What's new for 'JKB_daily1' in PubMed

This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
Do not reply directly to this message.

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

Sent on Wednesday, 2012 November 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]))

Click here to view complete results in PubMed (Results may change over time.)
To unsubscribe from these e-mail updates click here.

PubMed Results

Items 1 - 3 of 3

1.	Nat Med. 2012 Sep;18(9):1346-7. doi: 10.1038/nm.2930. The not-so-simple HDL story: A new era for quantifying HDL and cardiovascular risk? Heinecke JW. Department of Medicine, University of Washington, Seattle, Washington, USA. heinecke@u.washington.edu
	PMID: 22961165 [PubMed - indexed for MEDLINE]
	Related citations

2.	Nat Med. 2012 Sep;18(9):1344-6. doi: 10.1038/nm.2937. The not-so-simple HDL story: Is it time to revise the HDL cholesterol hypothesis? Rader DJ, Tall AR. Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. rader@mail.med.upenn.edu
	PMID: 22961164 [PubMed - indexed for MEDLINE]
	Related citations

3.	Nat Med. 2012 Sep;18(9):1434-40. On silico peptide microarrays for high-resolution mapping of antibody epitopes and diverse protein-protein interactions. Price JV, Tangsombatvisit S, Xu G, Yu J, Levy D, Baechler EC, Gozani O, Varma M, Utz PJ, Liu CL. Department of Medicine, Division of Immunology and Rheumatology, Stanford School of Medicine, Stanford, California, USA. Abstract We developed a new, silicon-based peptide array for a broad range of biological applications, including potential development as a real-time point-of-care platform. We used photolithography on silicon wafers to synthesize microarrays (Intel arrays) that contained every possible overlapping peptide within a linear protein sequence covering the N-terminal tail of human histone H2B. These arrays also included peptides with acetylated and methylated lysine residues, reflecting post-translational modifications of H2B. We defined minimum binding epitopes for commercial antibodies recognizing the modified and unmodified H2B peptides. We further found that this platform is suitable for the highly sensitive characterization of methyltransferases and kinase substrates. The Intel arrays also revealed specific H2B epitopes that are recognized by autoantibodies in individuals with systemic lupus erythematosus who have elevated disease severity. By combining emerging nonfluorescence-based detection methods with an underlying integrated circuit, we are now poised to create a truly transformative proteomics platform with applications in bioscience, drug development and clinical diagnostics. PMCID: PMC3491111 [Available on 2013/3/1]
	PMID: 22902875 [PubMed - indexed for MEDLINE]
	Related citations

What's new for 'JKB_daily1' in PubMed

This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
Do not reply directly to this message.

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

Sent on Tuesday, 2012 November 13
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]))

Click here to view complete results in PubMed (Results may change over time.)
To unsubscribe from these e-mail updates click here.

PubMed Results

Items 1 - 5 of 5

1.	Nature. 2012 Sep 27;489(7417):550-3. doi: 10.1038/nature11440. Response of salt-marsh carbon accumulation to climate change. Kirwan ML, Mudd SM. Department of Environmental Sciences, University of Virginia, PO Box 400123, Charlottesville, Virginia 24151, USA. mlk4n@virginia.edu Abstract About half of annual marine carbon burial takes place in shallow water ecosystems where geomorphic and ecological stability is driven by interactions between the flow of water, vegetation growth and sediment transport. Although the sensitivity of terrestrial and deep marine carbon pools to climate change has been studied for decades, there is little understanding of how coastal carbon accumulation rates will change and potentially feed back on climate. Here we develop a numerical model of salt marsh evolution, informed by recent measurements of productivity and decomposition, and demonstrate that competition between mineral sediment deposition and organic-matter accumulation determines the net impact of climate change on carbon accumulation in intertidal wetlands. We find that the direct impact of warming on soil carbon accumulation rates is more subtle than the impact of warming-driven sea level rise, although the impact of warming increases with increasing rates of sea level rise. Our simulations suggest that the net impact of climate change will be to increase carbon burial rates in the first half of the twenty-first century, but that carbon-climate feedbacks are likely to diminish over time.
	PMID: 23018965 [PubMed - indexed for MEDLINE]
	Related citations

2.	Nature. 2012 Sep 27;489(7417):485-6. doi: 10.1038/489485a. China buys US sequencing firm. Baker M.
	PMID: 23018943 [PubMed - indexed for MEDLINE]
	Related citations

3.	Nature. 2012 Sep 27;489(7417):513-8. doi: 10.1038/nature11514. Epub 2012 Sep 19. Genomic analysis of a key innovation in an experimental Escherichia coli population. Blount ZD, Barrick JE, Davidson CJ, Lenski RE. Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan 48824, USA. blountza@msu.edu Comment in Evolution: How the unicorn got its horn. [Nature. 2012] Evolution: How the unicorn got its horn.Hendrickson H, Rainey PB. Nature. 2012 Sep 27; 489(7417):504-5. Epub 2012 Sep 19. Abstract Evolutionary novelties have been important in the history of life, but their origins are usually difficult to examine in detail. We previously described the evolution of a novel trait, aerobic citrate utilization (Cit(+)), in an experimental population of Escherichia coli. Here we analyse genome sequences to investigate the history and genetic basis of this trait. At least three distinct clades coexisted for more than 10,000 generations before its emergence. The Cit(+) trait originated in one clade by a tandem duplication that captured an aerobically expressed promoter for the expression of a previously silent citrate transporter. The clades varied in their propensity to evolve this novel trait, although genotypes able to do so existed in all three clades, implying that multiple potentiating mutations arose during the population's history. Our findings illustrate the importance of promoter capture and altered gene regulation in mediating the exaptation events that often underlie evolutionary innovations. PMCID: PMC3461117 [Available on 2013/3/27]
	PMID: 22992527 [PubMed - indexed for MEDLINE]
	Related citations

4.	Nature. 2012 Sep 27;489(7417):504-5. doi: 10.1038/nature11487. Epub 2012 Sep 19. Evolution: How the unicorn got its horn. Hendrickson H, Rainey PB. Comment on Genomic analysis of a key innovation in an experimental Escherichia coli population. [Nature. 2012] Genomic analysis of a key innovation in an experimental Escherichia coli population.Blount ZD, Barrick JE, Davidson CJ, Lenski RE. Nature. 2012 Sep 27; 489(7417):513-8. Epub 2012 Sep 19.
	PMID: 22992522 [PubMed - indexed for MEDLINE]
	Related citations

5.	Nature. 2012 Sep 27;489(7417):519-25. doi: 10.1038/nature11404. Epub 2012 Sep 9. Comprehensive genomic characterization of squamous cell lung cancers. Cancer Genome Atlas Research Network, Hammerman PS, Hayes DN, Wilkerson MD, Schultz N, Bose R, Chu A, Collisson EA, Cope L, Creighton CJ, Getz G , Herman JG, Johnson BE, Kucherlapati R, Ladanyi M, Maher CA, Robertson G, Sander C, Shen R, Sinha R, Sivachenko A, Thomas RK, Travis WD, Tsao MS, Weinstein JN, Wigle DA, Baylin SB, Govindan R, Meyerson M. Collaborators: Hammerman PS, Lawrence MS, Voet D, Jing R, Cibulskis K, Sivachenko A, Stojanov P, McKenna A, Lander ES, Gabriel S, Getz G, Sougnez C, Imielinski M, Helman E, Hernandez B, Pho NH, Meyerson M, Chu A, Chun HJ, Mungall AJ, Pleasance E, Robertson A, Sipahimalani P, Stoll D, Balasundaram M, Birol I, Butterfield YS, Chuah E, Coope RJ, Corbett R, Dhalla N, Guin R, He A, Hirst C, Hirst M, Holt RA , Lee D, Li HI, Mayo M, Moore RA, Mungall K, Nip KM, Olshen A, Schein JE, Slobodan JR, Tam A, Thiessen N, Varhol R, Zeng T, Zhao Y, Jones SJ, Marra MA, Saksena G, Cherniack AD, Schumacher SE, Tabak B, Carter SL, Pho NH, Nguyen H, Onofrio RC, Crenshaw A, Ardlie K, Beroukhim R, Winckler W, Hammerman PS, Getz G, Meyerson M, Protopopov A, Zhang J, Hadjipanayis A, Lee S, Xi R, Yang L, Ren X, Zhang H, Shukla S, Chen PC, Haseley P, Lee E, Chin L, Park PJ, Kucherlapati R, Socci ND, Liang Y, Schultz N, Borsu L, Lash AE, Viale A, Sander C, Ladanyi M, Auman T, Hoadley KA, Wilkerson MD, Shi Y, Liquori C, Meng S, Li L, Turman YJ, Topal MD, Tan D, Waring S, Buda E, Walsh J, Jones CD, Mieczkowski PA, Singh D, Wu J, Gulabani A, Dolina P, Bodenheimer T, Hoyle AP, Simons JV, Soloway MG, Mose LE, Jefferys SR, Balu S, O'Connor BD, Prins JF, Liu J, Chiang DY, Hayes D, Perou CM, Cope L, Danilova L, Weisenberger DJ, Maglinte DT, Pan F, Van Den Berg DJ, Triche T Jr, Herman JG, Baylin SB, Laird PW, Getz G, Noble M, Voet D, Saksena G, Gehlenborg N, DiCara D, Zhang J, Zhang H, Wu CJ, Liu SY, Lawrence MS, Zou L, Sivachenko A, Lin P, Stojanov P, Jing R, Cho J, Nazaire MD, Robinson J, Thorvaldsdottir H, Mesirov J, Park PJ, Chin L, Schultz N, Sinha R, Ciriello G, Cerami E, Gross B, Jacobsen A, Gao J, Aksoy B, Weinhold N, Ramirez R, Taylor BS, Antipin Y, Reva B, Shen R, Mo Q, Seshan V, Paik PK, Ladanyi M, Sander C, Akbani R, Zhang N, Broom BM, Casasent T, Unruh A, Wakefield C, Cason R, Baggerly KA, Weinstein JN, Haussler D, Benz CC, Stuart JM, Zhu J, Szeto C, Scott GK, Yau C, Ng S, Goldstein T, Waltman P, Sokolov A, Ellrott K, Collisson EA, Zerbino D, Wilks C, Ma S, Craft B, Wilkerson MD, Auman J, Hoadley KA, Du Y, Cabanski C, Walter V, Singh D, Wu J, Gulabani A, Bodenheimer T, Hoyle AP, Simons JV, Soloway MG, Mose LE, Jefferys SR, Balu S, Marron J, Liu Y, Wang K, Liu J, Prins JF, Hayes D, Perou CM, Creighton CJ, Zhang Y, Travis WD, Rekhtman N, Yi J, Aubry MC, Cheney R, Dacic S, Flieder D, Funkhouser W, Illei P, Myers J, Tsao MS, Penny R, Mallery D, Shelton T, Hatfield M, Morris S, Yena P, Shelton C, Sherman M, Paulauskis J, Meyerson M, Baylin SB, Govindan R, Akbani R, Azodo I, Beer D, Bose R, Byers LA, Carbone D, Chang LW, Chiang D, Chu A, Chun E, Collisson E, Cope L, Creighton CJ, Danilova L, Ding L, Getz G, Hammerman PS, Hayes D, Hernandez B, Herman JG, Heymach J, Ida C, Imielinski M, Johnson B, Jurisica I, Kaufman J, Kosari F, Kucherlapati R, Kwiatkowski D, Ladanyi M, Lawrence MS, Maher CA, Mungall A, Ng S, Pao W, Peifer M, Penny R, Robertson G, Rusch V, Sander C, Schultz N, Shen R, Siegfried J, Sinha R, Sivachenko A, Sougnez C, Stoll D, Stuart J, Thomas RK, Tomaszek S, Tsao MS, Travis WD, Vaske C, Weinstein JN, Weisenberger D, Wheeler D, Wigle DA, Wilkerson MD, Wilks C, Yang P, Zhang JJ, Jensen MA, Sfeir R, Kahn AB, Chu AL, Kothiyal P, Wang Z, Snyder EE, Pontius J, Pihl TD, Ayala B, Backus M, Walton J, Baboud J, Berton DL, Nicholls MC, Srinivasan D, Raman R, Girshik S, Kigonya PA, Alonso S, Sanbhadti RN, Barletta SP, Greene JM, Pot DA, Tsao MS, Bandarchi-Chamkhaleh B, Boyd J, Weaver J, Wigle DA, Azodo IA, Tomaszek SC, Aubry MC, Ida CM, Yang P, Kosari F, Brock MV, Rogers K, Rutledge M, Brown T, Lee B, Shin J, Trusty D, Dhir R, Siegfried JM, Potapova O, Fedosenko KV, Nemirovich-Danchenko E, Rusch V, Zakowski M, Iacocca MV, Brown J, Rabeno B, Czerwinski C, Petrelli N, Fan Z, Todaro N, Eckman J, Myers J, Rathmell W, Thorne LB, Huang M, Boice L, Hill A, Penny R, Mallery D, Curley E, Shelton C, Yena P, Morrison C, Gaudioso C, Bartlett JM, Kodeeswaran S, Zanke B, Sekhon H, David K, Juhl H, Van Le X, Kohl B, Thorp R, Nguyen VT, Nguyen VB, Sussman H, Phu BD, Hajek R, Nguyen PH, Khan KZ, Muley T, Shaw KR, Sheth M, Yang L, Buetow K, Davidsen T, Demchok JA, Eley G, Ferguson M, Dillon LA, Schaefer C, Guyer MS, Ozenberger BA, Palchik JD, Peterson J, Sofia HJ, Thomson E. Eli and Edythe L. Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts 02142, USA. Abstract Lung squamous cell carcinoma is a common type of lung cancer, causing approximately 400,000 deaths per year worldwide. Genomic alterations in squamous cell lung cancers have not been comprehensively characterized, and no molecularly targeted agents have been specifically developed for its treatment. As part of The Cancer Genome Atlas, here we profile 178 lung squamous cell carcinomas to provide a comprehensive landscape of genomic and epigenomic alterations. We show that the tumour type is characterized by complex genomic alterations, with a mean of 360 exonic mutations, 165 genomic rearrangements, and 323 segments of copy number alteration per tumour. We find statistically recurrent mutations in 11 genes, including mutation of TP53 in nearly all specimens. Previously unreported loss-of-function mutations are seen in the HLA-A class I major histocompatibility gene. Significantly altered pathways included NFE2L2 and KEAP1 in 34%, squamous differentiation genes in 44%, phosphatidylinositol-3-OH kinase pathway genes in 47%, and CDKN2A and RB1 in 72% of tumours. We identified a potential therapeutic target in most tumours, offering new avenues of investigation for the treatment of squamous cell lung cancers. PMCID: PMC3466113 [Available on 2013/3/27]
	PMID: 22960745 [PubMed - indexed for MEDLINE]
	Related citations

What's new for 'JKB_daily1' in PubMed

This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
Do not reply directly to this message.

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

Sent on Wednesday, 2012 November 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]))

Click here to view complete results in PubMed (Results may change over time.)
To unsubscribe from these e-mail updates click here.

PubMed Results

Items 1 - 4 of 4

1.	Nature. 2012 Oct 11;490(7419):144. Fighting chance. [No authors listed]
	PMID: 23066547 [PubMed - indexed for MEDLINE]
	Related citations

2.	Nature. 2012 Oct 11;490(7419):143-4. Share alike. [No authors listed]
	PMID: 23066546 [PubMed - indexed for MEDLINE]
	Related citations

3.	Nature. 2012 Oct 11;490(7419):154-5. doi: 10.1038/490154a. Economics and genetics meet in uneasy union. Callaway E.
	PMID: 23060165 [PubMed - indexed for MEDLINE]
	Related citations

4.	Nature. 2012 Oct 11;490(7419):288-91. doi: 10.1038/nature11419. Epub 2012 Aug 15. Caspase-11 increases susceptibility to Salmonella infection in the absence of caspase-1. Broz P, Ruby T, Belhocine K, Bouley DM, Kayagaki N, Dixit VM, Monack DM. Department of Microbiology and Immunology, Stanford School of Medicine, Stanford University, California 94305, USA. Abstract Inflammasomes are cytosolic multiprotein complexes assembled by intracellular nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) and they initiate innate immune responses to invading pathogens and danger signals by activating caspase-1 (ref. 1). Caspase-1 activation leads to the maturation and release of the pro-inflammatory cytokines interleukin (IL)-1β and IL-18, as well as lytic inflammatory cell death known as pyroptosis. Recently, a new non-canonical inflammasome was described that activates caspase-11, a pro-inflammatory caspase required for lipopolysaccharide-induced lethality. This study also highlighted that previously generated caspase-1 knockout mice lack a functional allele of Casp11 (also known as Casp4), making them functionally Casp1 Casp11 double knockouts. Previous studies have shown that these mice are more susceptible to infections with microbial pathogens, including the bacterial pathogen Salmonella enterica serovar Typhimurium (S. typhimurium), but the individual contributions of caspase-1 and caspase-11 to this phenotype are not known. Here we show that non-canonical caspase-11 activation contributes to macrophage death during S. typhimurium infection. Toll-like receptor 4 (TLR4)-dependent and TIR-domain-containing adaptor-inducing interferon-β (TRIF)-dependent interferon-β production is crucial for caspase-11 activation in macrophages, but is only partially required for pro-caspase-11 expression, consistent with the existence of an interferon-inducible activator of caspase-11. Furthermore, Casp1(-/-) mice were significantly more susceptible to infection with S. typhimurium than mice lacking both pro-inflammatory caspases (Casp1(-/-) Casp11(-/-)). This phenotype was accompanied by higher bacterial counts, the formation of extracellular bacterial microcolonies in the infected tissue and a defect in neutrophil-mediated clearance. These results indicate that caspase-11-dependent cell death is detrimental to the host in the absence of caspase-1-mediated innate immunity, resulting in extracellular replication of a facultative intracellular bacterial pathogen. PMCID: PMC3470772 [Available on 2013/4/11]
	PMID: 22895188 [PubMed - indexed for MEDLINE]
	Related citations

What's new for 'JKB_daily1' in PubMed

This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
Do not reply directly to this message.

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

Sent on Tuesday, 2012 November 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]))

Click here to view complete results in PubMed (Results may change over time.)
To unsubscribe from these e-mail updates click here.

PubMed Results

Items 1 - 6 of 6

1.	Nature. 2012 Sep 13;489(7415):250-6. doi: 10.1038/nature11553. Genomic approaches to studying the human microbiota. Weinstock GM. The Genome Institute, Washington University, St. Louis, Missouri 63108, USA. gweinsto@genome.wustl.edu Abstract The human body is colonized by a vast array of microbes, which form communities of bacteria, viruses and microbial eukaryotes that are specific to each anatomical environment. Every community must be studied as a whole because many organisms have never been cultured independently, and this poses formidable challenges. The advent of next-generation DNA sequencing has allowed more sophisticated analysis and sampling of these complex systems by culture-independent methods. These methods are revealing differences in community structure between anatomical sites, between individuals, and between healthy and diseased states, and are transforming our view of human biology.
	PMID: 22972298 [PubMed - indexed for MEDLINE]
	Related citations

2.	Nature. 2012 Sep 13;489(7415):219. doi: 10.1038/489219a. Gut microbes and health. Lupp C, Skipper M, Weiss U.
	PMID: 22972294 [PubMed - indexed for MEDLINE]
	Related citations

3.	Nature. 2012 Sep 13;489(7415):208. doi: 10.1038/489208b. Genomics: ENCODE leads the way on big data. Gerstein M.
	PMID: 22972285 [PubMed - indexed for MEDLINE]
	Related citations

4.	Nature. 2012 Sep 13;489(7415):194-6. doi: 10.1038/489194a. Deep-sea research: Dive master. Monastersky R.
	PMID: 22972276 [PubMed - indexed for MEDLINE]
	Related citations

5.	Nat Genet. 2012 Jun 3;44(7):808-11. doi: 10.1038/ng.2309. Comparative population genomics of maize domestication and improvement. Hufford MB, Xu X, van Heerwaarden J, Pyhäjärvi T, Chia JM, Cartwright RA, Elshire RJ, Glaubitz JC, Guill KE, Kaeppler SM, Lai J, Morrell PL, Shannon LM, Song C, Springer NM, Swanson-Wagner RA, Tiffin P, Wang J, Zhang G, Doebley J, McMullen MD, Ware D, Buckler ES, Yang S, Ross-Ibarra J. Department of Plant Sciences, University of California, Davis, California, USA. Comment in A crop of maize variants. [Nat Genet. 2012] A crop of maize variants.Huang X, Han B. Nat Genet. 2012 Jun 27; 44(7):734-5. Epub 2012 Jun 27. Abstract Domestication and plant breeding are ongoing 10,000-year-old evolutionary experiments that have radically altered wild species to meet human needs. Maize has undergone a particularly striking transformation. Researchers have sought for decades to identify the genes underlying maize evolution, but these efforts have been limited in scope. Here, we report a comprehensive assessment of the evolution of modern maize based on the genome-wide resequencing of 75 wild, landrace and improved maize lines. We find evidence of recovery of diversity after domestication, likely introgression from wild relatives, and evidence for stronger selection during domestication than improvement. We identify a number of genes with stronger signals of selection than those previously shown to underlie major morphological changes. Finally, through transcriptome-wide analysis of gene expression, we find evidence both consistent with removal of cis-acting variation during maize domestication and improvement and suggestive of modern breeding having increased dominance in expression while targeting highly expressed genes.
	PMID: 22660546 [PubMed - indexed for MEDLINE]
	Related citations

6.	Nat Genet. 2012 Jun 3;44(7):803-7. doi: 10.1038/ng.2313. Maize HapMap2 identifies extant variation from a genome in flux. Chia JM, Song C, Bradbury PJ, Costich D, de Leon N, Doebley J, Elshire RJ, Gaut B, Geller L, Glaubitz JC, Gore M, Guill KE, Holland J, Hufford MB, Lai J, Li M, Liu X, Lu Y, McCombie R, Nelson R, Poland J, Prasanna BM, Pyhäjärvi T, Rong T, Sekhon RS, Sun Q, Tenaillon MI, Tian F, Wang J, Xu X, Zhang Z, Kaeppler SM, Ross-Ibarra J, McMullen MD, Buckler ES, Zhang G, Xu Y, Ware D. Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, USA. Comment in A crop of maize variants. [Nat Genet. 2012] A crop of maize variants.Huang X, Han B. Nat Genet. 2012 Jun 27; 44(7):734-5. Epub 2012 Jun 27. Abstract Whereas breeders have exploited diversity in maize for yield improvements, there has been limited progress in using beneficial alleles in undomesticated varieties. Characterizing standing variation in this complex genome has been challenging, with only a small fraction of it described to date. Using a population genetics scoring model, we identified 55 million SNPs in 103 lines across pre-domestication and domesticated Zea mays varieties, including a representative from the sister genus Tripsacum. We find that structural variations are pervasive in the Z. mays genome and are enriched at loci associated with important traits. By investigating the drivers of genome size variation, we find that the larger Tripsacum genome can be explained by transposable element abundance rather than an allopolyploid origin. In contrast, intraspecies genome size variation seems to be controlled by chromosomal knob content. There is tremendous overlap in key gene content in maize and Tripsacum, suggesting that adaptations from Tripsacum (for example, perennialism and frost and drought tolerance) can likely be integrated into maize.
	PMID: 22660545 [PubMed - indexed for MEDLINE]
	Related citations

What's new for 'JKB_daily1' in PubMed

This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
Do not reply directly to this message.

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

Sent on Saturday, 2012 November 03
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]))

Click here to view complete results in PubMed (Results may change over time.)
To unsubscribe from these e-mail updates click here.

PubMed Results

Items 1 - 2 of 2

1.	Science. 2012 Feb 3;335(6068):516-9. doi: 10.1126/science.335.6068.516. Genomics. China's sequencing powerhouse comes of age. Normile D.
	PMID: 22301291 [PubMed - indexed for MEDLINE]
	Related citations

2.	Science. 2012 Feb 3;335(6068):597-601. doi: 10.1126/science.1215173. Epub 2012 Jan 12. Innate response activator B cells protect against microbial sepsis. Rauch PJ, Chudnovskiy A, Robbins CS, Weber GF, Etzrodt M, Hilgendorf I, Tiglao E, Figueiredo JL, Iwamoto Y, Theurl I, Gorbatov R, Waring MT, Chicoine AT, Mouded M, Pittet MJ, Nahrendorf M, Weissleder R, Swirski FK. Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Abstract Recognition and clearance of a bacterial infection are a fundamental properties of innate immunity. Here, we describe an effector B cell population that protects against microbial sepsis. Innate response activator (IRA) B cells are phenotypically and functionally distinct, develop and diverge from B1a B cells, depend on pattern-recognition receptors, and produce granulocyte-macrophage colony-stimulating factor. Specific deletion of IRA B cell activity impairs bacterial clearance, elicits a cytokine storm, and precipitates septic shock. These observations enrich our understanding of innate immunity, position IRA B cells as gatekeepers of bacterial infection, and identify new treatment avenues for infectious diseases. PMCID: PMC3279743 Free PMC Article
	PMID: 22245738 [PubMed - indexed for MEDLINE]
	Related citations

What's new for 'JKB_daily1' in PubMed

This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
Do not reply directly to this message.

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

Sent on Thursday, 2012 November 01
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]))

Click here to view complete results in PubMed (Results may change over time.)
To unsubscribe from these e-mail updates click here.

PubMed Results

Item 1 of 1

1.	J Leukoc Biol. 2012 Sep;92(3):433-44. doi: 10.1189/jlb.0312166. Epub 2012 Jul 5. Plenary perspective: the complexity of constitutive and inducible gene expression in mononuclear phagocytes. Hume DA. The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Scotland, United Kingdom. David.Hume@roslin.ed.ac.uk Abstract Monocytes and macrophages differentiate from progenitor cells under the influence of colony-stimulating factors. Genome-scale data have enabled the identification of the set of genes that distinguishes macrophages from other cell types and the ways in which thousands of genes are regulated in response to pathogen challenge. Although there has been a focus on a small subset of lineage-enriched transcription factors, such as PU.1, more than one-half of the transcription factors in the genome can be expressed in macrophage lineage cells under some state of activation, and they interact in a complex network. The network architecture is conserved across species, but many of the target genes evolve rapidly and differ between mouse and human. The data and publication deluge related to macrophage biology require the development of new analytical tools and ways of presenting information in an accessible form. PMCID: PMC3427611 [Available on 2013/9/1]
	PMID: 22773680 [PubMed - indexed for MEDLINE]