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 Dec 14Search (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. 2011 Dec 1;365(22):2098-109.Genomics of cardiovascular disease.O'Donnell CJ, Nabel EG.SourceNational Heart, Lung, and Blood Institute and the Framingham Heart Study, National Institutes of Health, Bethesda, MD, USA. |
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2. | Lancet. 2011 Nov 19;378(9805):1769.Drug withdrawal sends critical care specialists back to basics.Mullard A. |
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3. | N Engl J Med. 2011 Nov 17;365(20):1942-4.Nitric oxide during altitude acclimatization.Janocha AJ, Koch CD, Tiso M, Ponchia A, Doctor A, Gibbons L, Gaston B, Beall CM, Erzurum SC. Free Article |
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4. | N Engl J Med. 2011 Nov 17;365(20):1916-24.Case records of the Massachusetts General Hospital. Case 35-2011: A 33-year-old woman with postpartum l eukocytosis and Gram-positive bacteremia.Soper DE, Lee SI, Kim JY, McDonald AG.SourceDepartment of Obstetrics and Gynecology, Medical University of South Carolina, Charleston, USA. |
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5. | Science. 2011 Nov 11;334(6057):799-802.Global DNA demethyl ation during mouse erythropoiesis in vivo.Shearstone JR, Pop R, Bock C, Boyle P, Meissner A, Socolovsky M.SourceDepartment of Pediatrics, University of Massachusetts Medical School, Worcester, MA 01605, USA. AbstractIn the mammalian genome, 5'-CpG-3' dinucleotides are frequently methylated, correlating with transcriptional silencing. Genome-wide demethylation is thought to occur only twice during development, in primordial germ cells and in the pre-implantation embryo. These demethylation events are followed by de novo methylation, setting up a pattern inherited throughout development and modified only at tissue-specific loci. We studied DNA methylation in differentiating mouse erythroblasts in vivo by using genomic-scale reduced representation bisulfite sequencing (RRBS). Demethylation at the erythroid-specific β-globin locus was coincident with global DNA demethylation at most genomic elements. Global demethylation was continuous throughout differentiation and required rapid DNA replication. Hence, DNA demethylation can occur globally during somatic cell differentiation, providing an experimental model for its study in development and disease. |
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6. | N Engl J Med. 2011 Oct 27;365(17):1612-23.Genomics and the multifactorial nature of human autoimmune disease.Cho JH, Gregersen PK.SourceDepartment of Medicine, Section of Digestive Diseases, Yale University, New Haven, CT 06520-8019, USA. judy.cho@yale.edu |
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7. | Nat Med. 2011 Oct 11;17(10):1194-5. doi: 10.1038/nm.2529.Moving ahead an HIV vaccine: use both arms to beat HIV.Walker BD, Ahmed R, Plotkin S.SourceRagon Institute of Massachusetts General Hospital, Massachusetts Instiute of Technology and Harvard, Massachusetts General Hospital, Boston, Massachusetts, USA. bwalker@partners.org |
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8. | Nat Med. 2011 Oct 11;17(10):1192-3. doi: 10.1038/nm1011-1192.Zinc fingers hit off target.Cheng L, Blazar B, High K, Porteus M.SourceInstitute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. |
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9. | Nat Med. 2011 Oct 11;17(10):1161. doi: 10.1038/nm1011-1161.Businesses ready whole-genome analysis services for researchers.Stokes T. |
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10. | Nat Med. 2011 Oct 11;17(10):1157. doi: 10.1038/nm1011-1157.Cancer drugs find a companion with new diagnostic tests.Schubert C. |
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11. | Nat Genet. 2011 Sep 28;43(10):923-5. doi: 10.1038/ng.953.Whole-genome sequencing data offer insights into human demography.Pritchard JK.Comment on |
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12. | Science. 2011 Nov 11;334(6057):814-7. Epub 2011 Sep 22.Failure to confirm XMRV/MLVs in the blood of patients with chronic fatigue syndrome: a multi-laboratory study.Simmons G, Glynn SA, Komaroff AL, Mikovits JA, Tobler LH, Hackett J Jr, Tang N, Switzer WM, Heneine W, Hewlett IK, Zhao J, Lo SC, Alter HJ, Linnen JM, Gao K, Coffin JM, Kearney MF, Ruscetti FW, Pfost MA, Bethel J, Kleinman S, Holmberg JA, Busch MP; Blood XMRV Scientific Research Working Group (SRWG).Collaborators: Glynn S, Holmberg JA, Bianco C, Busch MP, Dodd RY, Katz LM, Kleinman SH, Komaroff AL, Mikovits JA, Simmons G, Stramer SL, Tobler LH, Vernon SD, Alter H, Coffin J, Mangan DF, Ruscetti F, Kuehnert MJ, Hendry RM, Heneine W, Monroe SS, Switzer WM, Epstein J, Hewlett IK, Lo SC. SourceBlood Systems Research Institute and University of California, San Francisco, San Francisco, CA 94118, USA. AbstractMurine leukemia viruses (MLVs), including xenotropic-MLV-related virus (XMRV), have been controversially linked to chronic fatigue syndrome (CFS). To explore this issue in greater depth, we compiled coded replicate samples of blood from 15 subjects previously reported to be XMRV/MLV-positive (14 with CFS) and from 15 healthy donors previously determined to be negative for the viruses. These samples were distributed in a blinded fashion to nine laboratories, which performed assays designed to detect XMRV/MLV nucleic acid, virus replication, and antibody. Only two laboratories reported evidence of XMRV/MLVs; however, replicate sample results showed disagreement, and reactivity was similar among CFS subjects and negative controls. These results indicate that current assays do not reproducibly detect XMRV/MLV in blood samples and that blood donor screening is not warranted. |
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13. | Nat Genet. 2011 Sep 18;43(10):1031-4. doi: 10.1038/ng.937.Bayesian inference of ancient human demography from i ndividual genome sequences.Gronau I, Hubisz MJ, Gulko B, Danko CG, Siepel A.SourceDepartment of Biological Statistics and Computational Biology, Cornell University, Ithaca, New York, USA. Comment inAbstractWhole-genome sequences provide a rich source of information about human evolution. Here we describe an effort to estimate key evolutionary parameters based on the whole-genome sequences of six individuals from diverse human populations. We used a Bayesian, coalescent-based approach to obtain information about ancestral population sizes, divergence times and migration rates from inferred genealogies at many neutrally evolving loci across the genome. We introduce new methods for accommodating gene flow between populations and integrating over possible phasings of diploid genotypes. We also describe a custom pipeline for genotype inference to mitigate biases from heterogeneous sequencing technologies and coverage levels. Our analysis indicates that the San population of southern Africa diverged from other human populations approximately 108-157 thousand years ago, that Eurasians diverged from an ancestral African population 38-64 thousand years ago, and that the effective population size of the ancestors of all modern humans was ∼9,000. |
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14. | Nat Med. 2011 Sep 11;17(10):1231-4. doi: 10.1038/nm.2452.Evidence for osteocyte regulation of bone homeostasis through RANKL expression.Nakashima T, Hayashi M, Fukunaga T, Kurata K, Oh-Hora M, Feng JQ, Bonewald LF, Kodama T, Wutz A, Wagner EF, Penninger JM, Takayanagi H.SourceDepartment of Cell Signaling, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Yushima, Bunkyo-ku, Tokyo, Japan. Comment inAbstractOsteocytes embedded in bone have been postulated to orchestrate bone homeostasis by regulating both bone-forming osteoblasts and bone-resorbing osteoclasts. We find here that purified osteocytes express a much higher amount of receptor activator of nuclear factor-κB ligand (RANKL) and have a greater capacity to support osteoclastogenesis in vitro than osteoblasts and bone marrow stromal cells. Furthermore, the severe osteopetrotic phenotype that we observe in mice lacking RANKL specifically in osteocytes indicates that osteocytes are the major source of RANKL in bone remodeling in vivo. |
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15. | Nat Med. 2011 Sep 11;17(10):1235-41. doi: 10.1038/nm.2448.Matrix-embedded cells control osteoclast formation.Xiong J, Onal M, Jilka RL, Weinstein RS, Manolagas SC, O'Brien CA.SourceCenter for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences (UAMS), Little Rock, Arkansas, USA. Comment inAbstractOsteoclasts resorb the mineralized matrices formed by chondrocytes or osteoblasts. The cytokine receptor activator of nuclear factor-κB ligand (RANKL) is essential for osteoclast formation and thought to be supplied by osteoblasts or their precursors, thereby linking bone formation to resorption. However, RANKL is expressed by a variety of cell types, and it is unclear which of them are essential sources for osteoclast formation. Here we have used a mouse strain in which RANKL can be conditionally deleted and a series of Cre-deleter strains to demonstrate that hypertrophic chondrocytes and osteocytes, both of which are embedded in matrix, are essential sources of the RANKL that controls mineralized cartilage resorption and bone remodeling, respectively. Moreover, osteocyte RANKL is responsible for the bone loss associated with unloading. Contrary to the current paradigm, RANKL produced by osteoblasts or their progenitors does not contribute to adult bone remodeling. These results suggest that the rate-limiting step of matrix resorption is controlled by cells embedded within the matrix itself. |
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16. | Nat Genet. 2011 Aug 28;43(10):956-63. doi: 10.1038/ng.911.Whole-genome sequencing of multiple Arabidopsis thaliana populations.Cao J, Schneeberger K, Ossowski S, Günther T, Bender S, Fitz J, Koenig D, Lanz C, Stegle O, Lippert C, Wang X, Ott F, Müller J, Alonso-Blanco C, Borgwardt K, Schmid KJ, Weigel D.SourceMax Planck Institute for Developmental Biology, Tübingen, Germany. AbstractThe plant Arabidopsis thaliana occurs naturally in many different habitats throughout Eurasia. As a foundation for identifying genetic variation contributing to adaptation to diverse environments, a 1001 Genomes Project to sequence geographically diverse A. thaliana strains has been initiated. Here we present the first phase of this project, based on population-scale sequencing of 80 strains drawn from eight regions throughout the species' native range. We describe the majority of common small-scale polymorphisms as well as many larger insertions and deletions in the A. thaliana pan-genome, their effects on gene function, and the patterns of local and global linkage among these variants. The action of processes other than spontaneous mutation is identified by comparing the spectrum of mutations that have accumulated since A. thaliana diverged from its closest relative 10 million years ago with the spectrum observed in the laboratory. Recent species-wide selective sweeps are rare, and potentially deleterious mutations are more common in marginal populations. |
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17. | Nat Genet. 2011 Aug 28;43(10):984-9. doi: 10.1038/ng.921.Genome-wide association study in individuals of South Asian ancestry identifies six new type 2 diabetes susceptibility loci.< a href="http://www.ncbi.nlm.nih.gov/pubmed?term=%22Kooner%20JS%22%5BAuthor%5D">Kooner JS, Saleheen D, Sim X, Sehmi J, Zhang W, Frossard P, Been LF, Chia KS, Dimas AS, Hassanali N, Jafar T, Jowett JB, Li X, Radha V, Rees SD, Takeuchi F, Young R, Aung T, Basit A, Chidambaram M, Das D, Grundberg E, Hedman AK, Hydrie ZI, Islam M, Khor CC, Kowlessur S, Kristensen MM, Liju S, Lim WY, Matthews DR, Liu J, Morris AP, Nica AC, Pinidiyapathirage JM, Prokopenko I, Rasheed A, Samuel M, Shah N, Shera AS, Small KS, Suo C, Wickremasinghe AR, Wong TY, Yang M, Zhang F; DIAGRAM; MuTHER, Abecasis GR, Barnett AH, Caulfield M, Deloukas P, Frayling TM, Froguel P, Kato N, Katulanda P, Kelly MA, Liang J, Mohan V, Sanghera DK, Scott J, Seielstad M, Zimmet PZ, Elliott P, Teo YY, McCarthy MI, Danesh J, Tai ES, Chambers JC.SourceNational Heart and Lung Institute (NHLI), Imperial College London, Hammersmith Hospital, London, UK. j.kooner@imperial.ac.uk AbstractWe carried out a genome-wide association study of type-2 diabetes (T2D) in individuals of South Asian ancestry. Our discovery set included 5,561 individuals with T2D (cases) and 14,458 controls drawn from studies in London, Pakistan and Singapore. We identified 20 independent SNPs associated with T2D at P < 10(-4) for testing in a replication sample of 13,170 cases and 25,398 controls, also all of South Asian ancestry. In the combined analysis, we identified common genetic variants at six loci (GRB14, ST6GAL1, VPS26A, HMG20A, AP3S2 and HNF4A) newly associated with T2D (P = 4.1 × 10(-8) to P = 1.9 × 10(-11)). SNPs at GRB14 were also associated with insulin sensitivity (P = 5.0 × 10(-4)), and SNPs at ST6GAL1 and HNF4A were also associated with pancreatic beta-cell function (P = 0.02 and P = 0.001, respectively). Our findings provide additional insight into mechanisms underlying T2D and show the potential for new discovery from genetic association studies in South Asians, a population with increased susceptibility to T2D. |
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18. | Am J Pathol. 2011 Sep;179(3):1243-56. Epub 2011 Jul 14.Colony-stimulating factor-1 promotes kidney growth and repair via alteration of macrophage responses.Alikhan MA, Jones CV, Williams TM, Beckhouse AG, Fletcher AL, Kett MM, Sakkal S, Samuel CS, Ramsay RG, Deane JA, Wells CA, Little MH, Hume DA, Ricardo SD.SourceMonash Immunology and Stem Cell Laboratories (MISCL), Monash University, Melbourne, Australia. AbstractColony-stimulating factor (CSF)-1 controls the survival, proliferation, and differentiation of macrophages, which are recognized as scavengers and agents of the innate and the acquired immune systems. Because of their plasticity, macrophages are endowed with many other essential roles during development and tissue homeostasis. We present evidence that CSF-1 plays an important trophic role in postnatal organ growth and kidney repair. Notably, the injection of CSF-1 postnatally enhanced kidney weight and volume and was associated with increased numbers of tissue macrophages. Moreover, CSF-1 promotes postnatal renal repair in mice after ischemia-reperfusion injury by recruiting and influencing macrophages toward a reparative state. CSF-1 treatment rapidly accelerated renal repair with tubular epithelial cell replacement, attenuation of interstitial fibrosis, and functional recovery. Analysis of macrophages from CSF-1-treated kidneys showed increased expression of insulin-like growth factor-1 and anti-inflammatory genes that are known CSF-1 targets. Taken together, these data suggest that CSF-1 is important in kidney growth and the promotion of endogenous repair and resolution of inflammatory injury. Copyright © 2011 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved. |
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