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

Sent on Saturday, 2011 Feb 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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PubMed Results

Items 1 - 3 of 3

1.	Nat Med. 2011 Jan;17(1):7. Funds go toward biomedical business incubators in Mexico. Vargas-Parada L.
	PMID: 21217656 [PubMed - indexed for MEDLINE]
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2.	Nat Med. 2011 Jan;17(1):123-9. Epub 2010 Dec 12. Tumor-specific imaging through progression elevated gene-3 promoter-driven gene expression. Bhang HE, Gabrielson KL, Laterra J, Fisher PB, Pomper MG. Department of Pharmacology and Molecular Sciences, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA. Abstract Molecular-genetic imaging is advancing from a valuable preclinical tool to a guide for patient management. The strategy involves pairing an imaging reporter gene with a complementary imaging agent in a system that can be used to measure gene expression or protein interaction or track gene-tagged cells in vivo. Tissue-specific promoters can be used to delineate gene expression in certain tissues, particularly when coupled with an appropriate amplification mechanism. Here we show that the progression elevated gene-3 (PEG-3) promoter, derived from a rodent gene mediating tumor progression and metastatic phenotypes, can be used to drive imaging reporters selectively to enable detection of micrometastatic disease in mouse models of human melanoma and breast cancer using bioluminescence and radionuclide-based molecular imaging techniques. Because of its strong promoter activity, tumor specificity and capacity for clinical translation, PEG-3 promoter-driven gene expression may represent a practical, new system for facilitating cancer imaging and therapy.
	PMID: 21151140 [PubMed - indexed for MEDLINE]
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3.	Nat Med. 2011 Jan;17(1):64-70. Epub 2010 Dec 5. MicroRNA-124 promotes microglia quiescence and suppresses EAE by deactivating macrophages via the C/EBP-α-PU.1 pathway. Ponomarev ED, Veremeyko T, Barteneva N, Krichevsky AM, Weiner HL. Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. Comment in: Nat Rev Neurosci. 2011 Feb;12(2):61. Abstract MicroRNAs are a family of regulatory molecules involved in many physiological processes, including differentiation and activation of cells of the immune system. We found that brain-specific miR-124 is expressed in microglia but not in peripheral monocytes or macrophages. When overexpressed in macrophages, miR-124 directly inhibited the transcription factor CCAAT/enhancer-binding protein-α (C/EBP-α) and its downstream target PU.1, resulting in transformation of these cells from an activated phenotype into a quiescent CD45(low), major histocompatibility complex (MHC) class II(low) phenotype resembling resting microglia. During experimental autoimmune encephalomyelitis (EAE), miR-124 was downregulated in activated microglia. Peripheral administration of miR-124 in EAE caused systemic deactivation of macrophages, reduced activation of myelin-specific T cells and marked suppression of disease. Conversely, knockdown of miR-124 in microglia and macrophages resulted in activation of these cells in vitro and in vivo. These findings identify miR-124 both as a key regulator of microglia quiescence in the central nervous system and as a previously unknown modulator of monocyte and macrophage activation.
	PMID: 21131957 [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 Wednesday, 2011 Feb 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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Item 1 of 1

1.	Nature. 2011 Feb 3;470(7332):59-65. Mapping copy number variation by population-scale genome sequencing. Mills RE, Walter K, Stewart C, Handsaker RE, Chen K, Alkan C, Abyzov A, Yoon SC, Ye K, Cheetham RK, Chinwalla A, Conrad DF, Fu Y, Grubert F, Hajirasouliha I, Hormozdiari F, Iakoucheva LM, Iqbal Z, Kang S, Kidd JM, Konkel MK, Korn J, Khurana E, Kural D, Lam HY, Leng J, Li R, Li Y, Lin CY, Luo R, Mu XJ, Nemesh J, Peckham HE, Rausch T, Scally A, Shi X, Stromberg MP, Stütz AM, Urban AE, Walker JA, Wu J, Zhang Y, Zhang ZD, Batzer MA, Ding L, Marth GT, McVean G, Sebat J, Snyder M, Wang J, Ye K, Eichler EE, Gerstein MB, Hurles ME, Lee C, McCarroll SA, Korbel JO; 1000 Genomes Project. Collaborators: Altshuler DL, Durbin RM, Abecasis GR, Bentley DR, Chakravarti A, Clark AG, Collins FS, De La Vega FM, Donnelly P, Egholm M, Flicek P, Gabriel SB, Gibbs RA, Knoppers BM, Lander ES, Lehrach H, Mardis ER, McVean GA, Nickerson DA, Peltonen L, Schafer AJ, Sherry ST, Wang J, Wilson RK, Gibbs RA, Deiros D, Metzker M, Muzny D, Reid J, Wheeler D, Wang J, Li J, Jian M, Li G, Li R, Liang H, Tian G, Wang B, Wang J, Wang W, Yang H, Zhang X, Zheng H, Lander ES, Altshuler DL, Ambrogio L, Bloom T, Cibulskis K, Fennell TJ, Gabriel SB, Jaffe DB, Shefler E, Sougnez CL, Bentley DR, Gormley N, Humphray S, Kingsbury Z, Koko-Gonzales P, Stone J, McKernan KJ, Costa GL, Ichikawa JK, Lee CC, Sudbrak R, Lehrach H, Borodina TA, Dahl A, Davydov AN, Marquardt P, Mertes F, Nietfeld W, Rosenstiel P, Schreiber S, Soldatov AV, Timmermann B, Tolzmann M, Egholm M, Affourtit J, Ashworth D, Attiya S, Bachorski M, Buglione E, Burke A, Caprio A, Celone C, Clark S, Conners D, Desany B, Gu L, Guccione L, Kao K, Kebbel A, Knowlton J, Labrecque M, McDade L, Mealmaker C, Minderman M, Nawrocki A, Niazi F, Pareja K, Ramenani R, Riches D, Song W, Turcotte C, Wang S, Mardis ER, Wilson RK, Dooling D, Fulton L, Fulton R, Weinstock G, Durbin RM, Burton J, Carter DM, Churcher C, Coffey A, Cox A, Palotie A, Quail M, Skelly T, Stalker J, Swerdlow HP, Turner D, De Witte A, Giles S, Gibbs RA, Wheeler D, Bainbridge M, Challis D, Sabo A, Yu F, Yu J, Wang J, Fang X, Guo X, Li R, Li Y, Luo R, Tai S, Wu H, Zheng H, Zheng X, Zhou Y, Li G, Wang J, Yang H, Marth GT, Garrison EP, Huang W, Indap A, Kural D, Lee WP, Leong WF, Quinlan AR, Stewart C, Stromberg MP, Ward AN, Wu J, Lee C, Mills RE, Shi X, Daly MJ, DePristo MA, Altshuler DL, Ball AD, Banks E, Bloom T, Browning BL, Cibulskis K, Fennell TJ, Garimella KV, Grossman SR, Handsaker RE, Hanna M, Hartl C, Jaffe DB, Kernytsky AM, Korn JM, Li H, Maguire JR, McCarroll SA, McKenna A, Nemesh JC, Philippakis AA, Poplin RE, Price A, Rivas MA, Sabeti PC, Schaffner SF, Shefler E, Shlyakhter IA, Cooper DN, Ball EV, Mort M, Phillips AD, Stenson PD, Sebat J, Makarov V, Ye K, Yoon SC, Bustamante CD, Clark AG, Boyko A, Degenhardt J, Gravel S, Gutenkunst RN, Kaganovich M, Keinan A, Lacroute P, Ma X, Reynolds A, Clarke L, Flicek P, Cunningham F, Herrero J, Keenen S, Kulesha E, Leinonen R, McLaren WM, Radhakrishnan R, Smith RE, Zalunin V, Zheng-Bradley X, Korbel JO, Stütz AM, Humphray S, Bauer M, Cheetham RK, Cox T, Eberle M, James T, Kahn S, Murray L, Chakravarti A, Ye K, De La Vega FM, Fu Y, Hyland FC, Manning JM, McLaughlin SF, Peckham HE, Sakarya O, Sun YA, Tsung EF, Batzer MA, Konkel MK, Walker JA, Sudbrak R, Albrecht MW, Amstislavskiy VS, Herwig R, Parkhomchuk DV, Sherry ST, Agarwala R, Khouri H, Morgulis AO, Paschall JE, Phan LD, Rotmistrovsky KE, Sanders RD, Shumway MF, Xiao C, McVean GA, Auton A, Iqbal Z, Lunter G, Marchini JL, Moutsianas L, Myers S, Tumian A, Desany B, Knight J, Winer R, Craig DW, Beckstrom-Sternberg SM, Christoforides A, Kurdoglu AA, Pearson JV, Sinari SA, Tembe WD, Haussler D, Hinrichs AS, Katzman SJ, Kern A, Kuhn RM, Przeworski M, Hernandez RD, Howie B, Kelley JL, Melton SC, Abecasis GR, Li Y, Anderson P, Blackwell T, Chen W, Cookson WO, Ding J, Kang HM, Lathrop M, Liang L, Moffatt MF, Scheet P, Sidore C, Snyder M, Zhan X, Zöllner S, Awadalla P, Casals F, Idaghdour Y, Keebler J, Stone EA, Zilversmit M, Jorde L, Xing J, Eichler EE, Aksay G, Alkan C, Hajirasouliha I, Hormozdiari F, Kidd JM, Sahinalp SC, Sudmant PH, Mardis ER, Chen K, Chinwalla A, Ding L, Koboldt DC, McLellan MD, Dooling D, Weinstock G, Wallis JW, Wendl MC, Zhang Q, Durbin RM, Albers CA, Ayub Q, Balasubramaniam S, Barrett JC, Carter DM, Chen Y, Conrad DF, Danecek P, Dermitzakis ET, Hu M, Huang N, Hurles ME, Jin H, Jostins L, Keane TM, Le SQ, Lindsay S, Long Q, MacArthur DG, Montgomery SB, Parts L, Stalker J, Tyler-Smith C, Walter K, Zhang Y, Gerstein MB, Snyder M, Abyzov A, Balasubramanian S, Bjornson R, Du J, Grubert F, Habegger L, Haraksingh R, Jee J, Khurana E, Lam HY, Jeng J, Mu XJ, Urban AE, Zhang Z, Li Y, Luo R, Marth GT, Garrison EP, Kural D, Quinlan AR, Stewart C, Stromberg MP, Ward AN, Wu J, Lee C, Mills RE, Shi X, McCarroll SA, Bank E, DePristo MA, Handsaker RE, Hartl C, Korn JM, Li H, Nemesh JC, Sebat J, Makarov V, Ye K, Yoon S, Degenhardt J, Kaganovich M, Clarke L, Smith RE, Zheng-Bradley X, Korbel JO, Humphray S, Cheetham RK, Eberle M, Kahn S, Murray L, Ye K, De La Vega FM, Fu Y, Peckham HE, Sun YA, Batzer MA, Konkel MK, Walker JA, Xiao C, Iqbal Z, Desany B, Blackwell T, Snyder M, Xing J, Eichler EE, Aksay G, Alkan C, Hajirasouliha I, Hormozdiari F, Kidd JM, Chen K, Chinwalla A, Ding L, McLellan MD, Wallis JW, Hurles ME, Conrad DF, Walter K, Zhang Y, Gerstein MB, Snyder M, Abyzov A, Du J, Grubert F, Haraksingh R, Jee J, Khurana E, Lam HY, Leng J, Mu XJ, Urban AE, Zhang Z, Gibbs RA, Bainbridge M, Challis D, Coafra C, Dinh H, Kovar C, Lee S, Muzny D, Nazareth L, Reid J, Sabo A, Yu F, Yu J, Marth GT, Garrison EP, Indap A, Leong WF, Quinlan AR, Stewart C, Ward AN, Wu J, Cibulskis K, Fennell TJ, Gabriel SB, Garimella KV, Hartl C, Shefler E, Sougnez CL, Wilkinson J, Clark AG, Gravel S, Grubert F, Clarke L, Flicek P, Smith RE, Zheng-Bradley X, Sherry ST, Khouri HM, Paschall JE, Shumway MF, Xiao C, McVean GA, Katzman SJ, Abecasis GR, Blackwell T, Mardis ER, Dooling D, Fulton L, Fulton R, Koboldt DC, Durbin RM, Balasubramaniam S, Coffey A, Keane TM, MacArthur DG, Palotie A, Scott C, Stalker J, Tyler-Smith C, Gerstein MB, Balasubramanian S, Chakravarti A, Knoppers BM, Peltonen L, Abecasis GR, Bustamante CD, Gharani N, Gibbs RA, Jorde L, Kaye JS, Kent A, Li T, McGuire AL, McVean GA, Ossorio PN, Rotimi CN, Su Y, Toji LH, Tyler-Smith C, Brooks LD, Felsenfeld AL, McEwen JE, Abdallah A, Juenger CR, Clemm NC, Collins FS, Duncanson A, Green ED, Guyer MS, Peterson JL, Schafer AJ. Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. Abstract Genomic structural variants (SVs) are abundant in humans, differing from other forms of variation in extent, origin and functional impact. Despite progress in SV characterization, the nucleotide resolution architecture of most SVs remains unknown. We constructed a map of unbalanced SVs (that is, copy number variants) based on whole genome DNA sequencing data from 185 human genomes, integrating evidence from complementary SV discovery approaches with extensive experimental validations. Our map encompassed 22,025 deletions and 6,000 additional SVs, including insertions and tandem duplications. Most SVs (53%) were mapped to nucleotide resolution, which facilitated analysing their origin and functional impact. We examined numerous whole and partial gene deletions with a genotyping approach and observed a depletion of gene disruptions amongst high frequency deletions. Furthermore, we observed differences in the size spectra of SVs originating from distinct formation mechanisms, and constructed a map of SV hotspots formed by common mechanisms. Our analytical framework and SV map serves as a resource for sequencing-based association studies.
	PMID: 21293372 [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 Tuesday, 2011 Feb 22
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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PubMed Results

Items 1 - 13 of 13

1.	Science. 2011 Feb 4;331(6017):548. Genome-sequencing anniversary. Painting the genome for the public. Cortada X.
	PMID: 21292969 [PubMed - indexed for MEDLINE]
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2.	Science. 2011 Feb 4;331(6017):548. Genome-sequencing anniversary. Bringing genomics and genetics back together. Gibbs RA. Department of Molecular and Human Genetics, Human Genome Sequencing Center, Baylor College of Medicine, Houston, TX, USA.
	PMID: 21292968 [PubMed - indexed for MEDLINE]
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3.	Science. 2011 Feb 4;331(6017):548. Genome-sequencing anniversary. What defines us? Cole-Turner R. Pittsburgh Theological Seminary, Pittsburgh, PA, USA.
	PMID: 21292967 [PubMed - indexed for MEDLINE]
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4.	Science. 2011 Feb 4;331(6017):547. Genome-sequencing anniversary. The golden age of human population genetics. Przeworski M. University of Chicago, Chicago, IL, USA.
	PMID: 21292966 [PubMed - indexed for MEDLINE]
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5.	Science. 2011 Feb 4;331(6017):547. Genome-sequencing anniversary. Genomics and clinical relevance. Hudson T. Ontario Institute for Cancer Research, Toronto, Ontario, Canada.
	PMID: 21292965 [PubMed - indexed for MEDLINE]
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6.	Science. 2011 Feb 4;331(6017):546. Genome-sequencing anniversary. A celebration of the genome, part I. Jasny BR, Zahn LM.
	PMID: 21292964 [PubMed - indexed for MEDLINE]
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7.	Science. 2011 Feb 4;331(6017):546. Genome-sequencing anniversary. Faces of the genome. Collins FS. National Institutes of Health, Bethesda, MD, USA.
	PMID: 21292963 [PubMed - indexed for MEDLINE]
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8.	Science. 2011 Feb 4;331(6017):546-7. Genome-sequencing anniversary. The human genome at 10: successes and challen ges. Venter JC. J. Craig Venter Institute, Rockville, MD, USA.
	PMID: 21292962 [PubMed - indexed for MEDLINE]
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9.	Science. 2011 Feb 4;331(6017):530-1. Human genome 10th anniversary. The Human Genome (patent) Project. Kean S.
	PMID: 21292952 [PubMed - indexed for MEDLINE]
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10.	Science. 2011 Feb 4;331(6017):528-9. Human genome 10th anniversary. Human genetics in the clinic, one click away. Marshall E.
	PMID: 21292951 [PubMed - indexed for MEDLINE]
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11.	Science. 2011 Feb 4;331(6017):526-9. Human genome 10th anniversary. Waiting for the revolution. Marshall E.
	PMID: 21292950 [PubMed - indexed for MEDLINE]
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12.	Science. 2011 Feb 4;331(6017):511. Lessons from genomics. Alberts B. Free Article
	PMID: 21292941 [PubMed - indexed for MEDLINE]
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13.	Science. 2011 Feb 4;331(6017):593-6. Epub 2011 Jan 13. Aberrant overexpression of satellite rep eats in pancreatic and other epithelial cancers. Ting DT, Lipson D, Paul S, Brannigan BW, Akhavanfard S, Coffman EJ, Contino G, Deshpande V, Iafrate AJ, Letovsky S, Rivera MN, Bardeesy N, Maheswaran S, Haber DA. Massachusetts General Hospital Cancer Center and Department of Medicine, Harvard Medical School, Boston, MA 02114, USA. Abstract Satellite repeats in heterochromatin are transcribed into noncoding RNAs that have been linked to gene silencing and maintenance of chromosomal integrity. Using digital gene expression analysis, we showed that these transcripts are greatly overexpressed in mouse and human epithelial cancers. In 8 of 10 mouse pancreatic ductal adenocarcinomas (PDACs), pericentromeric satellites accounted for a mean 12% (range 1 to 50%) of all cellular transcripts, a mean 40-fold increase over that in normal tissue. In 15 of 15 human PDACs, alpha satellite transcripts were most abundant and HSATII transcripts were highly specific for cancer. Similar patterns were observed in cancers of the lung, kidney, ovary, colon, and prostate. Derepression of satellite transcripts correlated with overexpression of the long interspersed nuclear element 1 (LINE-1) retrotransposon and with aberrant expression of neuroendocrine-associated genes proximal to LINE-1 insertions. The overexpression of satellite transcripts in cancer may reflect global alterations in heterochromatin silencing and could potentially be useful as a biomarker for cancer detection.
	PMID: 21233348 [PubMed - indexed for MEDLINE]
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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Friday, 2011 Feb 18
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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Items 1 - 2 of 2

1.	Nature. 2011 Jan 20;469(7330):289-91. Get ready for the flood of fetal gene screening. Greely HT. Center for Law and the Biosciences, Stanford Law School, Stanford, California 94305, USA. hgreely@stanford.edu
	PMID: 21248817 [PubMed - indexed for MEDLINE]
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2.	N Engl J Med. 2011 Feb 10;364(6):524-34. Epub 2011 Jan 12. Effect of direct-to-consumer genomewide profiling to assess disease risk. Bloss CS, Schork NJ, Topol EJ. Scripps Genomic Medicine, Scripps Translational Science Institute, and Scripps Health, La Jolla, CA 92037, USA. Abstract BACKGROUND: The use of direct-to-consumer genomewide profiling to assess disease risk is controversial, and little is known about the effect of this technology on consumers. We examined the psychological, behavioral, and clinical effects of risk scanning with the Navigenics Health Compass, a commercially available test of uncertain clinical validity and utility. METHODS: We recruited subjects from health and technology companies who elected to purchase the Health Compass at a discounted rate. Subjects reported any changes in symptoms of anxiety, intake of dietary fat, and exercise behavior at a mean (±SD) of 5.6±2.4 months after testing, as compared with baseline, along with any test-related distress and the use of health-screening tests. RESULTS: From a cohort of 3639 enrolled subjects, 2037 completed follow-up. Primary analyses showed no significant differences between baseline and follow-up in anxiety symptoms (P=0.80), dietary fat intake (P=0.89), or exercise behavior (P=0.61). Secondary analyses revealed that test-related distress was positively correlated with the average estimated lifetime risk among all the assessed conditions (β=0.117, P<0.001). However, 90.3% of subjects who completed follow-up had scores indicating no test-related distress. There was no significant increase in the rate of use of screening tests associated with genomewide profiling, most of which are not considered appropriate for screening asymptomatic persons in any case. CONCLUSIONS: In a selected sample of subjects who completed follow-up after undergoing consumer genomewide testing, such testing did not result in any measurable short-term changes in psychological health, diet or exercise behavior, or use of screening tests. Potential effects of this type of genetic testing on the population at large are not known. (Funded by the National Institutes of Health and Scripps Health.).
	PMID: 21226570 [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, 2011 Feb 12
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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PubMed Results

Items 1 - 8 of 8

1.	Science. 2011 Jan 28;331(6016):463-7. Metagenomic discovery of biomass-degrading genes and genomes from cow rumen. Hess M, Sczyrba A, Egan R, Kim TW, Chokhawala H, Schroth G, Luo S, Clark DS, Chen F, Zhang T, Mackie RI, Pennacchio LA, Tringe SG, Visel A, Woyke T, Wang Z, Rubin EM. Department of Energy, Joint Genome Institute, Walnut Creek, CA 94598, USA. Abstract The paucity of enzymes that efficiently deconstruct plant polysaccharides represents a major bottleneck for industrial-scale conversion of cellulosic biomass into biofuels. Cow rumen microbes specialize in degradation of cellulosic plant material, but most members of this complex community resist cultivation. To characterize biomass-degrading genes and genomes, we sequenced and analyzed 268 gigabases of metagenomic DNA from microbes adherent to plant fiber incubated in cow rumen. From these data, we identified 27,755 putative carbohydrate-active genes and expressed 90 candidate proteins, of which 57% were enzymatically active against cellulosic substrates. We also assembled 15 uncultured microbial genomes, which were validated by complementary methods including single-cell genome sequencing. These data sets provide a substantially expanded catalog of genes and genomes participating in the deconstruction of cellulosic biomass.
	PMID: 21273488 [PubMed - indexed for MEDLINE]
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2.	Science. 2011 Jan 28;331(6016):430-4. Rapid pneumococcal evolution in response to clinical interventions. Croucher NJ, Harris SR, Fraser C, Quail MA, Burton J, van der Linden M, McGee L, von Gottberg A, Song JH, Ko KS, Pichon B, Baker S, Parry CM, Lambertsen LM, Shahinas D, Pillai DR, Mitchell TJ, Dougan G, Tomasz A, Klugman KP, Parkhill J, Hanage WP, Bentley SD. The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK. Comment in: Science. 2011 Jan 28;331(6016):407-9. Abstract Epidemiological studies of the naturally transformable bacterial pathogen Streptococcus pneumoniae have previously been confounded by high rates of recombination. Sequencing 240 isolates of the PMEN1 (Spain(23F)-1) multidrug-resistant lineage enabled base substitutions to be distinguished from polymorphisms arising through horizontal sequence transfer. More than 700 recombinations were detected, with genes encoding major antigens frequently affected. Among these were 10 capsule-switching events, one of which accompanied a population shift as vaccine-escape serotype 19A isolates emerged in the USA after the introduction of the conjugate polysaccharide vaccine. The evolution of resistance to fluoroquinolones, rifampicin, and macrolides was observed to occur on multiple occasions. This study details how genomic plasticity within lineages of recombinogenic bacteria can permit adaptation to clinical interventions over remarkably short time scales.
	PMID: 21273480 [PubMed - indexed for MEDLINE]
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3.	Science. 2011 Jan 28;331(6016):407-9. Genomics. The genomic view of bacterial diversification. Enright MC, Spratt BG. Biocontrol Ltd., Sharnbrook, Bedfordshire MK44 1LQ, UK. Comment on: Science. 2011 Jan 28;331(6016):430-4.
	PMID: 21273474 [PubMed - indexed for MEDLINE]
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4.	Nature. 2011 Jan 13;469(7329):162. Survey data are still vital to science. Gilbert J, O'Dor R, Vogel T.
	PMID: 21228857 [PubMed - indexed for MEDLINE]
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5.	Nature. 2011 Jan 13;469(7329):156-7. Bring on the biomarkers. Poste G. Complex A daptive Systems Initiative, Arizona State University, Scottsdale, Arizona 85257, USA. george.poste@asu.edu
	PMID: 21228852 [PubMed - indexed for MEDLINE]
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6.	Nature. 2011 Jan 13;469(7329):139-40. Cancer trial errors revealed. Samuel Reich E.
	PMID: 21228842 [PubMed - indexed for MEDLINE]
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7.	Nature. 2011 Jan 13;469(7329):216-20. Epub 2010 Dec 1. Integrative genomics identifies LMO1 as a neuroblastoma oncogene. Wang K, Diskin SJ, Zhang H, Attiyeh EF, Winter C, Hou C, Schnepp RW, Diamond M, Bosse K, Mayes PA, Glessner J, Kim C, Frackelton E, Garris M, Wang Q, Glaberson W, Chiavacci R, Nguyen L, Jagannathan J, Saeki N, Sasaki H, Grant SF, Iolascon A, Mosse YP, Cole KA, Li H, Devoto M, McGrady PW, London WB, Capasso M, Rahman N, Hakonarson H, Maris JM. The Center for Applied Genomics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA. Abstract Neuroblastoma is a childhood cancer of the sympathetic nervous system that accounts for approximately 10% of all paediatric oncology deaths. To identify genetic risk factors for neuroblastoma, we performed a genome-wide association study (GWAS) on 2,251 patients and 6,097 control subjects of European ancestry from four case series. Here we report a significant association within LIM domain only 1 (LMO1) at 11p15.4 (rs110419, combined P = 5.2 × 10(-16), odds ratio of risk allele = 1.34 (95% confidence interval 1.25-1.44)). The signal was enriched in the subset of patients with the most aggressive form of the disease. LMO1 encodes a cysteine-rich transcriptional regulator, and its paralogues (LMO2, LMO3 and LMO4) have each been previously implicated in cancer. In parallel, we analysed genome-wide DNA copy number alterations in 701 primary tumours. We found that the LMO1 locus was aberrant in 12.4% through a duplication event, and that this event was associated with more advanced disease (P < 0.0001) and survival (P = 0.041). The germline single nucleotide polymorphism (SNP) risk alleles and somatic copy number gains were associated with increased LMO1 expression in neuroblastoma cell lines and primary tumours, consistent with a gain-of-function role in tumorigenesis. Short hairpin RNA (shRNA)-mediated depletion of LMO1 inhibited growth of neuroblastoma cells with high LMO1 expression, whereas forced expression of LMO1 in neuroblastoma cells with low LMO1 expression enhanced proliferation. These data show that common polymorphisms at the LMO1 locus are strongly associated with susceptibility to developing neuroblastoma, but also may influence the likelihood of further somatic alterations at this locus, leading to malignant progression.
	PMID: 21124317 [PubMed - indexed for MEDLINE]
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8.	Nature. 2011 Jan 13;469(7329):221-5. Epub 2010 Dec 1. A role for mitochondria in NLRP3 inflammasome activation. Zhou R, Yazdi AS, Menu P, Tschopp J. Department of Biochemistry, Center of Immunity and Infection, University of Lausanne, Chemin des Boveresses 155, CH-1066 Epalinges, Switzerland. Abstract An inflammatory response initiated by the NLRP3 inflammasome is triggered by a variety of situations of host 'danger', including infection and metabolic dysregulation. Previous studies suggested that NLRP3 inflammasome activity is negatively regulated by autophagy and positively regulated by reactive oxygen species (ROS) derived from an uncharacterized organelle. Here we show that mitophagy/autophagy blockade leads to the accumulation of damaged, ROS-generating mitochondria, and this in turn activates the NLRP3 inflammasome. Resting NLRP3 localizes to endoplasmic reticulum structures, whereas on inflammasome activation both NLRP3 and its adaptor ASC redistribute to the perinuclear space where they co-localize with endoplasmic reticulum and mitochondria organelle clusters. Notably, both ROS generation and inflammasome activation are suppressed when mitochondrial activity is dysregulated by inhibition of the voltage-dependent anion channel. This indicates that NLRP3 inflammasome senses mitochondrial dysfunction and may explain the frequent association of mitochondrial damage with inflammatory diseases.
	PMID: 21124315 [PubMed - indexed for MEDLINE]
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