The Roslin Institute and Royal (Dick) School of Veterinary Studies, College of Medicine and Veterinary Medicine; University of Edinburgh, Edinburgh EH8 9YL, Scotland, UK. Abstract Macrophages (MΦs) colonize tissues during inflammation in two distinct ways: recruitment of monocyte precursors and proliferation of resident cells. We recently revealed a major role for IL-4 in the proliferative expansion of resident MΦs during a Th2-biased tissue nematode infection. We now show that proliferation of MΦs during intestinal as well as tissue nematode infection is restricted to sites of IL-4 production and requires MΦ-intrinsic IL-4R signaling. However, both IL-4Rα-dependent and -independent mechanisms contributed to MΦ proliferation during nematode infections. IL-4R-independent proliferation was controlled by a rise in local CSF-1 levels, but IL-4Rα expression conferred a competitive advantage with higher and more sustained proliferation and increased accumulation of IL-4Rα(+) compared with IL-4Rα(-) cells. Mechanistically, this occurred by conversion of IL-4Rα(+) MΦs from a CSF-1-dependent to -independent program of proliferation. Thus, IL-4 increases the relative density of tissue MΦs by overcoming the constraints mediated by the availability of CSF-1. Finally, although both elevated CSF1R and IL-4Rα signaling triggered proliferation above homeostatic levels, only CSF-1 led to the recruitment of monocytes and neutrophils. Thus, the IL-4 pathway of proliferation may have developed as an alternative to CSF-1 to increase resident MΦ numbers without coincident monocyte recruitment. PMCID: PMC3804948 [Available on 2014/4/21]
	PMID: 24101381 [PubMed - indexed for MEDLINE]
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6.	Nat Med. 2013 Oct;19(10):1207-8. doi: 10.1038/nm.3355. Therapeutically reeducating macrophages to treat GBM. Garris C, Pittet MJ. Author information: 1] Center for Systems Biology, Massachusetts General Hospital, Boston, Massachusetts, USA. [2] Graduate Program in Immunology, Harvard Medical School, Boston, Massachusetts, USA. Comment on CSF-1R inhibition alters macrophage polarization and blocks glioma progression. [Nat Med. 2013] CSF-1R inhibition alters macrophage polarization and blocks glioma progression.Pyonteck SM, Akkari L, Schuhmacher AJ, Bowman RL, Sevenich L, Quail DF, Olson OC, Quick ML, Huse JT, Teijeiro V, et al. Nat Med. 2013 Oct; 19(10):1264-72. Epub 2013 Sep 22. Abstract Glioblastoma multiforme (GBM) is the most common type of aggressive malignant brain cancer. The current lack of successful therapeutics means that this disease has a dismal prognosis. However, a new study in mice offers hope for patients with GBM by demonstrating the efficacy of a novel drug that targets GBM-associated macrophages (pages 1264–1272).
	PMID: 24100977 [PubMed - indexed for MEDLINE]
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7.	Nat Med. 2013 Oct;19(10):1264-72. doi: 10.1038/nm.3337. Epub 2013 Sep 22. CSF-1R inhibition alters macrophage polarization and blocks glioma progression. Pyonteck SM, Akkari L, Schuhmacher AJ, Bowman RL, Sevenich L, Quail DF, Olson OC, Quick ML, Huse JT, Teijeiro V, Setty M, Leslie CS, Oei Y, Pedraza A, Zhang J, Brennan CW, Sutton JC, Holland EC, Daniel D, Joyce JA. Author information: 1] Cancer Biology and Genetics, Memorial Sloan-Kettering Cancer Center (MSKCC), New York, New York, USA. [2]. Comment in Tumour microenvironment: Teaching old macrophages new tricks. [Nat Rev Cancer. 2013] Tumour microenvironment: Teaching old macrophages new tricks.Seton-Rogers S. Nat Rev Cancer. 2013 Nov; 13(11):753. Epub 2013 Oct 10. Therapeutically reeducating macrophages to treat GBM. [Nat Med. 2013] Therapeutically reeducating macrophages to treat GBM.Garris C, Pittet MJ. Nat Med. 2013 Oct; 19(10):1207-8. Abstract Glioblastoma multiforme (GBM) comprises several molecular subtypes, including proneural GBM. Most therapeutic approaches targeting glioma cells have failed. An alternative strategy is to target cells in the glioma microenvironment, such as tumor-associated macrophages and microglia (TAMs). Macrophages depend on colony stimulating factor-1 (CSF-1) for differentiation and survival. We used an inhibitor of the CSF-1 receptor (CSF-1R) to target TAMs in a mouse proneural GBM model, which significantly increased survival and regressed established tumors. CSF-1R blockade additionally slowed intracranial growth of patient-derived glioma xenografts. Surprisingly, TAMs were not depleted in treated mice. Instead, glioma-secreted factors, including granulocyte-macrophage CSF (GM-CSF) and interferon-γ (IFN-γ), facilitated TAM survival in the context of CSF-1R inhibition. Expression of alternatively activated M2 markers decreased in surviving TAMs, which is consistent with impaired tumor-promoting functions. These gene signatures were associated with enhanced survival in patients with proneural GBM. Our results identify TAMs as a promising therapeutic target for proneural gliomas and establish the translational potential of CSF-1R inhibition for GBM. PMCID: PMC3840724 [Available on 2014/4/1]
	PMID: 24056773 [PubMed - indexed for MEDLINE]
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8.	Nat Med. 2013 Oct;19(10):1318-24. doi: 10.1038/nm.3270. Epub 2013 Sep 15. Endogenous factor VIII synthesis from the intron 22-inverted F8 locus may modulate the immunogenicity of replacement therapy for hemophilia A. Pandey GS, Yanover C, Miller-Jenkins LM, Garfield S, Cole SA, Curran JE, Moses EK, Rydz N, Simhadri V, Kimchi-Sarfaty C, Lillicrap D, Viel KR, Przytycka TM, Pierce GF, Howard TE, Sauna ZE; PATH (Personalized Alternative Therapies for Hemophilia) Study Investigators. Collaborators: Lusher J, Chitlur M, Ameri A, Natarajan K, Iyer RV, Thompson AA, Watts RG, Kempton CL, Kessler C, Barrett JC, Martin EJ, Key N, Kruse-Jarres R, Lessinger C, Pratt KP, Josephson N, McRedmond K, Withycombe J, Walsh C, Matthews D, Mahlangu J, Krause A, Schwyzer R, Thejpal R, Rapiti N, Goga Y, Coetzee M, Stones D, Mann K, Butenas S, Almasy L, Blangero J, Carless M, Raja R, Reed E. Author information: Laboratory of Hemostasis, Division of Hematology, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland, USA. Abstract Neutralizing antibodies (inhibitors) to replacement factor VIII (FVIII, either plasma derived or recombinant) impair the effective management of hemophilia A. Individuals with hemophilia A due to major deletions of the FVIII gene (F8) lack antigenically cross-reactive material in their plasma ("CRM-negative"), and the prevalence of inhibitors in these individuals may be as high as 90%. Conversely, individuals with hemophilia A caused by F8 missense mutations are CRM-positive, and their overall prevalence of inhibitors is <10% (ref. 2). Individuals with the F8 intron 22 inversion (found in ∼50% of individuals with severe hemophilia A) have been grouped with the former on the basis of their genetic defect and CRM-negative status. However, only ∼20% of these individuals develop inhibitors. Here we demonstrate that the levels of F8 mRNA and intracellular FVIII protein in B lymphoblastoid cells and liver biopsies from individuals with the intron 22 inversion are comparable to those in healthy controls. These results support the hypothesis that most individuals with the intron 22 inversion are tolerized to FVIII and thus do not develop inhibitors. Furthermore, we developed a new pharmacogenetic algorithm that permits the stratification of inhibitor risk for individuals and subpopulations by predicting the immunogenicity of replacement FVIII using, as input, the number of putative T cell epitopes in the infused protein and the competence of major histocompatibility complex class II molecules to present such epitopes. This algorithm showed statistically significant accuracy in predicting the presence of inhibitors in 25 unrelated individuals with the intron 22 inversion.
	PMID: 24037092 [PubMed - indexed for MEDLINE]
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