What's new for 'JKB_daily1' in PubMed

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

Sent on Tuesday, 2012 June 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 - 6 of 6

1.	Nature. 2012 Apr 25;484(7395):524-8. doi: 10.1038/nature11042. Infection regulates pro-resolving mediators that lower antibiotic requirements. Chiang N, Fredman G, Bäckhed F, Oh SF, Vickery T, Schmidt BA, Serhan CN. Source Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA. Abstract Underlying mechanisms for how bacterial infections contribute to active resolution of acute inflammation are unknown. Here, we performed exudate leukocyte trafficking and mediator-metabololipidomics of murine peritoneal Escherichia coli infections with temporal identification of pro-inflammatory (prostaglandins and leukotrienes) and specialized pro-resolving mediators (SPMs). In self-resolving E. coli exudates (10(5) colony forming units, c.f.u.), the dominant SPMs identified were resolvin (Rv) D5 and protectin D1 (PD1), which at 12 h were at significantly greater levels than in exudates from higher titre E. coli (10(7) c.f.u.)-challenged mice. Germ-free mice had endogenous RvD1 and PD1 levels higher than in conventional mice. RvD1 and RvD5 (nanograms per mouse) each reduced bacterial titres in blood and exudates, E. coli-induced hypothermia and increased survival, demonstrating the first actions of RvD5. With human polymorphonuclear neutrophils and macrophages, RvD1, RvD5 and PD1 each directly enhanced phagocytosis of E. coli, and RvD5 counter-regulated a panel of pro-inflammatory genes, including NF-κB and TNF-α. RvD5 activated the RvD1 receptor, GPR32, to enhance phagocytosis. With self-limited E. coli infections, RvD1 and the antibiotic ciprofloxacin accelerated resolution, each shortening resolution intervals (R(i)). Host-directed RvD1 actions enhanced ciprofloxacin's therapeutic actions. In 10(7) c.f.u. E. coli infections, SPMs (RvD1, RvD5, PD1) together with ciprofloxacin also heightened host antimicrobial responses. In skin infections, SPMs enhanced vancomycin clearance of Staphylococcus aureus. These results demonstrate that specific SPMs are temporally and differentially regulated during infections and that they are anti-phlogistic, enhance containment and lower antibiotic requirements for bacterial clearance. PMCID: PMC3340015 [Available on 2012/10/26]
	PMID: 22538616 [PubMed - indexed for MEDLINE]
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2.	Nature. 2012 Apr 25;484(7395):455. doi: 10.1038/484455d. Biobanks: Validate gene findings before telling donors. Hansson MG. Comment on Incidental benefits. [Nature. 2012] Incidental benefits.[No authors listed]Nature. 2012 Mar 21; 483(7390):373. Epub 2012 Mar 21. DNA donor rights affirmed. [Nature. 2012] DNA donor rights affirmed.Hayden EC. Nature. 2012 Mar 21; 483(7390):387. Epub 2012 Mar 21.
	PMID: 22538599 [PubMed - indexed for MEDLINE]
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3.	Nature. 2012 Apr 25;484(7395):455. doi: 10.1038/484455b. Molecular biology: Protect the DNA of museum specimens. Shepherd L, Perrie L.
	PMID: 22538597 [PubMed - indexed for MEDLINE]
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4.	Nat Med. 2012 Mar 6;18(3):363-74. doi: 10.1038/nm.2627. The cellular and signaling networks linking the immune system and metabolism in disease. Osborn O, Olefsky JM. Source Department of Medicine, Division of Endocrinology and Metabolism, University of California-San Diego, La Jolla, California, USA. Abstract It is now recognized that obesity is driving the type 2 diabetes epidemic in Western countries. Obesity-associated chronic tissue inflammation is a key contributing factor to type 2 diabetes and cardiovascular disease, and a number of studies have clearly demonstrated that the immune system and metabolism are highly integrated. Recent advances in deciphering the various cellular and signaling networks that participate in linking the immune and metabolic systems together have contributed to understanding of the pathogenesis of metabolic diseases and may also inform new therapeutic strategies based on immunomodulation. Here we discuss how these various networks underlie the etiology of the inflammatory component of insulin resistance, with a particular focus on the central roles of macrophages in adipose tissue and liver.
	PMID: 22395709 [PubMed - indexed for MEDLINE]
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5.	Nat Med. 2012 Mar 6;18(3):326. doi: 10.1038/nm0312-326. Genomics contest underscores challenges of personalized medicine. Scudellari M.
	PMID: 22395677 [PubMed - indexed for MEDLINE]
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6.	Nat Med. 2012 Feb 19;18(3):405-12. doi: 10.1038/nm.2653. Wnt5a-Ror2 signaling between osteoblast-lineage cells and osteoclast precursors enhances osteoclastogenesis. Maeda K, Kobayashi Y, Udagawa N, Uehara S, Ishihara A, Mizoguchi T, Kikuchi Y, Takada I, Kato S, Kani S, Nishita M, Marumo K, Martin TJ, Minami Y, Takahashi N. Source Institute for Oral Science, Matsumoto Dental University, Nagano, Japan. Comment in Bone cells crosstalk: noncanonical Roring in the Wnt. [Cell Metab. 2012] Bone cells crosstalk: noncanonical Roring in the Wnt.Baron R, Saito H, Gori F. Cell Metab. 2012 Apr 4; 15(4):415-7. Abstract The signaling molecule Wnt regulates bone homeostasis through β-catenin-dependent canonical and β-catenin-independent noncanonical pathways. Impairment of canonical Wnt signaling causes bone loss in arthritis and osteoporosis; however, it is unclear how noncanonical Wnt signaling regulates bone resorption. Wnt5a activates noncanonical Wnt signaling through receptor tyrosine kinase-like orphan receptor (Ror) proteins. We showed that Wnt5a-Ror2 signaling between osteoblast-lineage cells and osteoclast precursors enhanced osteoclastogenesis. Osteoblast-lineage cells expressed Wnt5a, whereas osteoclast precursors expressed Ror2. Mice deficient in either Wnt5a or Ror2, and those with either osteoclast precursor-specific Ror2 deficiency or osteoblast-lineage cell-specific Wnt5a deficiency showed impaired osteoclastogenesis. Wnt5a-Ror2 signals enhanced receptor activator of nuclear factor-κB (RANK) expression in osteoclast precursors by activating JNK and recruiting c-Jun on the promoter of the gene encoding RANK, thereby enhancing RANK ligand (RANKL)-induced osteoclastogenesis. A soluble form of Ror2 acted as a decoy receptor of Wnt5a and abrogated bone destruction in mouse arthritis models. Our results suggest that the Wnt5a-Ror2 pathway is crucial for osteoclastogenesis in physiological and pathological environments and represents a therapeutic target for bone diseases, including arthritis.
	PMID: 22344299 [PubMed - indexed for MEDLINE]
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