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

Sent on Wednesday, 2013 July 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.	Lancet. 2013 Jul 13;382(9887):119. doi: 10.1016/S0140-6736(13)61551-2. Mary-Claire King: taking genes beyond the lab. Watts G.
	PMID: 23849913 [PubMed - indexed for MEDLINE]
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2.	Nature. 2013 Jul 4;499(7456):43-9. doi: 10.1038/nature12222. Epub 2013 Jun 23. Comprehensive molecular characterization of clear cell renal cell carcinoma. Cancer Genome Atlas Research Network. Collaborators: Creighton CJ, Morgan M, Gunaratne PH, Wheeler DA, Gibbs RA, Robertson A, Chu A, Beroukhim R, Cibulskis K, Signoretti S, Vandin F, Wu HT, Raphael BJ, Verhaak RG, Tamboli P, Torres-Garcia W, Akbani R, Weinstein JN, Reuter V, Hsieh JJ, Brannon A, Hakimi A, Jacobsen A, Ciriello G, Reva B, Ricketts CJ, Linehan W, Stuart JM, Rathmell W, Shen H, Laird PW, Muzny D, Davis C, Morgan M, Xi L, Chang K, Kakkar N, Treviño LR, Benton S, Reid JG, Morton D, Doddapaneni H, Han Y, Lewis L, Dinh H, Kovar C, Zhu Y, Santibanez J, Wang M, Hale W, Kalra D, Creighton CJ, Wheeler DA, Gibbs RA, Getz G, Cibulskis K, Lawrence MS, Sougnez C, Carter SL, Sivachenko A, Lichtenstein L, Stewart C, Voet D, Fisher S, Gabriel SB, Lander E, Beroukhim R, Schumacher SE, Tabak B, Saksena G, Onofrio RC, Carter SL, Cherniack AD, Gentry J, Ardlie K, Sougnez C, Getz G, Gabriel SB, Meyerson M, Robertson A, Chu A, Chun HJ, Mungall AJ, Sipahimalani P, Stoll D, Ally A, Balasundaram M, Butterfield YS, Carlsen R, Carter C, Chuah E, Coope RJ, Dhalla N, Gorski S, Guin R, Hirst C, Hirst M, Holt RA, Lebovitz C, Lee D, Li HI, Mayo M, Moore RA, Pleasance E, Plettner P, Schein JE, Shafiei A, Slobodan JR, Tam A, Thiessen N, Varhol RJ, Wye N, Zhao Y, Birol I, Jones SJ, Marra MA, Auman JT, Tan D, Jones CD, Hoadley KA, Mieczkowski PA, Mose LE, Jefferys SR, Topal MD, Liquori C, Turman YJ, Shi Y, Waring S, Buda E, Walsh J, Wu J, Bodenheimer T, Hoyle AP, Simons JV, Soloway MG, Balu S, Parker JS, Hayes D, Perou CM, Kucherlapati R, Park P, Shen H, Triche T Jr, Weisenberger DJ, Lai PH, Bootwalla MS, Maglinte DT, Mahurkar S, Berman BP, Van Den Berg DJ, Cope L, Baylin SB, Laird PW, Creighton CJ, Wheeler DA, Getz G, Noble MS, DiCara D, Zhang H, Cho J, Heiman DI, Gehlenborg N, Voet D, Mallard W, Lin P, Frazer S, Stojanov P, Liu Y, Zhou L, Kim J, Lawrence MS, Chin L, Vandin F, Wu HT, Raphael BJ, Benz C, Yau C, Reynolds SM, Shmulevich I, Verhaak RG, Torres-Garcia W, Vegesna R, Kim H, Zhang W, Cogdell D, Jonasch E, Ding Z, Lu Y, Akbani R, Zhang N, Unruh AK, Casasent TD, Wakefield C, Tsavachidou D, Chin L, Mills GB, Weinstein JN, Jacobsen A, Brannon R, Ciriello G, Schultz N, Hakimi A, Reva B, Antipin Y, Gao J, Cerami E, Gross B, Aksoy BA, Sinha R, Weinhold N, Sumer S, Taylor BS, Shen R, Ostrovnaya I, Hsieh JJ, Berger MF, Ladanyi M, Sander C, Fei SS, Stout A, Spellman PT, Rubin DL, Liu TT, Stuart JM, Ng S, Paull EO, Carlin D, Goldstein T, Waltman P, Ellrott K, Zhu J, Haussler D, Gunaratne PH, Xiao W, Shelton C, Gardner J, Penny R, Sherman M, Mallery D, Morris S, Paulauskis J, Burnett K, Shelton T, Signoretti S, Kaelin WG, Choueiri T, Atkins MB, Penny R, Burnett K, Mallery D, Curley E, Tickoo S, Reuter V, Rathmell W, Thorne L, Boice L, Huang M, Fisher JC, Linehan WM, Vocke CD, Peterson J, Worrell R, Merino MJ, Schmidt LS, Tamboli P, Czerniak BA, Aldape KD, Wood CG, Boyd J, Weaver J, Iacocca MV, Petrelli N, Witkin G, Brown J, Czerwinski C, Huelsenbeck-Dill L, Rabeno B, Myers J, Morrison C, Bergsten J, Eckman J, Harr J, Smith C, Tucker K, Zach LA, Bshara W, Gaudioso C, Morrison C, Dhir R, Maranchie J, Nelson J, Parwani A, Potapova O, Fedosenko K, Cheville JC, Thompson RH, Signoretti S, Kaelin WG, Atkins MB, Tickoo S, Reuter V, Linehan WM, Vocke CD, Peterson J, Merino MJ, Schmidt LS, Tamboli P, Mosquera JM, Rubin MA, Blute ML, Rathmell W, Pihl T, Jensen M, Sfeir R, Kahn A, Chu A, Kothiyal P , Snyder E, Pontius J, Ayala B, Backus M, Walton J, Baboud J, Berton D, Nicholls M, Srinivasan D, Raman R, Girshik S, Kigonya P, Alonso S, Sanbhadti R, Barletta S, Pot D, Sheth M, Demchok JA, Davidsen T, Wang Z, Yang L, Tarnuzzer RW, Zhang J, Eley G, Ferguson ML, Mills Shaw KR, Guyer MS, Ozenberger BA, Sofia HJ. Abstract Genetic changes underlying clear cell renal cell carcinoma (ccRCC) include alterations in genes controlling cellular oxygen sensing (for example, VHL) and the maintenance of chromatin states (for example, PBRM1). We surveyed more than 400 tumours using different genomic platforms and identified 19 significantly mutated genes. The PI(3)K/AKT pathway was recurrently mutated, suggesting this pathway as a potential therapeutic target. Widespread DNA hypomethylation was associated with mutation of the H3K36 methyltransferase SETD2, and integrative analysis suggested that mutations involving the SWI/SNF chromatin remodelling complex (PBRM1, ARID1A, SMARCA4) could have far-reaching effects on other pathways. Aggressive cancers demonstrated evidence of a metabolic shift, involving downregulation of genes involved in the TCA cycle, decreased AMPK and PTEN protein levels, upregulation of the pentose phosphate pathway and the glutamine transporter genes, increased acetyl-CoA carboxylase protein, and altered promoter methylation of miR-21 (also known as MIR21) and GRB10. Remodelling cellular metabolism thus constitutes a recurrent pattern in ccRCC that correlates with tumour stage and severity and offers new views on the opportunities for disease treatment.
	PMID: 23792563 [PubMed - indexed for MEDLINE]
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3.	Nature. 2013 Jul 4;499(7456):79-82. doi: 10.1038/nature12223. Epub 2013 May 15. Variation and genetic control of protein abundance in humans. Wu L, Candille SI, Choi Y, Xie D, Jiang L, Li-Pook-Than J, Tang H, Snyder M. Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA. Abstract Gene expression differs among individuals and populations and is thought to be a major determinant of phenotypic variation. Although variation and genetic loci responsible for RNA expression levels have been analysed extensively in human populations, our knowledge is limited regarding the differences in human protein abundance and the genetic basis for this difference. Variation in messenger RNA expression is not a perfect surrogate for protein expression because the latter is influenced by an array of post-transcriptional regulatory mechanisms, and, empirically, the correlation between protein and mRNA levels is generally modest. Here we used isobaric tag-based quantitative mass spectrometry to determine relative protein levels of 5,953 genes in lymphoblastoid cell lines from 95 diverse individuals genotyped in the HapMap Project. We found that protein levels are heritable molecular phenotypes that exhibit considerable variation between individuals, populations and sexes. Levels of specific sets of proteins involved in the same biological process covary among individuals, indicating that these processes are tightly regulated at the protein level. We identified cis-pQTLs (protein quantitative trait loci), including variants not detected by previous transcriptome studies. This study demonstrates the feasibility of high-throughput human proteome quantification that, when integrated with DNA variation and transcriptome information, adds a new dimension to the characterization of gene expression regulation.
	PMID: 23676674 [PubMed - indexed for MEDLINE]
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What's new for 'JKB_daily1' in PubMed

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Sent on Friday, 2013 July 26
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. 2013 Jul 18;369(3):289-90. doi: 10.1056/NEJMc1302295. Metagenomic analysis of tuberculosis in a mummy. Chan JZ, Sergeant MJ, Lee OY, Minnikin DE, Besra GS, Pap I, Spigelman M, Donoghue HD, Pallen MJ. Free Article
	PMID: 23863071 [PubMed - indexed for MEDLINE]

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Sent on Wednesday, 2013 July 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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1.	Science. 2013 Jul 12;341(6142):137-8. doi: 10.1126/science.1242217. Epub 2013 Jun 27. Genetics. Moving beyond "isolated" gene patents. Rai AK, Cook-Deegan R. Duke University School of Law, Durham, NC 27708, USA. rai@law.duke.edu
	PMID: 23811224 [PubMed - indexed for MEDLINE]

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Sent on Saturday, 2013 July 20
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.	PLoS One. 2013;8(1):e54935. doi: 10.1371/journal.pone.0054935. Epub 2013 Jan 31. The function of the conserved regulatory element within the second intron of the mammalian Csf1r locus. Sauter KA, Bouhlel MA, O'Neal J, Sester DP, Tagoh H, Ingram RM, Pridans C, Bonifer C, Hume DA. Developmental Biology, The Roslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Roslin, United Kingdom. Abstract The gene encoding the receptor for macrophage colony-stimulating factor (CSF-1R) is expressed exclusively in cells of the myeloid lineages as well as trophoblasts. A conserved element in the second intron, Fms-Intronic Regulatory Element (FIRE), is essential for macrophage-specific transcription of the gene. However, the molecular details of how FIRE activity is regulated and how it impacts the Csf1r promoter have not been characterised. Here we show that agents that down-modulate Csf1r mRNA transcription regulated promoter activity altered the occupancy of key FIRE cis-acting elements including RUNX1, AP1, and Sp1 binding sites. We demonstrate that FIRE acts as an anti-sense promoter in macrophages and reversal of FIRE orientation within its native context greatly reduced enhancer activity in macrophages. Mutation of transcription initiation sites within FIRE also reduced transcription. These results demonstrate that FIRE is an orientation-specific transcribed enhancer element. PMCID: PMC3561417 Free PMC Article
	PMID: 23383005 [PubMed - indexed for MEDLINE]

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Sent on Wednesday, 2013 July 17
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. 2013 Jun 27;498(7455):S10-1. doi: 10.1038/498S10a. Epigenetics: reversible tags. Wright J.
	PMID: 23803942 [PubMed - indexed for MEDLINE]
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2.	Lancet. 2013 Jun 22;381(9884):2222. doi: 10.1016/S0140-6736(13)60682-0. Deep coma and diffuse white matter abnormalities caused by sepsis-associated encephalopathy. Luitse MJ, van Asch CJ, Klijn CJ. Department of Neurology, University Medical Center Utrecht, The Netherlands. m.luitse-2@umcutrecht.nl
	PMID: 23791345 [PubMed - indexed for MEDLINE]
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3.	Nature. 2013 Jun 27;498(7455):511-5. doi: 10.1038/nature12209. Epub 2013 Jun 2. Rev-Erbs repress macrophage gene expression by inhibiting enhancer-directed transcription. Lam MT, Cho H, Lesch HP, Gosselin D, Heinz S , Tanaka-Oishi Y, Benner C, Kaikkonen MU, Kim AS, Kosaka M, Lee CY, Watt A, Grossman TR, Rosenfeld MG, Evans RM, Glass CK. Department of Cellular and Molecular Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA. Abstract Rev-Erb-α and Rev-Erb-β are nuclear receptors that regulate the expression of genes involved in the control of circadian rhythm, metabolism and inflammatory responses. Rev-Erbs function as transcriptional repressors by recruiting nuclear receptor co-repressor (NCoR)-HDAC3 complexes to Rev-Erb response elements in enhancers and promoters of target genes, but the molecular basis for cell-specific programs of repression is not known. Here we present evidence that in mouse macrophages Rev-Erbs regulate target gene expression by inhibiting the functions of distal enhancers that are selected by macrophage-lineage-determining factors, thereby establishing a macrophage-specific program of repression. Remarkably, the repressive functions of Rev-Erbs are associated with their ability to inhibit the transcription of enhancer-derived RNAs (eRNAs). Furthermore, targeted degradation of eRNAs at two enhancers subject to negative regulation by Rev-Erbs resulted in reduced expression of nearby messenger RNAs, suggesting a direct role of these eRNAs in enhancer function. By precisely defining eRNA start sites using a modified form of global run-on sequencing that quantifies nascent 5' ends, we show that transfer of full enhancer activity to a target promoter requires both the sequences mediating transcription-factor binding and the specific sequences encoding the eRNA transcript. These studies provide evidence for a direct role of eRNAs in contributing to enhancer functions and suggest that Rev-Erbs act to suppress gene expression at a distance by repressing eRNA transcription.
	PMID: 23728303 [PubMed - indexed for MEDLINE]
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1.	Lancet. 2013 Jun 29;381(9885):2250. doi: 10.1016/S0140-6736(13)61476-2. Sepsis definitions - Authors' reply. Vincent JL, Opal SM, Marshall JC, Tracey KJ. Comment on Sepsis definitions: time for change. [Lancet. 2013] Sepsis definitions: time for change.Vincent JL, Opal SM, Marshall JC, Tracey KJ. Lancet. 2013 Mar 2; 381(9868):774-5. Sepsis definitions. [Lancet. 2013] Sepsis definitions.Lucas S. Lancet. 2013 Jun 29; 381(9885):2249. Sepsis definitions. [Lancet. 2013] Sepsis definitions.Cascio A, Iaria C. Lancet. 2013 Jun 29; 381(9885):2249. Sepsis definitions. [Lancet. 2013] Sepsis definitions.Inoue K, Takano H. Lancet. 2013 Jun 29; 381(9885):2249-50.
	PMID: 23809556 [PubMed - indexed for MEDLINE]
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2.	Lancet. 2013 Jun 29;381(9885):2249-50. doi: 10.1016/S0140-6736(13)61475-0. Sepsis definitions. Inoue K, Takano H. Comment in Sepsis definitions - Authors' reply. [Lancet. 2013] Sepsis definitions - Authors' reply.Vincent JL, Opal SM, Marshall JC, Tracey KJ. Lancet. 2013 Jun 29; 381(9885):2250. Comment on Sepsis definitions: time for change. [Lancet. 2013] Sepsis definitions: time for change.Vincent JL, Opal SM, Marshall JC, Tracey KJ. Lancet. 2013 Mar 2; 381(9868):774-5.
	PMID: 23809554 [PubMed - indexed for MEDLINE]
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3.	Lancet. 2013 Jun 29;381(9885):2249. doi: 10.1016/S0140-6736(13)61473-7. Sepsis definitions. Cascio A, Iaria C. Comment in Sepsis definitions - Authors' reply. [Lancet. 2013] Sepsis definitions - Authors' reply.Vincent JL, Opal SM, Marshall JC, Tracey KJ. Lancet. 2013 Jun 29; 381(9885):2250. Comment on Sepsis definitions: time for change. [Lancet. 2013] Sepsis definitions: time for change.Vincent JL, Opal SM, Marshall JC, Tracey KJ. Lancet. 2013 Mar 2; 381(9868):774-5.
	PMID: 23809553 [PubMed - indexed for MEDLINE]
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4.	Lancet. 2013 Jun 29;381(9885):2249. doi: 10.1016/S0140-6736(13)61474-9. Sepsis definitions. Lucas S. Comment in Sepsis definitions - Authors' reply. [Lancet. 2013] Sepsis definitions - Authors' reply.Vincent JL, Opal SM, Marshall JC, Tracey KJ. Lancet. 2013 Jun 29; 381(9885):2250. Comment on Sepsis definitions: time for change. [Lancet. 2013] Sepsis definitions: time for change.Vincent JL, Opal SM, Marshall JC, Tracey KJ. Lancet. 2013 Mar 2; 381(9868):774-5.
	PMID: 23809552 [PubMed - indexed for MEDLINE]
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1.	Nature. 2013 Jun 20;498(7454):371-5. doi: 10.1038/nature12175. Epub 2013 May 26. Neutrophil swarms require LTB4 and integrins at sites of cell death in vivo. Lämmermann T, Afonso PV, Angermann BR, Wang JM, Kastenmüller W, Parent CA, Germain RN. Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-0421, USA. laemmermannt@niaid.nih.gov Abstract Neutrophil recruitment from blood to extravascular sites of sterile or infectious tissue damage is a hallmark of early innate immune responses, and the molecular events leading to cell exit from the bloodstream have been well defined. Once outside the vessel, individual neutrophils often show extremely coordinated chemotaxis and cluster formation reminiscent of the swarming behaviour of insects. The molecular players that direct this response at the single-cell and population levels within the complexity of an inflamed tissue are unknown. Using two-photon intravital microscopy in mouse models of sterile injury and infection, we show a critical role for intercellular signal relay among neutrophils mediated by the lipid leukotriene B4, which acutely amplifies local cell death signals to enhance the radius of highly directed interstitial neutrophil recruitment. Integrin receptors are dispensable for long-distance migration, but have a previously unappreciated role in maintaining dense cellular clusters when congregating neutrophils rearrange the collagenous fibre network of the dermis to form a collagen-free zone at the wound centre. In this newly formed environment, integrins, in concert with neutrophil-derived leukotriene B4 and other chemoattractants, promote local neutrophil interaction while forming a tight wound seal. This wound seal has borders that cease to grow in kinetic concert with late recruitment of monocytes and macrophages at the edge of the displaced collagen fibres. Together, these data provide an initial molecular map of the factors that contribute to neutrophil swarming in the extravascular space of a damaged tissue. They reveal how local events are propagated over large-range distances, and how auto-signalling produces coordinated, self-organized neutrophil-swarming behaviour that isolates the wound or infectious site from surrounding viable tissue.
	PMID: 23708969 [PubMed - indexed for MEDLINE]

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1.	Nat Med. 2013 May;19(5):530. doi: 10.1038/nm0513-530. Establish good genomic practice to guide medicine forward. Barker RW, Brindley DA, Schuh A. Oxford-UCL Centre for the Advancement of Sustainable Medical Innovation, University of Oxford, Oxford, UK.
	PMID: 23652098 [PubMed - indexed for MEDLINE]
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2.	Nat Med. 2013 May;19(5):576-85. doi: 10.1038/nm.3145. Epub 2013 Apr 7. Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis. Koeth RA, Wang Z, Levison BS, Buffa JA, Org E , Sheehy BT, Britt EB, Fu X, Wu Y, Li L, Smith JD, DiDonato JA, Chen J, Li H, Wu GD, Lewis JD, Warrier M, Brown JM, Krauss RM, Tang WH, Bushman FD, Lusis AJ, Hazen SL. Department of Cellular & Molecular Medicine, Cleveland Clinic, Cleveland, Ohio, USA. Comment in Meat-metabolizing bacteria in atherosclerosis. [Nat Med. 2013] Meat-metabolizing bacteria in atherosclerosis.Bäckhed F. Nat Med. 2013 May; 19(5):533-4. Abstract Intestinal microbiota metabolism of choline and phosphatidylcholine produces trimethylamine (TMA), which is further metabolized to a proatherogenic species, trimethylamine-N-oxide (TMAO). We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice. Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism. The presence of specific bacterial taxa in human feces was associated with both plasma TMAO concentration and dietary status. Plasma L-carnitine levels in subjects undergoing cardiac evaluation (n = 2,595) predicted increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events (myocardial infarction, stroke or death), but only among subjects with concurrently high TMAO levels. Chronic dietary L-carnitine supplementation in mice altered cecal microbial composition, markedly enhanced synthesis of TMA and TMAO, and increased atherosclerosis, but this did not occur if intestinal microbiota was concurrently suppressed. In mice with an intact intestinal microbiota, dietary supplementation with TMAO or either carnitine or choline reduced in vivo reverse cholesterol transport. Intestinal microbiota may thus contribute to the well-established link between high levels of red meat consumption and CVD risk. PMCID: PMC3650111 [Available on 2013/11/1]
	PMID: 23563705 [PubMed - indexed for MEDLINE]
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3.	Nat Med. 2013 May;19(5):608-13. doi: 10.1038/nm.3146. Epub 2013 Mar 31. PPARβ/δ governs Wnt signaling and bone turnover. Scholtysek C, Katzenbeisser J, Fu H, Uderhardt S, Ipseiz N, Stoll C, Zaiss MM, Stock M, Donhauser L, Böhm C, Kleyer A, Hess A , Engelke K, David JP, Djouad F, Tuckermann JP, Desvergne B, Schett G, Krönke G. Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nürnberg, Erlangen, Germany. Abstract Peroxisome proliferator-activated receptors (PPARs) act as metabolic sensors and central regulators of fat and glucose homeostasis. Furthermore, PPARγ has been implicated as major catabolic regulator of bone mass in mice and humans. However, a potential involvement of other PPAR subtypes in the regulation of bone homeostasis has remained elusive. Here we report a previously unrecognized role of PPARβ/δ as a key regulator of bone turnover and the crosstalk between osteoblasts and osteoclasts. In contrast to activation of PPARγ, activation of PPARβ/δ amplified Wnt-dependent and β-catenin-dependent signaling and gene expression in osteoblasts, resulting in increased expression of osteoprotegerin (OPG) and attenuation of osteoblast-mediated osteoclastogenesis. Accordingly, PPARβ/δ-deficient mice had lower Wnt signaling activity, lower serum concentrations of OPG, higher numbers of osteoclasts and osteopenia. Pharmacological activation of PPARβ/δ in a mouse model of postmenopausal osteoporosis led to normalization of the altered ratio of tumor necrosis factor superfamily, member 11 (RANKL, also called TNFSF11) to OPG, a rebalancing of bone turnover and the restoration of normal bone density. Our findings identify PPARβ/δ as a promising target for an alternative approach in the treatment of osteoporosis and related diseases.
	PMID: 23542786 [PubMed - indexed for MEDLINE]
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1.	Science. 2013 Jun 21;340(6139):1388-9. doi: 10.1126/science.340.6139.1388. Human genetics. Agency nixes deCODE's new data-mining plan. Kaiser J.
	PMID: 23788773 [PubMed - indexed for MEDLINE]