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

Sent on Tuesday, 2010 Aug 31
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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1.	Nature. 2010 Jul 15;466(7304):295. Brazil's biotech boom. [No authors listed]
	PMID: 20631753 [PubMed - indexed for MEDLINE]

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, 2010 Aug 25
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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1.	Science. 2010 Aug 13;329(5993):849-53. Activation of beta-catenin in dendritic cells regulates immunity versus tolerance in the intestine. Manicassamy S, Reizis B, Ravindran R, Nakaya H, Salazar-Gonzalez RM, Wang YC, Pulendran B. Emory Vaccine Center, and Yerkes National Primate Research Center, 954 Gatewood Road, Atlanta, GA 30329, USA. Comment in: Science. 2010 Aug 13;329(5993):767-9. Abstract Dendritic cells (DCs) play a vital role in initiating robust immunity against pathogens as well as maintaining immunological tolerance to self antigens. However, the intracellular signaling networks that program DCs to become tolerogenic remain unknown. We report here that the Wnt-beta-catenin signaling in intestinal dendritic cells regulates the balance between inflammatory versus regulatory responses in the gut. beta-catenin in intestinal dendritic cells was required for the expression of anti-inflammatory mediators such as retinoic acid-metabolizing enzymes, interleukin-10, and transforming growth factor-beta, and the stimulation of regulatory T cell induction while suppressing inflammatory effector T cells. Furthermore, ablation of beta-catenin expression in DCs enhanced inflammatory responses and disease in a mouse model of inflammatory bowel disease. Thus, beta-catenin signaling programs DCs to a tolerogenic state, limiting the inflammatory response.
	PMID: 20705860 [PubMed - indexed for MEDLINE]
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2.	Science. 2010 Aug 13;329(5993):740-2. Human Evolution. Tracing evolution's recent fingerprints. Gibbons A.
	PMID: 20705825 [PubMed - indexed for MEDLINE]
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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Saturday, 2010 Aug 21
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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1.	Science. 2010 Aug 6;329(5992):614-5. Cancer research. As questions grow, Duke halts trials, launches investigation. Couzin-Frankel J.
	PMID: 20688986 [PubMed - indexed for MEDLINE]

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

Sent on Saturday, 2010 Aug 14
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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1.	Nat Genet. 2010 Aug;42(8):648-50. Variation across the allele frequency spectrum. Gloyn AL, McCarthy MI. Comment on: Nat Genet. 2010 Aug;42(8):684-7.
	PMID: 20664646 [PubMed - indexed for MEDLINE]
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2.	Nat Genet. 2010 Aug;42(8):641-5. Collaborative genomics for human health and cooperation in the Mediterranean region. Ozçelik T, Kanaan M, Avraham KB, Yannoukakos D, Mégarbané A, Tadmouri GO, Middleton L, Romeo G, King MC, Levy-Lahad E. Department of Molecular Biology and Genetics, Bilkent University, Ankara, Turkey. tozcelik@bilkent.edu.tr Abstract The US government has proposed the development of scientific centers of excellence to solve global challenges. We propose such a center of excellence devoted to the genomic analysis of Mediterranean populations of all creeds. This genomic focus is rooted in the region's demographic history, builds on the area's rapidly developing expertise in human genetics, and will yield scientific discoveries of both local and global significance. The genome sequence data of Mediterranean populations will offer unique insights into human evolution and early human migration. The potent combination of highly consanguineous populations in the Mediterranean's southern and eastern rims and regional medical and scientific expertise could lead to the identification and characterization of many genes responsible for human disease. Such discoveries will enable genetic knowledge to be translated into medical knowledge that will benefit local populations and contribute substantially to the understanding of the genetic bases of human diseases worldwide.
	PMID: 20664644 [PubMed - indexed for MEDLINE]
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3.	Nat Genet. 2010 Aug;42(8):639. Basin of attraction. [No authors listed]
	PMID: 20664643 [PubM ed - indexed for MEDLINE]
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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, 2010 Aug 11
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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1.	Science. 2010 Jul 23;329(5990):397-8. Medicine. Wnt fans the flames in obesity. Oh da Y, Olefsky JM. Department of Medicine, Division of Endocrinology and Metabolism, University of California, San Diego, La Jolla, CA 92093, USA. Comment on: Science. 2010 Jul 23;329(5990):454-7.
	PMID: 20651140 [PubMed - indexed for MEDLINE]
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2.	Science. 2010 Jul 23;329(5990):393-4. Information access. Prepublication data release, latency, and genome commons. Contreras JL. School of Law, Washington University in St. Louis, St. Louis, MO 63130, USA. jlcontreras@wulaw.wustl.edu
	PMID: 20651137 [PubMed - indexed for MEDLINE]
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3.	Science. 2010 Jul 23;329(5990):454-7. Epub 2010 Jun 17. Sfrp5 is an anti-inflammatory adipokine that modulates m etabolic dysfunction in obesity. Ouchi N, Higuchi A, Ohashi K, Oshima Y, Gokce N, Shibata R, Akasaki Y, Shimono A, Walsh K. Molecular Cardiology and Whitaker Cardiovascular Institute, Boston University School of Medicine, 715 Albany Street, W611, Boston, MA 02118, USA. nouchi@bu.edu Comment in: Science. 2010 Jul 23;329(5990):397-8. Nat Rev Drug Discov. 2010 Aug;9(8):594. Nat Rev Immunol. 2010 Aug;10(8):540. Abstract Adipose tissue secretes proteins referred to as adipokines, many of which promote inflammation and disrupt glucose homeostasis. Here we show that secreted frizzled-related protein 5 (Sfrp5), a protein previously linked to the Wnt signaling pathway, is an anti-inflammatory adipokine whose expression is perturbed in models of obesity and type 2 diabetes. Sfrp5-deficient mice fed a high-calorie diet developed severe glucose intolerance and hepatic steatosis, and their adipose tissue showed an accumulation of activated macrophages that was associated with activation of the c-Jun N-terminal kinase signaling pathway. Adenovirus-mediated delivery of Sfrp5 to mouse models of obesity ameliorated glucose intolerance and hepatic steatosis. Thus, in the setting of obesity, Sfrp5 secretion by adipocytes exerts salutary effects on metabolic dysfunction by controlling inflammatory cells within adipose tissue.
	PMID: 20558665 [PubMed - indexed for MEDLINE]
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What's new for 'JKB_daily1' in PubMed

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

Sent on Saturday, 2010 Aug 07
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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1.	Nature. 2010 Jul 1;466(7302):38-40. Autophagy: Snapshot of the network. Levine B, Ranganathan R. Comment on: Nature. 2010 Jul 1;466(7302):68-76.
	PMID: 20596005 [PubMed - indexed for MEDLINE]
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2.	Nature. 2010 Jul 1;466(7302):24-6. Climate science: An erosion of trust? Tollefson J.
	PMID: 20595989 [PubMed - indexed for MEDLINE]
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3.	Nature. 2010 Jul 1;466(7302):20. Strong medicine for French research. Arnold Munnich interviewed by Declan Butler. Munnich A.
	PMID: 20595986 [PubMed - indexed for MEDLINE]
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4.	Nature. 2010 Jul 1;466(7302):68-76. Epub 2010 Jun 20. Network organization of the human autophagy system. Behrends C, Sowa ME, Gygi SP, Harper JW. Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA. Comment in: Nature. 2010 Jul 1;466(7302):38-40. Abstract Autophagy, the process by which proteins and organelles are sequestered in autophagosomal vesicles and delivered to the lysosome/vacuole for degradation, provides a primary route for turnover of stable and defective cellular proteins. Defects in this system are linked with numerous human diseases. Although conserved protein kinase, lipid kinase and ubiquitin-like protein conjugation subnetworks controlling autophagosome formation and cargo recruitment have been defined, our understanding of the global organization of this system is limited. Here we report a proteomic analysis of the autophagy interaction network in human cells under conditions of ongoing (basal) autophagy, revealing a network of 751 interactions among 409 candidate interacting proteins with extensive connectivity among subnetworks. Many new autophagy interaction network components have roles in vesicle trafficking, protein or lipid phosphorylation and protein ubiquitination, and affect autophagosome number or flux when depleted by RNA interference. The six ATG8 orthologues in humans (MAP1LC3/GABARAP proteins) interact with a cohort of 67 proteins, with extensive binding partner overlap between family members, and frequent involvement of a conserved surface on ATG8 proteins known to interact with LC3-interacting regions in partner proteins. These studies provide a global view of the mammalian autophagy interaction landscape and a resource for mechanistic analysis of this critical protein homeostasis pathway. PMCID: PMC2901998 [Available on 2011/1/1]
	PMID: 20562859 [PubMed - indexed for MEDLINE]
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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Friday, 2010 Aug 06
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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1.	N Engl J Med. 2010 Jul 22;363(4):301-4. Epub 2010 Jun 15. The path to personalized medicine. Hamburg MA, Collins FS. Food and Drug Administration, Silver Spring, Maryland, USA.
	PMID: 20551152 [PubMed - indexed for MEDLINE]
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2.	Science. 2010 Jul 16;329(5989):294-6. Epub 2010 Jun 3. Staphylococcus aureus nonribosomal peptide secondary metabolites regulate virulence.< /a> Wyatt MA, Wang W, Roux CM, Beasley FC, Heinrichs DE, Dunman PM, Magarvey NA. Department of Biochemistry and Biomedical Sciences, M. G. DeGroote Institute for Infectious Disease Research, McMaster University, Hamilton, Ontario L8N 3Z5, Canada. Abstract Staphylococcus aureus is a major human pathogen that is resistant to numerous antibiotics in clinical use. We found two nonribosomal peptide secondary metabolites--the aureusimines, made by S. aureus--that are not antibiotics, but function as regulators of virulence factor expression and are necessary for productive infections. In vivo mouse models of bacteremia showed that strains of S. aureus unable to produce aureusimines were attenuated and/or cleared from major organs, including the spleen, liver, and heart. Targeting aureusimine synthesis may offer novel leads for anti-infective drugs.
	PMID: 20522739 [PubMed - indexed for MEDLINE]
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