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  • 1
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    Nonthermal plasma induces head and neck cancer cell death: the potential involvement of mitogen-activated protein kinase-dependent mitochondrial reactive oxygen species (2014)
    Springer Nature
    Details
    Publication Date: 2014-02-14
    Description: Nonthermal plasma induces head and neck cancer cell death: the potential involvement of mitogen-activated protein kinase-dependent mitochondrial reactive oxygen species Cell Death and Disease 5, e1056 (February 2014). doi:10.1038/cddis.2014.33 Authors: S U Kang, J-H Cho, J W Chang, Y S Shin, K I Kim, J K Park, S S Yang, J-S Lee, E Moon, K Lee & C-H Kim
    Keywords: nonthermal plasmaapoptosisMAPKROShead and neck cancer
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 2
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    Perpendicular magnetic anisotropy of amorphous [CoSiB/Pt]N thin films (2015)
    American Institute of Physics (AIP)
    Details
    Publication Date: 2015-01-23
    Description: Materials with perpendicular magnetic anisotropy (PMA) have been intensively studied for high-density nonvolatile memory such as spin-transfer-torque magnetic random access memory with low switching current density and high thermal stability. Compared with crystalline PMA multilayers, considerable works have been done on amorphous PMA multilayers because the amorphous materials are expected to have lower pinning site density as well as smaller domain wall width. This study is an overview of the PMA properties of amorphous [CoSiB/Pt] N multilayers with varying N, where the energy contribution is changed from domain wall energy to magnetostatic energy around N = 6. By measuring the field-induced domain wall motion, we obtain the creep exponent of μ = 1/4. These results in the amorphous PMA multilayers of [CoSiB/Pt] N demonstrate possible potential as a free layer for PMA-based memory devices.
    Print ISSN: 0021-8979
    Electronic ISSN: 1089-7550
    Topics: Physics
    Published by American Institute of Physics (AIP)
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  • 3
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    A sub-kpc-scale binary active galactic nucleus with double narrow-line regions (2013)
    Oxford University Press
    Details
    Publication Date: 2013-12-06
    Description: We present the kinematic properties of a type-2 Quasi stellar object (QSO), SDSS J132323.33–015941.9 at z ~ 0.35, based on the analysis of Very Large Telescope integral field spectroscopy and Hubble Space Telescope ( HST ) imaging, which suggest that the target is a binary active galactic nucleus (AGN) with double narrow-line regions. The QSO features double-peaked emission lines ([O iii ] and Hβ) which can be decomposed into two kinematic components. The flux-weighted centroids of the blue and red components are separated by ~0.2 arcsec (0.8 kpc in projection) and coincide with the location of the two stellar cores detected in the HST broad-band images, implying that both stellar cores host an active black hole. The line-of-sight velocity of the blue component is comparable to the luminosity-weighted velocity of stars in the host galaxy, while the red component is redshifted by ~240 km s –1 , consistent with typical velocity offsets of two cores in a late stage of a galaxy merger. If confirmed, the target is one of the rare cases of sub-kpc-scale binary AGNs, providing a test-bed for understanding the binary AGN population.
    Print ISSN: 0035-8711
    Electronic ISSN: 1365-2966
    Topics: Physics
    Published by Oxford University Press
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  • 4
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    MYC enhancer and lncRNA [Genetics] (2014)
    National Academy of Sciences
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    Publication Date: 2014-03-19
    Description: The mechanism by which the 8q24 MYC enhancer region, including cancer-associated variant rs6983267, increases cancer risk is unknown due to the lack of protein-coding genes at 8q24.21. Here we report the identification of long noncoding RNAs named cancer-associated region long noncoding RNAs (CARLos) in the 8q24 region. The expression of...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 5
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    Finding the missing heritability of complex diseases (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-10-09
    Description: Genome-wide association studies have identified hundreds of genetic variants associated with complex human diseases and traits, and have provided valuable insights into their genetic architecture. Most variants identified so far confer relatively small increments in risk, and explain only a small proportion of familial clustering, leading many to question how the remaining, 'missing' heritability can be explained. Here we examine potential sources of missing heritability and propose research strategies, including and extending beyond current genome-wide association approaches, to illuminate the genetics of complex diseases and enhance its potential to enable effective disease prevention or treatment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831613/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831613/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manolio, Teri A -- Collins, Francis S -- Cox, Nancy J -- Goldstein, David B -- Hindorff, Lucia A -- Hunter, David J -- McCarthy, Mark I -- Ramos, Erin M -- Cardon, Lon R -- Chakravarti, Aravinda -- Cho, Judy H -- Guttmacher, Alan E -- Kong, Augustine -- Kruglyak, Leonid -- Mardis, Elaine -- Rotimi, Charles N -- Slatkin, Montgomery -- Valle, David -- Whittemore, Alice S -- Boehnke, Michael -- Clark, Andrew G -- Eichler, Evan E -- Gibson, Greg -- Haines, Jonathan L -- Mackay, Trudy F C -- McCarroll, Steven A -- Visscher, Peter M -- P50 GM065509/GM/NIGMS NIH HHS/ -- P50 GM065509-080006/GM/NIGMS NIH HHS/ -- R01 HG003229/HG/NHGRI NIH HHS/ -- R01 HL072904/HL/NHLBI NIH HHS/ -- R01 HL072904-07/HL/NHLBI NIH HHS/ -- R01 MH084695/MH/NIMH NIH HHS/ -- U01 HL084706/HL/NHLBI NIH HHS/ -- UL1 RR024992/RR/NCRR NIH HHS/ -- England -- Nature. 2009 Oct 8;461(7265):747-53. doi: 10.1038/nature08494.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Human Genome Research Institute, Building 31, Room 4B09, 31 Center Drive, MSC 2152, Bethesda, Maryland 20892-2152, USA. manoliot@mail.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19812666" target="_blank"〉PubMed〈/a〉
    Keywords: Genetic Diseases, Inborn/*genetics ; Genetic Predisposition to Disease/*genetics ; Genetics, Medical/*methods/trends ; Genome-Wide Association Study/methods/trends ; Humans ; Inheritance Patterns/genetics ; Pedigree
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
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    A genome-wide association study identifies IL23R as an inflammatory bowel disease gene (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-28
    Description: The inflammatory bowel diseases Crohn's disease and ulcerative colitis are common, chronic disorders that cause abdominal pain, diarrhea, and gastrointestinal bleeding. To identify genetic factors that might contribute to these disorders, we performed a genome-wide association study. We found a highly significant association between Crohn's disease and the IL23R gene on chromosome 1p31, which encodes a subunit of the receptor for the proinflammatory cytokine interleukin-23. An uncommon coding variant (rs11209026, c.1142G〉A, p.Arg381Gln) confers strong protection against Crohn's disease, and additional noncoding IL23R variants are independently associated. Replication studies confirmed IL23R associations in independent cohorts of patients with Crohn's disease or ulcerative colitis. These results and previous studies on the proinflammatory role of IL-23 prioritize this signaling pathway as a therapeutic target in inflammatory bowel disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4410764/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4410764/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duerr, Richard H -- Taylor, Kent D -- Brant, Steven R -- Rioux, John D -- Silverberg, Mark S -- Daly, Mark J -- Steinhart, A Hillary -- Abraham, Clara -- Regueiro, Miguel -- Griffiths, Anne -- Dassopoulos, Themistocles -- Bitton, Alain -- Yang, Huiying -- Targan, Stephan -- Datta, Lisa Wu -- Kistner, Emily O -- Schumm, L Philip -- Lee, Annette T -- Gregersen, Peter K -- Barmada, M Michael -- Rotter, Jerome I -- Nicolae, Dan L -- Cho, Judy H -- DK62413/DK/NIDDK NIH HHS/ -- DK62420/DK/NIDDK NIH HHS/ -- DK62422/DK/NIDDK NIH HHS/ -- DK62423/DK/NIDDK NIH HHS/ -- DK62429/DK/NIDDK NIH HHS/ -- DK62431/DK/NIDDK NIH HHS/ -- DK62432/DK/NIDDK NIH HHS/ -- P30 DK063491/DK/NIDDK NIH HHS/ -- P30 DK063491-019004/DK/NIDDK NIH HHS/ -- P30 DK063491-029004/DK/NIDDK NIH HHS/ -- P30 DK063491-039004/DK/NIDDK NIH HHS/ -- P30 DK063491-049004/DK/NIDDK NIH HHS/ -- U01 DK062420/DK/NIDDK NIH HHS/ -- U01 DK062422/DK/NIDDK NIH HHS/ -- U01 DK062423/DK/NIDDK NIH HHS/ -- U01 DK062429/DK/NIDDK NIH HHS/ -- U01 DK062432/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 Dec 1;314(5804):1461-3. Epub 2006 Oct 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, School of Medicine, University of Pittsburgh, University of Pittsburgh Medical Center Presbyterian, Mezzanine Level, C-Wing, 200 Lothrop Street, Pittsburgh, PA 15213, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17068223" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Case-Control Studies ; Chromosomes, Human, Pair 1/genetics ; Cohort Studies ; Colitis, Ulcerative/genetics ; Crohn Disease/*genetics ; Genetic Markers ; Genetic Predisposition to Disease ; Genetic Testing ; Genome, Human ; Haplotypes ; Humans ; Interleukin-23/metabolism ; Jews/genetics ; Linkage Disequilibrium ; *Polymorphism, Single Nucleotide ; Receptors, Interleukin/*genetics/physiology ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 7
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    Angiopoietin 2 induces astrocyte apoptosis via αvβ5-integrin signaling in diabetic retinopathy (2016)
    Springer Nature
    Details
    Publication Date: 2016-02-19
    Description: Angiopoietin 2 induces astrocyte apoptosis via αvβ5-integrin signaling in diabetic retinopathy Cell Death and Disease 7, e2101 (February 2016). doi:10.1038/cddis.2015.347 Authors: J-H Yun, S W Park, J H Kim, Y-J Park, C-H Cho & J H Kim
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 8
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    IL-22BP is regulated by the inflammasome and modulates tumorigenesis in the intestine (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-10-19
    Description: Chronic mucosal inflammation and tissue damage predisposes patients to the development of colorectal cancer. This association could be explained by the hypothesis that the same factors and pathways important for wound healing also promote tumorigenesis. A sensor of tissue damage should induce these factors to promote tissue repair and regulate their action to prevent development of cancer. Interleukin 22 (IL-22), a cytokine of the IL-10 superfamily, has an important role in colonic epithelial cell repair, and its levels are increased in the blood and intestine of inflammatory bowel disease patients. This cytokine can be neutralized by the soluble IL-22 receptor, known as the IL-22 binding protein (IL-22BP, also known as IL22RA2); however, the significance of endogenous IL-22BP in vivo and the pathways that regulate this receptor are unknown. Here we describe that IL-22BP has a crucial role in controlling tumorigenesis and epithelial cell proliferation in the colon. IL-22BP is highly expressed by dendritic cells in the colon in steady-state conditions. Sensing of intestinal tissue damage via the NLRP3 or NLRP6 inflammasomes led to an IL-18-dependent downregulation of IL-22BP, thereby increasing the ratio of IL-22/IL-22BP. IL-22, which is induced during intestinal tissue damage, exerted protective properties during the peak of damage, but promoted tumour development if uncontrolled during the recovery phase. Thus, the IL-22-IL-22BP axis critically regulates intestinal tissue repair and tumorigenesis in the colon.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3493690/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3493690/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huber, Samuel -- Gagliani, Nicola -- Zenewicz, Lauren A -- Huber, Francis J -- Bosurgi, Lidia -- Hu, Bo -- Hedl, Matija -- Zhang, Wei -- O'Connor, William Jr -- Murphy, Andrew J -- Valenzuela, David M -- Yancopoulos, George D -- Booth, Carmen J -- Cho, Judy H -- Ouyang, Wenjun -- Abraham, Clara -- Flavell, Richard A -- DK-P30-34989/DK/NIDDK NIH HHS/ -- P30 DK034989/DK/NIDDK NIH HHS/ -- R01 DK077905/DK/NIDDK NIH HHS/ -- R01DK077905/DK/NIDDK NIH HHS/ -- U19 AI082713/AI/NIAID NIH HHS/ -- U19-AI082713/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Nov 8;491(7423):259-63. doi: 10.1038/nature11535. Epub 2012 Oct 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23075849" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Transformation, Neoplastic ; Colitis/complications/metabolism/pathology ; Colon/metabolism/pathology ; Colonic Neoplasms/complications/metabolism/pathology ; Disease Models, Animal ; Down-Regulation ; Epithelial Cells/metabolism/pathology ; Genes, APC ; Inflammasomes/*metabolism ; Interleukin-18/metabolism ; Interleukins/deficiency/genetics/metabolism ; Intestines/*metabolism/*pathology ; Mice ; Mice, Knockout ; Receptors, Interleukin/deficiency/genetics/*metabolism ; Time Factors ; Weight Loss
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 9
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    Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-11-07
    Description: Crohn's disease and ulcerative colitis, the two common forms of inflammatory bowel disease (IBD), affect over 2.5 million people of European ancestry, with rising prevalence in other populations. Genome-wide association studies and subsequent meta-analyses of these two diseases as separate phenotypes have implicated previously unsuspected mechanisms, such as autophagy, in their pathogenesis and showed that some IBD loci are shared with other inflammatory diseases. Here we expand on the knowledge of relevant pathways by undertaking a meta-analysis of Crohn's disease and ulcerative colitis genome-wide association scans, followed by extensive validation of significant findings, with a combined total of more than 75,000 cases and controls. We identify 71 new associations, for a total of 163 IBD loci, that meet genome-wide significance thresholds. Most loci contribute to both phenotypes, and both directional (consistently favouring one allele over the course of human history) and balancing (favouring the retention of both alleles within populations) selection effects are evident. Many IBD loci are also implicated in other immune-mediated disorders, most notably with ankylosing spondylitis and psoriasis. We also observe considerable overlap between susceptibility loci for IBD and mycobacterial infection. Gene co-expression network analysis emphasizes this relationship, with pathways shared between host responses to mycobacteria and those predisposing to IBD.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3491803/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3491803/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jostins, Luke -- Ripke, Stephan -- Weersma, Rinse K -- Duerr, Richard H -- McGovern, Dermot P -- Hui, Ken Y -- Lee, James C -- Schumm, L Philip -- Sharma, Yashoda -- Anderson, Carl A -- Essers, Jonah -- Mitrovic, Mitja -- Ning, Kaida -- Cleynen, Isabelle -- Theatre, Emilie -- Spain, Sarah L -- Raychaudhuri, Soumya -- Goyette, Philippe -- Wei, Zhi -- Abraham, Clara -- Achkar, Jean-Paul -- Ahmad, Tariq -- Amininejad, Leila -- Ananthakrishnan, Ashwin N -- Andersen, Vibeke -- Andrews, Jane M -- Baidoo, Leonard -- Balschun, Tobias -- Bampton, Peter A -- Bitton, Alain -- Boucher, Gabrielle -- Brand, Stephan -- Buning, Carsten -- Cohain, Ariella -- Cichon, Sven -- D'Amato, Mauro -- De Jong, Dirk -- Devaney, Kathy L -- Dubinsky, Marla -- Edwards, Cathryn -- Ellinghaus, David -- Ferguson, Lynnette R -- Franchimont, Denis -- Fransen, Karin -- Gearry, Richard -- Georges, Michel -- Gieger, Christian -- Glas, Jurgen -- Haritunians, Talin -- Hart, Ailsa -- Hawkey, Chris -- Hedl, Matija -- Hu, Xinli -- Karlsen, Tom H -- Kupcinskas, Limas -- Kugathasan, Subra -- Latiano, Anna -- Laukens, Debby -- Lawrance, Ian C -- Lees, Charlie W -- Louis, Edouard -- Mahy, Gillian -- Mansfield, John -- Morgan, Angharad R -- Mowat, Craig -- Newman, William -- Palmieri, Orazio -- Ponsioen, Cyriel Y -- Potocnik, Uros -- Prescott, Natalie J -- Regueiro, Miguel -- Rotter, Jerome I -- Russell, Richard K -- Sanderson, Jeremy D -- Sans, Miquel -- Satsangi, Jack -- Schreiber, Stefan -- Simms, Lisa A -- Sventoraityte, Jurgita -- Targan, Stephan R -- Taylor, Kent D -- Tremelling, Mark -- Verspaget, Hein W -- De Vos, Martine -- Wijmenga, Cisca -- Wilson, David C -- Winkelmann, Juliane -- Xavier, Ramnik J -- Zeissig, Sebastian -- Zhang, Bin -- Zhang, Clarence K -- Zhao, Hongyu -- International IBD Genetics Consortium (IIBDGC) -- Silverberg, Mark S -- Annese, Vito -- Hakonarson, Hakon -- Brant, Steven R -- Radford-Smith, Graham -- Mathew, Christopher G -- Rioux, John D -- Schadt, Eric E -- Daly, Mark J -- Franke, Andre -- Parkes, Miles -- Vermeire, Severine -- Barrett, Jeffrey C -- Cho, Judy H -- 068545/Z/02/Wellcome Trust/United Kingdom -- 083948/Z/07/Z/Wellcome Trust/United Kingdom -- 085475/B/08/Z/Wellcome Trust/United Kingdom -- 085475/Z/08/Z/Wellcome Trust/United Kingdom -- 089120/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- AI062773/AI/NIAID NIH HHS/ -- CA141743/CA/NCI NIH HHS/ -- CZB/4/540/Chief Scientist Office/United Kingdom -- DK043351/DK/NIDDK NIH HHS/ -- DK062413/DK/NIDDK NIH HHS/ -- DK062420/DK/NIDDK NIH HHS/ -- DK062422/DK/NIDDK NIH HHS/ -- DK062423/DK/NIDDK NIH HHS/ -- DK062429/DK/NIDDK NIH HHS/ -- DK062429-S1/DK/NIDDK NIH HHS/ -- DK062431/DK/NIDDK NIH HHS/ -- DK062432/DK/NIDDK NIH HHS/ -- DK063491/DK/NIDDK NIH HHS/ -- DK076984/DK/NIDDK NIH HHS/ -- DK084554/DK/NIDDK NIH HHS/ -- DK83756/DK/NIDDK NIH HHS/ -- ETM/137/Chief Scientist Office/United Kingdom -- ETM/75/Chief Scientist Office/United Kingdom -- G0000934/British Heart Foundation/United Kingdom -- G0600329/Medical Research Council/United Kingdom -- G0800675/Medical Research Council/United Kingdom -- G0800759/Medical Research Council/United Kingdom -- G1002033/Medical Research Council/United Kingdom -- K23 DK097142/DK/NIDDK NIH HHS/ -- M01-RR00425/RR/NCRR NIH HHS/ -- P01 DK046763/DK/NIDDK NIH HHS/ -- P01DK046763/DK/NIDDK NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- R01 CA141743/CA/NCI NIH HHS/ -- R01 DK055731/DK/NIDDK NIH HHS/ -- T32 GM007205/GM/NIGMS NIH HHS/ -- T32GM07205/GM/NIGMS NIH HHS/ -- U01 DK062418/DK/NIDDK NIH HHS/ -- U01 DK062420/DK/NIDDK NIH HHS/ -- U01 DK062422/DK/NIDDK NIH HHS/ -- U01 DK062429/DK/NIDDK NIH HHS/ -- U01 DK062431/DK/NIDDK NIH HHS/ -- U01 DK062432/DK/NIDDK NIH HHS/ -- UL1 TR000005/TR/NCATS NIH HHS/ -- UL1 TR000124/TR/NCATS NIH HHS/ -- UL1 TR000124-01/TR/NCATS NIH HHS/ -- Medical Research Council/United Kingdom -- England -- Nature. 2012 Nov 1;491(7422):119-24. doi: 10.1038/nature11582.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1HH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23128233" target="_blank"〉PubMed〈/a〉
    Keywords: Colitis, Ulcerative/genetics/immunology/microbiology/physiopathology ; Crohn Disease/genetics/immunology/microbiology/physiopathology ; Genetic Predisposition to Disease/*genetics ; Genome, Human/genetics ; *Genome-Wide Association Study ; Haplotypes/genetics ; *Host-Pathogen Interactions/genetics/immunology ; Humans ; Inflammatory Bowel Diseases/*genetics/immunology/*microbiology/physiopathology ; Mycobacterium/*immunology/pathogenicity ; Mycobacterium Infections/genetics/microbiology ; Mycobacterium tuberculosis/immunology/pathogenicity ; Phenotype ; Polymorphism, Single Nucleotide/genetics ; Reproducibility of Results
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 10
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    Long-term Loss and Re-formation of the Outer Radiation Belt (2013)
    Wiley
    Details
    Publication Date: 2013-05-28
    Description: [1]  The Earth's outer radiation belt is known to vary often and significantly on various time scales. In this study we have used the data of various instruments onboard the THEMIS spacecraft to study long-term changes of the outer radiation belt electrons around the year 2009. We find that the entire outer belt became extremely weak for nearly a year and was practically lost a few times, each time lasting ~20 days up to ~2 months, before eventually re-forming. This was revealed at a wide energy range from several tens of keV to up to 719 keV, which was covered by the THEMIS spacecraft measurements. The loss of the outer belt was associated with extremely weak solar wind conditions, i.e., low interplanetary magnetic field magnitude and slow solar wind speed. In particular, this set greatly reduced magnetospheric convection and/or injections for a prolonged time interval, which led to a large expansion of the plasmasphere, even beyond geosynchronous altitude and thus invading the majority of the typical outer belt territory for the same prolonged time interval. Consequently, pre existing electrons inside the plasmasphere had enough time to be lost into the atmosphere gradually over a time scale of several days without being supplied with fresh electrons from the plasma sheet under the same reduced convection and/or injections. Plasmaspheric hiss waves with an amplitude of up to a few tens of pT persisted to exist during the gradual decay periods, implying that they are likely responsible for the continual loss of the electrons inside the plasmasphere. A complete re-formation of the outer belt to full intensity was then realized over an interval of a few months. During the re-formation process, the magnetospheric convection and/or injections increased, which led to a gradual increase of whistler chorus wave activity, contraction of the plasmasphere and supply of the plasma sheet electrons at high L-shells. This set first an outward increasing profile of the phase space density, which eventually developed into a profile with a peak at low L of ~5 over a time scale of 1–2 days. In this latter stage, a local acceleration at low L-shells is found to be clearly needed although the radial diffusion process can contribute to some extent, in particular, for particles with a low first adiabatic invariant value.
    Print ISSN: 0148-0227
    Topics: Geosciences , Physics
    Published by Wiley on behalf of American Geophysical Union (AGU).
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