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

Sent on Friday, 2014 January 24
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. 2014 Jan 10;343(6167):204-8. doi: 10.1126/science.1244705. Internalization of Salmonella by macrophages induces formation of nonreplicating persisters. Helaine S, Cheverton AM, Watson KG, Faure LM, Matthews SA, Holden DW. Author information: Section of Microbiology, Medical Research Council Centre for Molecular Bacteriology and Infection, Imperial College London, Armstrong Road, London SW7 2AZ, UK. Abstract Many bacterial pathogens cause persistent infections despite repeated antibiotic exposure. Bacterial persisters are antibiotic-tolerant cells, but little is known about their growth status and the signals and pathways leading to their formation in infected tissues. We used fluorescent single-cell analysis to identify Salmonella persisters during infection. These were part of a nonreplicating population formed immediately after uptake by macrophages and were induced by vacuolar acidification and nutritional deprivation, conditions that also induce Salmonella virulence gene expression. The majority of 14 toxin-antitoxin modules contributed to intracellular persister formation. Some persisters resumed intracellular growth after phagocytosis by naïve macrophages. Thus, the vacuolar environment induces phenotypic heterogeneity, leading to either bacterial replication or the formation of nonreplicating persisters that could provide a reservoir for relapsing infection.
	PMID: 24408438 [PubMed - indexed for MEDLINE]
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2.	Science. 2014 Jan 10;343(6167):117. doi: 10.1126/science.1247701. EMBO at 50. Nurse P. Author information: Paul Nurse is Secretary General of EMBO.
	PMID: 24408402 [PubMed - indexed for MEDLINE]
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3.	N Engl J Med. 2014 Jan 9;370(2):158. doi: 10.1056/NEJMicm1306161. Images in clinical medicine. Emphysematous aortitis after endovascular graft. Huang YL, Wu MT. Author information: Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan. Free Article
	PMID: 24401053 [PubMed - indexed for MEDLINE]
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4.	Nat Med. 2013 Nov;19(11):1423-37. doi: 10.1038/nm.3394. Microenvironmental regulation of tumor progression and metastasis. Quail DF, Joyce JA. Author information: Cancer Biology and Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York, USA. Abstract Cancers develop in complex tissue environments, which they depend on for sustained growth, invasion and metastasis. Unlike tumor cells, stromal cell types within the tumor microenvironment (TME) are genetically stable and thus represent an attractive therapeutic target with reduced risk of resistance and tumor recurrence. However, specifically disrupting the pro-tumorigenic TME is a challenging undertaking, as the TME has diverse capacities to induce both beneficial and adverse consequences for tumorigenesis. Furthermore, many studies have shown that the microenvironment is capable of normalizing tumor cells, suggesting that re-education of stromal cells, rather than targeted ablation per se, may be an effective strategy for treating cancer. Here we discuss the paradoxical roles of the TME during specific stages of cancer progression and metastasis, as well as recent therapeutic attempts to re-educate stromal cells within the TME to have anti-tumorigenic effects.
	PMID: 24202395 [PubMed - indexed for MEDLINE]
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5.	Nat Med. 2013 Nov;19(11):1368-9. doi: 10.1038/nm.3387. An endogenous factor mediates shock-induced injury. Ward PA. Author information: Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA. Comment on Cold-inducible RNA-binding protein (CIRP) triggers inflammatory responses in hemorrhagic shock and sepsis. [Nat Med. 2013] Cold-inducible RNA-binding protein (CIRP) triggers inflammatory responses in hemorrhagic shock and sepsis.Qiang X, Yang WL, Wu R, Zhou M, Jacob A, Dong W, Kuncewitch M, Ji Y, Yang H, Wang H, et al. Nat Med. 2013 Nov; 19(11):1489-95. Epub 2013 Oct 6.
	PMID: 24202382 [PubMed - indexed for MEDLINE]
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6.	Nat Med. 2013 Nov;19(11):1354-5. doi: 10.1038/nm1113-1354. Pharmacogenetic tests yield bonus benefit: better drug adherence. Dolgin E.
	PMID: 24202373 [PubMed - indexed for MEDLINE]
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7.	Nat Med. 2013 Nov;19(11):1529-33. doi: 10.1038/nm.3351. Epub 2013 Oct 27. Loss of immune escape mutations during persistent HCV infection in pregnancy enhances replication of vertically transmitted viruses. Honegger JR, Kim S, Price AA, Kohout JA, McKnight KL, Prasad MR, Lemon SM, Grakoui A, Walker CM. Author information: 1] The Center for Vaccines and Immunity, Nationwide Children's Hospital, Columbus, Ohio, USA. [2] Department of Pediatrics, The Ohio State University School of Medicine, Columbus, Ohio, USA. Abstract Globally, about 1% of pregnant women are persistently infected with the hepatitis C virus (HCV). Mother-to-child transmission of HCV occurs in 3-5% of pregnancies and accounts for most new childhood infections. HCV-specific CD8(+) cytotoxic T lymphocytes (CTLs) are vital in the clearance of acute HCV infections, but in the 60-80% of infections that persist, these cells become functionally exhausted or select for mutant viruses that escape T cell recognition. Increased HCV replication during pregnancy suggests that maternofetal immune tolerance mechanisms may further impair HCV-specific CTLs, limiting their selective pressure on persistent viruses. To assess this possibility, we characterized circulating viral quasispecies during and after consecutive pregnancies in two women. This revealed a loss of some escape mutations in HLA class I epitopes during pregnancy that was associated with emergence of more fit viruses. CTL selective pressure was reimposed after childbirth, at which point escape mutations in these epitopes again predominated in the quasispecies and viral load dropped sharply. Importantly, the viruses transmitted perinatally were those with enhanced fitness due to reversion of escape mutations. Our findings indicate that the immunoregulatory changes of pregnancy reduce CTL selective pressure on HCV class I epitopes, thereby facilitating vertical transmission of viruses with optimized replicative fitness. PMCID: PMC3823809 [Available on 2014/5/1]
	PMID: 24162814 [PubMed - indexed for MEDLINE]
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8.	Nat Med. 2013 Nov;19(11):1489-95. doi: 10.1038/nm.3368. Epub 2013 Oct 6. Cold-inducible RNA-binding protein (CIRP) triggers inflammatory responses in hemorrhagic shock and sepsis. Qiang X, Yang WL, Wu R, Zhou M, Jacob A, Dong W, Kuncewitch M, Ji Y, Yang H, Wang H, Fujita J, Nicastro J, Coppa GF, Tracey KJ, Wang P. Author information: 1] Center for Translational Research, The Feinstein Institute for Medical Research, Manhasset, New York, USA. [2]. Comment in An endogenous factor mediates shock-induced injury. [Nat Med. 2013] An endogenous factor mediates shock-induced injury.Ward PA. Nat Med. 2013 Nov; 19(11):1368-9. Abstract A systemic inflammatory response is observed in patients undergoing hemorrhagic shock and sepsis. Here we report increased levels of cold-inducible RNA-binding protein (CIRP) in the blood of individuals admitted to the surgical intensive care unit with hemorrhagic shock. In animal models of hemorrhage and sepsis, CIRP is upregulated in the heart and liver and released into the circulation. In macrophages under hypoxic stress, CIRP translocates from the nucleus to the cytosol and is released. Recombinant CIRP stimulates the release of tumor necrosis factor-α (TNF-α) and HMGB1 from macrophages and induces inflammatory responses and causes tissue injury when injected in vivo. Hemorrhage-induced TNF-α and HMGB1 release and lethality were reduced in CIRP-deficient mice. Blockade of CIRP using antisera to CIRP attenuated inflammatory cytokine release and mortality after hemorrhage and sepsis. The activity of extracellular CIRP is mediated through the Toll-like receptor 4 (TLR4)-myeloid differentiation factor 2 (MD2) complex. Surface plasmon resonance analysis indicated that CIRP binds to the TLR4-MD2 complex, as well as to TLR4 and MD2 individually. In particular, human CIRP amino acid residues 106-125 bind to MD2 with high affinity. Thus, CIRP is a damage-associated molecular pattern molecule that promotes inflammatory responses in shock and sepsis. PMCID: PMC3826915 [Available on 2014/5/1]
	PMID: 24097189 [PubMed - indexed for MEDLINE]
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