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

Sent on Thursday, 2013 October 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.	BMC Genomics. 2013 May 15;14:332. doi: 10.1186/1471-2164-14-332. Structural and functional annotation of the porcine immunome. Dawson HD, Loveland JE, Pascal G, Gilbert JG, Uenishi H, Mann KM, Sang Y, Zhang J, Carvalho-Silva D, Hunt T, Hardy M, Hu Z, Zhao SH, Anselmo A, Shinkai H, Chen C, Badaoui B, Berman D, Amid C, Kay M, Lloyd D, Snow C, Morozumi T, Cheng RP, Bystrom M, Kapetanovic R, Schwartz JC, Kataria R, Astley M, Fritz E, Steward C, Thomas M, Wilming L, Toki D, Archibald AL, Bed'Hom B, Beraldi D, Huang TH, Ait-Ali T, Blecha F, Botti S, Freeman TC, Giuffra E, Hume DA, Lunney JK, Murtaugh MP, Reecy JM, Harrow JL, Rogel-Gaillard C, Tuggle CK. USDA-ARS, Beltsville Human Nutrition Research Center, Diet, Genomics, Immunology Laboratory, Beltsville, MD 20705, USA. Abstract BACKGROUND: The domestic pig is known as an excellent model for human immunology and the two species share many pathogens. Susceptibility to infectious disease is one of the major constraints on swine performance, yet the structure and function of genes comprising the pig immunome are not well-characterized. The completion of the pig genome provides the opportunity to annotate the pig immunome, and compare and contrast pig and human immune systems. RESULTS: The Immune Response Annotation Group (IRAG) used computational curation and manual annotation of the swine genome assembly 10.2 (Sscrofa10.2) to refine the currently available automated annotation of 1,369 immunity-related genes through sequence-based comparison to genes in other species. Within these genes, we annotated 3,472 transcripts. Annotation provided evidence for gene expansions in several immune response families, and identified artiodactyl-specific expansions in the cathelicidin and type 1 Interferon families. We found gene duplications for 18 genes, including 13 immune response genes and five non-immune response genes discovered in the annotation process. Manual annotation provided evidence for many new alternative splice variants and 8 gene duplications. Over 1,100 transcripts without porcine sequence evidence were detected using cross-species annotation. We used a functional approach to discover and accurately annotate porcine immune response genes. A co-expression clustering analysis of transcriptomic data from selected experimental infections or immune stimulations of blood, macrophages or lymph nodes identified a large cluster of genes that exhibited a correlated positive response upon infection across multiple pathogens or immune stimuli. Interestingly, this gene cluster (cluster 4) is enriched for known general human immune response genes, yet contains many un-annotated porcine genes. A phylogenetic analysis of the encoded proteins of cluster 4 genes showed that 15% exhibited an accelerated evolution as compared to 4.1% across the entire genome. CONCLUSIONS: This extensive annotation dramatically extends the genome-based knowledge of the molecular genetics and structure of a major portion of the porcine immunome. Our complementary functional approach using co-expression during immune response has provided new putative immune response annotation for over 500 porcine genes. Our phylogenetic analysis of this core immunome cluster confirms rapid evolutionary change in this set of genes, and that, as in other species, such genes are important components of the pig's adaptation to pathogen challenge over evolutionary time. These comprehensive and integrated analyses increase the value of the porcine genome sequence and provide important tools for global analyses and data-mining of the porcine immune response. PMCID: PMC3658956 Free PMC Article
	PMID: 23676093 [PubMed - indexed for MEDLINE]

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

Sent on Wednesday, 2013 October 30
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

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1.	Science. 2013 Oct 4;342(6154):1235587. doi: 10.1126/science.1235587. Integrative annotation of variants from 1092 humans: application to cancer genomics. Khurana E, Fu Y, Colonna V, Mu XJ, Kang HM, Lappalainen T, Sboner A, Lochovsky L, Chen J, Harmanci A, Das J, Abyzov A, Balasubramanian S, Beal K, Chakravarty D, Challis D, Chen Y, Clarke D, Clarke L, Cunningham F, Evani US, Flicek P, Fragoza R, Garrison E, Gibbs R, Gümüs ZH, Herrero J, Kitabayashi N, Kong Y, Lage K, Liluashvili V, Lipkin SM, MacArthur DG, Marth G, Muzny D, Pers TH, Ritchie GR, Rosenfeld JA, Sisu C, Wei X, Wilson M, Xue Y, Yu F; 1000 Genomes Project Consortium, Dermitzakis ET, Yu H, Rubin MA, Tyler-Smith C, Gerstein M, Abecasis GR, Auton A, Brooks LD, DePristo MA, Durbin RM, Handsaker RE, McVean GA. Collaborators: Altshuler DM, Durbin RM, Abecasis GR, Bentley DR, Chakravarti A, Clark AG, Donnelly P, Eichler EE, Flicek P, Gabriel SB, Gibbs RA, Green ED, Hurles ME, Knoppers BM, Korbel JO, Lander ES, Lee C, Lehrach H, Mardis ER, Marth GT, McVean GA, Nickerson DA, Schmidt JP, Sherry ST, Wang J, Wilson RK, Gibbs RA, Dinh H, Kovar C, Lee S, Lewis L, Muzny D, Reid J, Wang M, Wang J, Fang X, Guo X, Jian M, Jiang H, Jin X, Li G, Li J, Li Y, Li Z, Liu X, Lu Y, Ma X, Su Z, Tai S, Tang M, Wang B, Wang G, Wu H, Wu R, Yin Y, Zhang W, Zhao J, Zhao M, Zheng X, Zhou Y, Lander ES, Altshuler DM, Gabriel SB, Gupta N, Flicek P, Clarke L, Leinonen R, Smith RE, Zheng-Bradley X, Bentley DR, Grocock R, Humphray S, James T, Kingsbury Z, Lehrach H, Sudbrak R, Albrecht MW, Amstislavskiy VS, Borodina TA, Lienhard M, Mertes F, Sultan M, Timmermann B, Yaspo ML, Sherry ST, McVean GA, Mardis ER, Wilson RK, Fulton L, Fulton R, Weinstock GM, Durbin RM, Balasubramaniam S, Burton J, Danecek P, Keane TM, Kolb-Kokocinski A, McCarthy S, Stalker J, Quail M, Schmidt JP, Davies CJ, Gollub J, Webster T, Wong B, Zhan Y, Auton A, Gibbs RA, Yu F, Bainbridge M, Challis D, Evani US, Lu J, Muzny D, Nagaswamy U, Reid J, Sabo A, Wang Y, Yu J, Wang J, Coin LJ, Fang L, Guo X, Jin X, Li G, Li Q, Li Y, Li Z, Lin H, Liu B, Luo R, Qin N, Shao H, Wang B, Xie Y, Ye C, Yu C, Zhang F, Zheng H, Zhu H, Marth GT, Garrison EP, Kural D, Lee WP, Leong WF, Ward AN, Wu J, Zhang M, Lee C, Griffin L, Hsieh CH, Mills RE, Shi X, von Grotthuss M, Zhang C, Daly MJ, DePristo MA, Altshuler DM, Banks E, Bhatia G, Carneiro MO, del Angel G, Gabriel SB, Genovese G, Gupta N, Handsaker RE, Hartl C, Lander ES, McCarroll SA, Nemesh JC, Poplin RE, Schaffner SF, Shakir K, Yoon SC, Lihm J, Makarov V, Jin H, Kim W, Kim KC, Korbel JO, Rausch T, Flicek P, Beal K, Clarke L, Cunningham F, Herrero J, McLaren WM, Ritchie GR, Smith RE, Zheng-Bradley X, Clark AG, Gottipati S, Keinan A, Rodriguez-Flores JL, Sabeti PC, Grossman SR, Tabrizi S, Tariyal R, Cooper DN, Ball EV, Stenson PD, Bentley DR, Barnes B, Bauer M, Cheetham R, Cox T, Eberle M, Humphray S, Kahn S, Murray L , Peden J, Shaw R, Ye K, Batzer MA, Konkel MK, Walker JA, MacArthur DG, Lek M, Sudbrak R, Amstislavskiy VS, Herwig R, Shriver MD, Bustamante CD, Byrnes JK, De La Vega M, Gravel S, Kenny EE, Kidd JM, Lacroute P, Maples BK, Moreno-Estrada A, Zakharia F, Halperin E, Baran Y, Craig DW, Christoforides A, Homer N, Izatt T, Kurdoglu AA, Sinari SA, Squire K, Sherry ST, Xiao C, Sebat J, Bafna V, Ye K, Burchard EG, Hernandez RD, Gignoux CR, Haussler D, Katzman SJ, Kent W, Howie B, Ruiz-Linares A, Dermitzakis ET, Lappalainen T, Devine SE, Liu X, Maroo A, Tallon LJ, Rosenfeld JA, Michelson LP, Abecasis GR, Kang HM, Anderson P, Angius A, Bigham A, Blackwell T, Busonero F, Cucca F, Fuchsberger C, Jones C, Jun G, Li Y, Lyons R, Maschio A, Porcu E, Reinier F, Sanna S, Schlessinger D, Sidore C, Tan A, Trost MK, Awadalla P, Hodgkinson A, Lunter G, McVean GA, Marchini JL, Myers S, Churchhouse C, Delaneau O, Gupta-Hinch A, Iqbal Z, Mathieson I, Rimmer A, Xifara DK, Oleksyk TK, Fu Y, Liu X, Xiong M, Jorde L, Witherspoon D, Xing J, Eichler EE, Browning BL, Alkan C, Hajirasouliha I, Hormozdiari F, Ko A, Sudmant PH, Mardis ER, Chen K, Chinwalla A, Ding L, Dooling D, Koboldt DC, McLellan MD, Wallis JW, Wendl MC, Zhang Q, Durbin RM, Hurles ME, Tyler-Smith C, Albers CA, Ayub Q, Balasubramaniam S, Chen Y, Coffey AJ, Colonna V, Danecek P, Huang N, Jostins L, Keane TM, Li H, McCarthy S, Scally A, Stalker J, Walter K, Xue Y, Zhang Y, Gerstein MB, Abyzov A, Balasubramanian S, Chen J, Clarke D, Fu Y, Habegger L, Harmanci AO, Jin M, Khurana E, Mu XJ, Sisu C, Li Y, Luo R, Zhu H, Lee C, Griffin L, Hsieh CH, Mills RE, Shi X, von Grotthuss M, Zhang C, Marth GT, Garrison EP, Kural D, Lee WP, Ward AN, Wu J, Zhang M, McCarroll SA, Altshuler DM, Banks E, del Angel G, Genovese G, Handsaker RE, Hartl C, Nemesh JC, Shakir K, Yoon SC, Lihm J, Makarov V, Degenhardt J, Flicek P, Clarke L, Smith RE, Zheng-Bradley X, Korbel JO, Rausch T, Stütz AM, Bentley DR, Barnes B, Cheetham R, Eberle M, Humphray S, Kahn S, Murray L, Shaw R, Ye K, Batzer MA, Konkel MK, Walker JA, Lacroute P, Craig DW, Homer N, Church D, Xiao C, Sebat J, Bafna V, Michaelson JJ, Ye K, Devine SE, Liu X, Maroo A, Tallon LJ, Lunter G, McVean GA, Iqbal Z, Witherspoon D, Xing J, Eichler EE, Alkan C, Hajirasouliha I, Hormozdiari F, Ko A, Sudmant PH, Chen K, Chinwalla A, Ding L, McLellan MD, Wallis JW, Hurles ME, Blackburne B, Li H, Lindsay SJ, Ning Z, Scally A, Walter K, Zhang Y, Gerstein MB, Abyzov A, Chen J, Clarke D, Khurana E, Mu XJ, Sisu C, Gibbs RA, Yu F, Bainbridge M, Challis D, Evani US, Kovar C, Lewis L, Lu J, Muzny D, Nagaswamy U, Reid J, Sabo A, Yu J, Guo X, Li Y, Wu R, Marth GT, Garrison EP, Leong WF, Ward AN, del Angel G, DePristo MA, Gabriel SB, Gupta N, Hartl C, Poplin RE, Clark AG, Rodriguez-Flores JL, Flicek P, Clarke L, Smith RE, Zheng-Bradley X, MacArthur DG, Bustamante CD, Gravel S, Craig DW, Christoforides A, Homer N, Izatt T, Sherry ST, Xiao C, Dermitzakis ET, Abecasis GR, Kang HM, McVean GA, Mardis ER, Dooling D, Fulton L, Fulton R, Koboldt DC, Durbin RM, Balasubramaniam S, Keane TM, McCarthy S, Stalker J, Gerstein MB, Balasubramanian S, Habegger L, Garrison EP, Gibbs RA, Bainbridge M, Muzny D, Yu F, Yu J, del Angel G, Handsaker RE, Makarov V, Rodriguez-Flores JL, Jin H, Kim W, Kim KC, Flicek P, Beal K, Clarke L, Cunningham F, Herrero J, McLaren WM, Ritchie GR, Zheng-Bradley X, Tabrizi S, MacArthur DG, Lek M, Bustamante CD, De La Vega FM, Craig DW, Kurdoglu AA, Lappalainen T, Rosenfeld JA, Michelson LP, Awadalla P, Hodgkinson A, McVean GA, Chen K, Tyler-Smith C, Chen Y, Colonna V, Frankish A, Harrow J, Xue Y, Gerstein MB, Abyzov A, Balasubramanian S, Chen J, Clarke D, Fu Y, Harmanci AO, Jin M, Khurana E, Mu XJ, Sisu C, Gibbs RA, Kovar C, Kalra D, Hale W, Fowler G, Muzny D, Reid J, Wang J, Guo X, Li G, Li Y, Zheng X, Altshuler DM, Flicek P, Clarke L, Barker J, Kelman G, Kulesha E, Leinonen R, McLaren WM, Radhakrishnan R, Roa A, Smirnov D, Smith RE, Streeter I, Toneva I, Vaughan B, Zheng-Bradley X, Bentley DR, Cox T, Humphray S, Kahn S, Sudbrak R, Albrecht MW, Lienhard M, Craig DW, Izatt T, Kurdoglu AA, Sherry ST, Ananiev V, Belaia Z, Beloslyudtsev D, Bouk N, Chen C, Church D, Cohen R, Cook C, Garner J, Hefferon T, Kimelman M, Liu C, Lopez J, Meric P, O'Sullivan C, Ostapchuk Y, Phan L, Ponomarov S, Schneider V, Shekhtman E, Sirotkin K, Slotta D, Xiao C, Zhang H, Haussler D, Abecasis GR, McVean GA, Alkan C, Ko A, Dooling D, Durbin RM, Balasubramaniam S, Keane TM, McCarthy S, Stalker J, Chakravarti A, Knoppers BM, Abecasis GR, Barnes KC, Beiswanger C, Burchard E, Bustamante CD, Cai H, Cao H, Durbin RM, Gharani N, Gibbs RA, Gignoux CR, Gravel S, Henn B, Jones D, Jorde L, Kaye JS, Keinan A, Kent A, Kerasidou A, Li Y, Mathias R, McVean G, Moreno-Estrada A, Ossorio PN, Parker M, Reich D, Rotimi CN, Royal CD, Sandoval K, Su Y, Sudbrak R, Tian Z, Timmermann B, Tishkoff S, Toji LH, Tyler-Smith C, Via M, Wang Y, Yang H, Yang L, Zhu J, Bodmer W, Bedoya G, Ruiz-Linares A, Ming CZ, Yang G, You CJ, Peltonen L, Garcia-Montero A, Orfao A, Dutil J, Martinez-Cruzado JC, Oleksyk TK, Brooks LD, Felsenfeld AL, McEwen JE, Clemm NC, Duncanson A, Dunn M, Green ED, Guyer MS, Peterson JL. Program in Computational Biology and Bioinformatics, Yale University, New Haven, CT 06520, USA. Abstract Interpreting variants, especially noncoding ones, in the increasing number of personal genomes is challenging. We used patterns of polymorphisms in functionally annotated regions in 1092 humans to identify deleterious variants; then we experimentally validated candidates. We analyzed both coding and noncoding regions, with the former corroborating the latter. We found regions particularly sensitive to mutations ("ultrasensitive") and variants that are disruptive because of mechanistic effects on transcription-factor binding (that is, "motif-breakers"). We also found variants in regions with higher network centrality tend to be deleterious. Insertions and deletions followed a similar pattern to single-nucleotide variants, with some notable exceptions (e.g., certain deletions and enhancers). On the basis of these patterns, we developed a computational tool (FunSeq), whose application to ~90 cancer genomes reveals nearly a hundred candidate noncoding drivers.
	PMID: 24092746 [PubMed - indexed for MEDLINE]
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2.	Nature. 2013 Aug 22;500(7463):453-7. doi: 10.1038/nature12326. Epub 2013 Jul 21. Genomic evidence for ameiotic evolution in the bdelloid rotifer Adineta vaga. Flot JF, Hespeels B, Li X, Noel B, Arkhipova I, Danchin EG, Hejnol A, Henrissat B, Koszul R, Aury JM, Barbe V, Barthélémy RM, Bast J, Bazykin GA, Chabrol O, Couloux A, Da Rocha M, Da Silva C, Gladyshev E, Gouret P, Hallatschek O, Hecox-Lea B, Labadie K, Lejeune B, Piskurek O, Poulain J, Rodriguez F, Ryan JF, Vakhrusheva OA, Wajnberg E, Wirth B, Yushenova I, Kellis M, Kondrashov AS, Mark Welch DB, Pontarotti P, Weissenbach J, Wincker P, Jaillon O, Van Doninck K. University of Namur, Department of Biology, URBE, Laboratory of Evolutionary Genetics and Ecology, 5000 Namur, Belgium. jean-francois.flot@ds.mpg.de Abstract Loss of sexual reproduction is considered an evolutionary dead end for metazoans, but bdelloid rotifers challenge this view as they appear to have persisted asexually for millions of years. Neither male sex organs nor meiosis have ever been observed in these microscopic animals: oocytes are formed through mitotic divisions, with no reduction of chromosome number and no indication of chromosome pairing. However, current evidence does not exclude that they may engage in sex on rare, cryptic occasions. Here we report the genome of a bdelloid rotifer, Adineta vaga (Davis, 1873), and show that its structure is incompatible with conventional meiosis. At gene scale, the genome of A. vaga is tetraploid and comprises both anciently duplicated segments and less divergent allelic regions. However, in contrast to sexual species, the allelic regions are rearranged and sometimes even found on the same chromosome. Such structure does not allow meiotic pairing; instead, we find abundant evidence of gene conversion, which may limit the accumulation of deleterious mutations in the absence of meiosis. Gene families involved in resistance to oxidation, carbohydrate metabolism and defence against transposons are significantly expanded, which may explain why transposable elements cover only 3% of the assembled sequence. Furthermore, 8% of the genes are likely to be of non-metazoan origin and were probably acquired horizontally. This apparent convergence between bdelloids and prokaryotes sheds new light on the evolutionary significance of sex.
	PMID: 23873043 [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 Friday, 2013 October 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. 2013 Sep 20;341(6152):1390-4. doi: 10.1126/science.1244040. Epub 2013 Aug 29. Pivotal roles of cGAS-cGAMP signaling in antiviral defense and immune adjuvant effects. Li XD, Wu J, Gao D, Wang H, Sun L, Chen ZJ. Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9148, USA. Abstract Invasion of microbial DNA into the cytoplasm of animal cells triggers a cascade of host immune reactions that help clear the infection; however, self DNA in the cytoplasm can cause autoimmune diseases. Biochemical approaches led to the identification of cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) synthase (cGAS) as a cytosolic DNA sensor that triggers innate immune responses. Here, we show that cells from cGAS-deficient (cGas(-/-)) mice, including fibroblasts, macrophages, and dendritic cells, failed to produce type I interferons and other cytokines in response to DNA transfection or DNA virus infection. cGas(-/-) mice were more susceptible to lethal infection with herpes simplex virus 1 (HSV1) than wild-type mice. We also show that cGAMP is an adjuvant that boosts antigen-specific T cell activation and antibody production in mice.
	PMID: 23989956 [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, 2013 October 23
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 Oct 17;369(16):1572. doi: 10.1056/NEJMc1311596. Metagenomic analysis of tuberculosis--current limitations. Hingley-Wilson SM. University of Surrey, Guildford, United Kingdom s.hingley-wilson@surrey.ac.uk. Comment on Metagenomic analysis of tuberculosis in a mummy. [N Engl J Med. 2013] 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. N Engl J Med. 2013 Jul 18; 369(3):289-90.
	PMID: 24131193 [PubMed - indexed for MEDLINE]
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2.	N Engl J Med. 2013 Oct 3;369(14):1381-2. doi: 10.1056/NEJMc1301936. Primaquine failure and cytochrome P-450 2D6 in Plasmodium vivax malaria. Bennett JW, Pybus BS, Yadava A, Tosh D, Sousa JC, McCarthy WF, Deye G, Melendez V, Ockenhouse CF. Free Article
	PMID: 24088113 [PubMed - indexed for MEDLINE]
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3.	Science. 2013 Sep 6;341(6150):1078. doi: 10.1126/science.1244986. Retrospective. Tony Pawson (1952-2013). Hunter T. Salk Institute, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA. hunter@salk.edu
	PMID: 24009385 [PubMed - indexed for MEDLINE]
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4.	Nat Med. 2012 Aug;18(8):1217-23. doi: 10.1038/nm.2843. Epub 2012 Jul 22. The pulmonary endothelial glycocalyx regulates neutrophil adhesion and lung injury during experimental sepsis. Schmidt EP, Yang Y, Janssen WJ, Gandjeva A, Perez MJ, Barthel L, Zemans RL, Bowman JC, Koyanagi DE, Yunt ZX, Smith LP, Cheng SS, Overdier KH, Thompson KR, Geraci MW, Douglas IS, Pearse DB, Tuder RM. Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, Program in Translational Lung Research, University of Colorado School of Medicine, Aurora, Colorado, USA; Denver Health Medical Center, Denver, Colorado, USA. eric.schmidt@ucdenver.edu Abstract Sepsis, a systemic inflammatory response to infection, commonly progresses to acute lung injury (ALI), an inflammatory lung disease with high morbidity. We postulated that sepsis-associated ALI is initiated by degradation of the pulmonary endothelial glycocalyx, leading to neutrophil adherence and inflammation. Using intravital microscopy, we found that endotoxemia in mice rapidly induced pulmonary microvascular glycocalyx degradation via tumor necrosis factor-α (TNF-α)-dependent mechanisms. Glycocalyx degradation involved the specific loss of heparan sulfate and coincided with activation of endothelial heparanase, a TNF-α-responsive, heparan sulfate-specific glucuronidase. Glycocalyx degradation increased the availability of endothelial surface adhesion molecules to circulating microspheres and contributed to neutrophil adhesion. Heparanase inhibition prevented endotoxemia-associated glycocalyx loss and neutrophil adhesion and, accordingly, attenuated sepsis-induced ALI and mortality in mice. These findings are potentially relevant to human disease, as sepsis-associated respiratory failure in humans was associated with higher plasma heparan sulfate degradation activity; moreover, heparanase content was higher in human lung biopsies showing diffuse alveolar damage than in normal human lung tissue. PMCID: PMC3723751 Free PMC Article
	PMID: 22820644 [PubMed - indexed for MEDLINE]
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