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Sent on Saturday, 2012 April 28
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. 2012 Apr 7;379(9823):1291. Christine Petit: interdisciplinary geneticist. Watts G.
	PMID: 22483022 [PubMed - indexed for MEDLINE]

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Sent on Saturday, 2012 April 21
Search: (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))

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1.	Nat Genet. 2012 Feb 27;44(3):233. doi: 10.1038/ng.2216. On not reinventing the wheel. [No authors listed] Abstract An alphabet soup of organizations and initiatives across the world are concerned with identifying, collecting and evaluating disease-causing human gene variants and using them to diagnose and treat rare diseases. Despite increasing standardization of nomenclature and technology, our efforts still need coordination to produce a pipeline leading from discovery to delivery.
	PMID: 22366856 [PubMed - indexed for MEDLINE]
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2.	Nat Genet. 2012 Feb 5;44(3):243-6. doi: 10.1038/ng.1074. Differential confounding of rare and common variants in spatially structured populations. Mathieson I, McVean G. Source Wellcome Trust Centre for Human Genetics, University of Oxford, UK. mathii@well.ox.ac.uk Abstract Well-powered genome-wide association studies, now made possible through advances in technology and large-scale collaborative projects, promise to characterize the contribution of rare variants to complex traits and disease. However, while population structure is a known confounder of association studies, it remains unknown whether methods developed to control stratification are equally effective for rare variants. Here, we demonstrate that rare variants can show a stratification that is systematically different from, and typically stronger than, common variants, and this is not necessarily corrected by existing methods. We show that the same process leads to inflation for load-based tests and can obscure signals at truly associated variants. Furthermore, we show that populations can display spatial structure in rare variants, even when Wright's fixation index F(ST) is low, but that allele frequency-dependent metrics of allele sharing can reveal localized stratification. These results underscore the importance of collecting and integrating spatial information in the genetic analysis of complex traits. PMCID: PMC3303124 [Available on 2012/8/5]
	PMID: 22306651 [PubMed - indexed for MEDLINE]
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3.	Nat Genet. 2012 Jan 29;44(3):352-5. doi: 10.1038/ng.1072. Pneumococcal genome sequencing tracks a vaccine escape variant formed through a multi-fragment recombination event. Golubchik T, Brueggemann AB, Street T, Gertz RE Jr, Spencer CC, Ho T, Giannoulatou E, Link-Gelles R, Harding RM, Beall B, Peto TE, Moore MR, Donnelly P, Crook DW, Bowden R. Source Department of Statistics, University of Oxford, UK. Abstract Streptococcus pneumoniae ('pneumococcus') causes an estimated 14.5 million cases of serious disease and 826,000 deaths annually in children under 5 years of age(1). The highly effective introduction of the PCV7 pneumococcal vaccine in 2000 in the United States(2,3) provided an unprecedented opportunity to investigate the response of an important pathogen to widespread, vaccine-induced selective pressure. Here, we use array-based sequencing of 62 isolates from a US national monitoring program to study five independent instances of vaccine escape recombination(4), showing the simultaneous transfer of multiple and often large (up to at least 44 kb) DNA fragments. We show that one such new strain quickly became established, spreading from east to west across the United States. These observations clarify the roles of recombination and selection in the population genomics of pneumococcus and provide proof of principle of the considerable value of combining genomic and epidemiological information in the surveillance and enhanced understanding of infectious diseases. PMCID: PMC3303117 [Available on 2012/7/29]
	PMID: 22286217 [PubMed - indexed for MEDLINE]
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4.	Nat Genet. 2012 Jan 29;44(3):285-90. doi: 10.1038/ng.1050. Chromosome-scale selective sweeps shape Caenorhabditis elegans genomic diversity. Andersen EC, Gerke JP, Shapiro JA, Crissman JR, Ghosh R, Bloom JS, Félix MA, Kruglyak L. Source Lewis-Sigler Institute for Integrative Genomics, Princeton University, New Jersey, USA. Comment in Nat Genet. 2012 Mar;44(3):237-8. Abstract The nematode Caenorhabditis elegans is central to research in molecular, cell and developmental biology, but nearly all of this research has been conducted on a single strain of C. elegans. Little is known about the population genomic and evolutionary history of this species. We characterized C. elegans genetic variation using high-throughput selective sequencing of a worldwide collection of 200 wild strains and identified 41,188 SNPs. Notably, C. elegans genome variation is dominated by a set of commonly shared haplotypes on four of its six chromosomes, each spanning many megabases. Population genetic modeling showed that this pattern was generated by chromosome-scale selective sweeps that have reduced variation worldwide; at least one of these sweeps probably occurred in the last few hundred years. These sweeps, which we hypothesize to be a result of human activity, have drastically reshaped the global C. elegans population in the recent past.
	PMID: 22286215 [PubMed - indexed for MEDLINE]
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Sent on Friday, 2012 April 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.	Science. 2012 Apr 6;336(6077):86-90. Epub 2012 Mar 22. A lineage of myeloid cells independent of Myb and hematopoietic stem cells. Schulz C, Gomez Perdiguero E, Chorro L, Szabo-Rogers H, Cagnard N, Kierdorf K, Prinz M, Wu B, Jacobsen SE, Pollard JW, Frampton J, Liu KJ, Geissmann F. Source Centre for Molecular and Cellular Biology of Inflammation, New Hunt's House, King's College London, Great Maze Pond, London SE1 1UL, UK. Abstract Macrophages and dendritic cells (DCs) are key components of cellular immunity and are thought to originate and renew from hematopoietic stem cells (HSCs). However, some macrophages develop in the embryo before the appearance of definitive HSCs. We thus reinvestigated macrophage development. We found that the transcription factor Myb was required for development of HSCs and all CD11b(high) monocytes and macrophages, but was dispensable for yolk sac (YS) macrophages and for the development of YS-derived F4/80(bright) macrophages in several tissues, such as liver Kupffer cells, epidermal Langerhans cells, and microglia--cell populations that all can persist in adult mice independently of HSCs. These results define a lineage of tissue macrophages that derive from the YS and are genetically distinct from HSC progeny.
	PMID: 22442384 [PubMed - indexed for MEDLINE]
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2.	Nature. 2012 Mar 21;483(7390):408. doi: 10.1038/483408a. Renato Dulbecco (1914-2012). Verma IM. Source Salk Institute, La Jolla, California 92037, USA. verma@salk.edu
	PMID: 22437605 [PubMed - indexed for MEDLINE]
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3.	Nature. 2012 Mar 21;483(7390):387. doi: 10.1038/483387a. DNA donor rights affirmed. Hayden EC.
	PMID: 22437587 [PubMed - indexed for MEDLINE]
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4.	Nature. 2012 Mar 21;483(7390):373. doi: 10.1038/483373a. Incidental benefits. [No authors listed]
	PMID: 22437569 [PubMed - indexed for MEDLINE]
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5.	Nature. 2012 Mar 7;483(7388):169-75. doi: 10.1038/nature10842. Insights into hominid evolution from the gorilla genome sequence. Scally A, Dutheil JY, Hillier LW, Jordan GE, Goodhead I, Herrero J, Hobolth A, Lappalainen T, Mailund T, Marques-Bonet T, McCarthy S, Montgomery SH, Schwalie PC, Tang YA, Ward MC, Xue Y, Yngvadottir B, Alkan C, Andersen LN, Ayub Q, Ball EV, Beal K, Bradley BJ, Chen Y, Clee CM, Fitzgerald S, Graves TA, Gu Y, Heath P, Heger A, Karakoc E, Kolb-Kokocinski A, Laird GK, Lunter G, Meader S, Mort M, Mullikin JC, Munch K, O'Connor TD, Phillips AD, Prado-Martinez J, Rogers AS, Sajjadian S, Schmidt D, Shaw K, Simpson JT, Stenson PD, Turner DJ, Vigilant L, Vilella AJ, Whitener W, Zhu B, Cooper DN, de Jong P, Dermitzakis ET, Eichler EE, Flicek P, Goldman N, Mundy NI, Ning Z, Odom DT, Ponting CP, Quail MA, Ryder OA, Searle SM, Warren WC, Wilson RK, Schierup MH, Rogers J, Tyler-Smith C, Durbin R. Source Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton CB10 1SA, UK. Comment in Nature. 2012 Mar 8;483(7388):164-5. Abstract Gorillas are humans' closest living relatives after chimpanzees, and are of comparable importance for the study of human origins and evolution. Here we present the assembly and analysis of a genome sequence for the western lowland gorilla, and compare the whole genomes of all extant great ape genera. We propose a synthesis of genetic and fossil evidence consistent with placing the human-chimpanzee and human-chimpanzee-gorilla speciation events at approximately 6 and 10 million years ago. In 30% of the genome, gorilla is closer to human or chimpanzee than the latter are to each other; this is rarer around coding genes, indicating pervasive selection throughout great ape evolution, and has functional consequences in gene expression. A comparison of protein coding genes reveals approximately 500 genes showing accelerated evolution on each of the gorilla, human and chimpanzee lineages, and evidence for parallel acceleration, particularly of genes involved in hearing. We also compare the western and eastern gorilla species, estimating an average sequence divergence time 1.75 million years ago, but with evidence for more recent genetic exchange and a population bottleneck in the eastern species. The use of the genome sequence in these and future analyses will promote a deeper understanding of great ape biology and evolution. PMCID: PMC3303130 [Available on 2012/9/8]
	PMID: 22398555 [PubMed - indexed for MEDLINE]
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6.	Nature. 2012 Mar 7;483(7388):158. doi: 10.1038/483158c. Genetics research: Clinical standards not practical in the lab. Lindpaintner K. Comment on Nature. 2012 Feb 16;482(7385):300-1.
	PMID: 22398544 [PubMed - indexed for MEDLINE]
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7.	Nature. 2012 Mar 7;483(7388):134-5. doi: 10.1038/483134a. Trouble at the text mine. Van Noorden R.
	PMID: 22398532 [PubMed - indexed for MEDLINE]
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8.	Nature. 2012 Feb 15;483(7390):479-83. doi: 10.1038/nature10866. IDH1 mutation is sufficient to establish the glioma hypermethylator phenotype. Turcan S, Rohle D, Goenka A, Walsh LA, Fang F, Yilmaz E, Campos C, Fabius AW, Lu C, Ward PS, Thompson CB, Kaufman A, Guryanova O, Levine R, Heguy A, Viale A, Morris LG, Huse JT, Mellinghoff IK, Chan TA. Source Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA. Abstract Both genome-wide genetic and epigenetic alterations are fundamentally important for the development of cancers, but the interdependence of these aberrations is poorly understood. Glioblastomas and other cancers with the CpG island methylator phenotype (CIMP) constitute a subset of tumours with extensive epigenomic aberrations and a distinct biology. Glioma CIMP (G-CIMP) is a powerful determinant of tumour pathogenicity, but the molecular basis of G-CIMP remains unresolved. Here we show that mutation of a single gene, isocitrate dehydrogenase 1 (IDH1), establishes G-CIMP by remodelling the methylome. This remodelling results in reorganization of the methylome and transcriptome. Examination of the epigenome of a large set of intermediate-grade gliomas demonstrates a distinct G-CIMP phenotype that is highly dependent on the presence of IDH mutation. Introduction of mutant IDH1 into primary human astrocytes alters specific histone marks, induces extensive DNA hypermethylation, and reshapes the methylome in a fashion that mirrors the changes observed in G-CIMP-positive lower-grade gliomas. Furthermore, the epigenomic alterations resulting from mutant IDH1 activate key gene expression programs, characterize G-CIMP-positive proneural glioblastomas but not other glioblastomas, and are predictive of improved survival. Our findings demonstrate that IDH mutation is the molecular basis of CIMP in gliomas, provide a framework for understanding oncogenesis in these gliomas, and highlight the interplay between genomic and epigenomic changes in human cancers.
	PMID: 22343889 [PubMed - indexed for MEDLINE]
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Sent on Thursday, 2012 April 19
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. 2012 Feb 29;483(7387):20-2. doi: 10.1038/483020a. Rare diseases: Genomics, plain and simple. Gura T.
	PMID: 22382959 [PubMed - indexed for MEDLINE]
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2.	Nature. 2012 Feb 28;483(7387):15-6. doi: 10.1038/483015b. Structural biologists share their toys. Callaway E.
	PMID: 22382954 [PubMed - indexed for MEDLINE]
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3.	Nature. 2012 Feb 29;483(7387):5-6. doi: 10.1038/483005b. The great beyond. [No authors listed]
	PMID: 22382938 [PubMed - indexed for MEDLINE]
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4.	Nature. 2012 Feb 29;483(7387):S7. doi: 10.1038/483S7a. Q&A: Controversy and intellect. Interview by Julie Corliss. Dunn B.
	PMID: 22378127 [PubMed - indexed for MEDLINE]
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Sent on Tuesday, 2012 April 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.	Science. 2012 Mar 30;335(6076):1590-1. IBI* series winner. Adapting to osmotic stress and the process of science. Gasper BJ, Minchella DJ, Weaver GC, Csonka LN, Gardner SM. Source Department of Biological Sciences, Purdue University, West Lafayette, IN 47907, USA.
	PMID: 22461603 [PubMed - indexed for MEDLINE]
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2.	Science. 2012 Mar 30;335(6076):1587. Retrospective. Renato Dulbecco (1914-2012). Baltimore D. Source Biology Department, California Institute of Technology, Pasadena, CA 91125, USA. baltimo@caltech.edu
	PMID: 22461601 [PubMed - indexed for MEDLINE]
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3.	Science. 2012 Mar 30;335(6076):1573; author reply 1573. Comment on "Disentangling the drivers of β diversity along latitudinal and elevational gradients". Tuomisto H, Ruokolainen K. Source Department of Biology, University of Turku, Turku, Finland. hanna.tuomisto@utu.fi Comment on Science. 2011 Sep 23;333(6050):1755-8. Abstract Kraft et al. (Report, 23 September 2011, p. 1755) argued that the latitudinal trend in β diversity is spurious and just reflects a trend in γ diversity. Their results depend on the idiosyncrasies of their data, especially the latitudinally varying degree of undersampling and a local sampling setup that is not suitable for analyzing drivers of β diversity.
	PMID: 22461591 [PubMed - indexed for MEDLINE]
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4.	Science. 2012 Mar 30;335(6076):1573; author reply 1573. Comment on "Disentangling the drivers of β diversity along latitudinal and elevational gradients". Qian H, Wang X, Zhang Y. Source Research and Collections Center, Illinois State Museum, Springfield, IL 62703, USA. hqian@museum.state.il.us Comment on Science. 2011 Sep 23;333(6050):1755-8. Abstract Kraft et al. (Report, 23 September 2011, p. 1755) analyzed two data sets and concluded that "there is no need to invoke differences in the mechanisms of community assembly in temperate versus tropical systems to explain these global-scale patterns of β diversity." We show that their conclusion is based on inappropriate data and inadequate methods of analysis.
	PMID: 22461590 [PubMed - indexed for MEDLINE]
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Sent on Wednesday, 2012 April 11
Search: (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))

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1.	Lancet. 2012 Mar 24;379(9821):1088. 2012 Gairdner International Awards go to US scientists. Webster PC.
	PMID: 22451963 [PubMed - indexed for MEDLINE]
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2.	Hum Genet. 2012 Mar;131(3):423-33. Epub 2011 Sep 9. High altitude adaptation in Daghestani populations from the Caucasus. Pagani L, Ayub Q, MacArthur DG, Xue Y, Baillie JK, Chen Y, Kozarewa I, Turner DJ, Tofanelli S, Bulayeva K, Kidd K, Paoli G, Tyler-Smith C. Source The Wellcome Trust Sanger Institute, Hinxton, UK. lp8@sanger.ac.uk Abstract We have surveyed 15 high-altitude adaptation candidate genes for signals of positive selection in North Caucasian highlanders using targeted re-sequencing. A total of 49 unrelated Daghestani from three ethnic groups (Avars, Kubachians, and Laks) living in ancient villages located at around 2,000 m above sea level were chosen as the study population. Caucasian (Adygei living at sea level, N = 20) and CEU (CEPH Utah residents with ancestry from northern and western Europe; N = 20) were used as controls. Candidate genes were compared with 20 putatively neutral control regions resequenced in the same individuals. The regions of interest were amplified by long-PCR, pooled according to individual, indexed by adding an eight-nucleotide tag, and sequenced using the Illumina GAII platform. 1,066 SNPs were called using false discovery and false negative thresholds of ~6%. The neutral regions provided an empirical null distribution to compare with the candidate genes for signals of selection. Two genes stood out. In Laks, a non-synonymous variant within HIF1A already known to be associated with improvement in oxygen metabolism was rediscovered, and in Kubachians a cluster of 13 SNPs located in a conserved intronic region within EGLN1 showing high population differentiation was found. These variants illustrate both the common pathways of adaptation to high altitude in different populations and features specific to the Daghestani populations, showing how even a mildly hypoxic environment can lead to genetic adaptation. PMCID: PMC3312735 Free PMC Article
	PMID: 21904933 [PubMed - indexed for MEDLINE]
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Sent on Tuesday, 2012 April 10
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. 2012 Mar 23;335(6075):1496-9. MARF1 regulates essential oogenic processes in mice. Su YQ, Sugiura K, Sun F, Pendola JK, Cox GA, Handel MA, Schimenti JC, Eppig JJ. Source The Jackson Laboratory, Bar Harbor, ME 04609, USA. Abstract Development of fertilization-competent oocytes depends on integrated processes controlling meiosis, cytoplasmic development, and maintenance of genomic integrity. We show that meiosis arrest female 1 (MARF1) is required for these processes in mammalian oocytes. Mutations of Marf1 cause female infertility characterized by up-regulation of a cohort of transcripts, increased retrotransposon expression, defective cytoplasmic maturation, and meiotic arrest. Up-regulation of protein phosphatase 2 catalytic subunit (PPP2CB) is key to the meiotic arrest phenotype. Moreover, Iap and Line1 retrotransposon messenger RNAs are also up-regulated, and, concomitantly, DNA double-strand breaks are elevated in mutant oocytes. Therefore MARF1, by suppressing levels of specific transcripts, is an essential regulator of important oogenic processes leading to female fertility and the development of healthy offspring.
	PMID: 22442484 [PubMed - indexed for MEDLINE]
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2.	Science. 2012 Mar 23;335(6075):1457. Retrospective. Oscar Miller (1925-2012). McKnight S, Beyer A, Gall J. Source Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. steven.mcknight@utsouthwestern.edu
	PMID: 22442474 [PubMed - indexed for MEDLINE]
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Sent on Tuesday, 2012 April 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]))

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1.	Science. 2012 Mar 16;335(6074):1344-8. Climatic niche shifts are rare among terrestrial plant invaders. Petitpierre B, Kueffer C, Broennimann O, Randin C, Daehler C, Guisan A. Source Department of Ecology and Evolution, University of Lausanne, Lausanne, Switzerland. Abstract The assumption that climatic niche requirements of invasive species are conserved between their native and invaded ranges is key to predicting the risk of invasion. However, this assumption has been challenged recently by evidence of niche shifts in some species. Here, we report the first large-scale test of niche conservatism for 50 terrestrial plant invaders between Eurasia, North America, and Australia. We show that when analog climates are compared between regions, fewer than 15% of species have more than 10% of their invaded distribution outside their native climatic niche. These findings reveal that substantial niche shifts are rare in terrestrial plant invaders, providing support for an appropriate use of ecological niche models for the prediction of both biological invasions and responses to climate change.
	PMID: 22422981 [PubMed - indexed for MEDLINE]
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2.	Science. 2012 Mar 16;335(6074):1317-21. Human evolution out of Africa: the role of refugia and climate change. Stewart JR, Stringer CB. Source School of Applied Sciences, Bournemouth University, Talbot Campus, Poole, Dorset, UK. jstewart@bournemouth.ac.uk Abstract Although an African origin of the modern human species is generally accepted, the evolutionary processes involved in the speciation, geographical spread, and eventual extinction of archaic humans outside of Africa are much debated. An additional complexity has been the recent evidence of limited interbreeding between modern humans and the Neandertals and Denisovans. Modern human migrations and interactions began during the buildup to the Last Glacial Maximum, starting about 100,000 years ago. By examining the history of other organisms through glacial cycles, valuable models for evolutionary biogeography can be formulated. According to one such model, the adoption of a new refugium by a subgroup of a species may lead to important evolutionary changes.
	PMID: 22422974 [PubMed - indexed for MEDLINE]
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3.	Science. 2012 Mar 16;335(6074):1316. Retrospective. Norton Zinder (1928-2012). Lodish H, Fedoroff N. Source Whitehead Institute for Biomedical Research and the Massachusetts Institute of Technology, Cambridge, MA 02142, USA. lodish@wi.mit.edu
	PMID: 22422973 [PubMed - indexed for MEDLINE]
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